Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Complement C4: A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.Complement C4a: The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A.Complement C1q: A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.Complement C3a: The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.Complement C5a: The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.Complement Activation: The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.Complement C4b: The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Complement C5: C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.Complement C3b: The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.Complement System Proteins: Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).Complement C6: A 105-kDa serum glycoprotein with significant homology to the other late complement components, C7-C9. It is a polypeptide chain cross-linked by 32 disulfide bonds. C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. It is encoded by gene C6.Complement C3c: A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.Complement C3d: A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001).Complement C2: A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Complement C9: A 63-kDa serum glycoprotein encoded by gene C9. Monomeric C9 (mC9) binds the C5b-8 complex to form C5b-9 which catalyzes the polymerization of C9 forming C5b-p9 (MEMBRANE ATTACK COMPLEX) and transmembrane channels leading to lysis of the target cell. Patients with C9 deficiency suffer from recurrent bacterial infections.Receptors, Complement: Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.Complement C1s: A 77-kDa subcomponent of complement C1, encoded by gene C1S, is a SERINE PROTEASE existing as a proenzyme (homodimer) in the intact complement C1 complex. Upon the binding of COMPLEMENT C1Q to antibodies, the activated COMPLEMENT C1R cleaves C1s into two chains, A (heavy) and B (light, the serine protease), linked by disulfide bonds yielding the active C1s. The activated C1s, in turn, cleaves COMPLEMENT C2 and COMPLEMENT C4 to form C4b2a (CLASSICAL C3 CONVERTASE).Complement Membrane Attack Complex: A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.Complement C1r: A 80-kDa subcomponent of complement C1, existing as a SERINE PROTEASE proenzyme in the intact complement C1 complex. When COMPLEMENT C1Q is bound to antibodies, the changed tertiary structure causes autolytic activation of complement C1r which is cleaved into two chains, A (heavy) and B (light, the serine protease), connected by disulfide bonds. The activated C1r serine protease, in turn, activates COMPLEMENT C1S proenzyme by cleaving the Arg426-Ile427 bond. No fragment is released when either C1r or C1s is cleaved.Complement Inactivator Proteins: Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.Complement C7: A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.Complement C3-C5 Convertases: Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.Complement Factor B: A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.Complement Pathway, Alternative: Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement Pathway, Classical: Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement C8: A 150-kDa serum glycoprotein composed of three subunits with each encoded by a different gene (C8A; C8B; and C8G). This heterotrimer contains a disulfide-linked C8alpha-C8gamma heterodimer and a noncovalently associated C8beta chain. C8 is the next component to bind the C5-7 complex forming C5b-8 that binds COMPLEMENT C9 and acts as a catalyst in the polymerization of C9.Complement C1: The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.Receptors, Complement 3b: Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.Complement Factor H: An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).Complement C5b: The larger fragment generated from the cleavage of C5 by C5 CONVERTASE that yields COMPLEMENT C5A and C5b (beta chain + alpha' chain, the residual alpha chain, bound by disulfide bond). C5b remains bound to the membrane and initiates the spontaneous assembly of the late complement components to form C5b-8-poly-C9, the MEMBRANE ATTACK COMPLEX.Complement C2a: The COOH-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S. It is a SERINE PROTEASE. C2a combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Receptor, Anaphylatoxin C5a: A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.Complement Activating Enzymes: Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.Complement Inactivating Agents: Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.Complement Hemolytic Activity Assay: A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Receptors, Complement 3d: Molecular sites on or in B-lymphocytes, follicular dendritic cells, lymphoid cells, and epithelial cells that recognize and combine with COMPLEMENT C3D. Human complement receptor 2 (CR2) serves as a receptor for both C3dg and the gp350/220 glycoprotein of HERPESVIRUS 4, HUMAN, and binds the monoclonal antibody OKB7, which blocks binding of both ligands to the receptor.Anaphylatoxins: Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE CONTRACTION; mast cell HISTAMINE RELEASE; PLATELET AGGREGATION; and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.Complement Fixation Tests: Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.Complement Factor D: A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.Complement Factor I: A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.Complement C4b-Binding Protein: A serum protein that regulates the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It binds as a cofactor to COMPLEMENT FACTOR I which then hydrolyzes the COMPLEMENT C4B in the CLASSICAL PATHWAY C3 CONVERTASE (C4bC2a).Complement C3b Inactivator Proteins: Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.Antigens, CD55: GPI-linked membrane proteins broadly distributed among hematopoietic and non-hematopoietic cells. CD55 prevents the assembly of C3 CONVERTASE or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.Complement C3-C5 Convertases, Classical Pathway: Important enzymes in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Complement C2b: The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.Antigens, CD59: Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)Cobra Venoms: Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Steroid 21-Hydroxylase: An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Complement C3-C5 Convertases, Alternative Pathway: Important enzymes in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Complement C1 Inhibitor Protein: An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Complement C3 Convertase, Alternative Pathway: A serine protease that is the complex of COMPLEMENT C3B and COMPLEMENT FACTOR BB. It cleaves multiple COMPLEMENT C3 into COMPLEMENT C3A (anaphylatoxin) and COMPLEMENT C3B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY.Complement C5 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 5 into COMPLEMENT 5A (anaphylatoxin) and COMPLEMENT 5B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of CLASSICAL PATHWAY C3 CONVERTASE (C4b2a) with an additional COMPLEMENT C3B, or C4b2a3b.Complement C3 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 3 into COMPLEMENT 3A (anaphylatoxin) and COMPLEMENT 3B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of COMPLEMENT 4B and COMPLEMENT 2A (C4b2a).Antigens, CD46: A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.Opsonin Proteins: Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Lupus Erythematosus, Systemic: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Complement C5 Convertase, Alternative Pathway: A serine protease that cleaves multiple COMPLEMENT C5 into COMPLEMENT C5A (anaphylatoxin) and COMPLEMENT C5B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. It is the complex of ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) with an additional COMPLEMENT C3B, or C3bBb3b.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Complement Pathway, Mannose-Binding Lectin: Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Properdin: A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.Complement C5a, des-Arginine: A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Mice, Inbred C57BLMacrophage-1 Antigen: An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.Serum: The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.Glomerulonephritis, Membranoproliferative: Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.Immunoglobulin M: A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.Genetic Complementation Test: A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Schistosoma: A genus of trematode flukes belonging to the family Schistosomatidae. There are over a dozen species. These parasites are found in man and other mammals. Snails are the intermediate hosts.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Glomerulonephritis: Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.Arteriolosclerosis: Thickening of the walls of small ARTERIES or ARTERIOLES due to cell proliferation or HYALINE deposition.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Cloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Immunity, Innate: The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Antigens, CD: Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.Mice, Inbred BALB CBlood Bactericidal Activity: The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.Mannose-Binding Lectin: A specific mannose-binding member of the collectin family of lectins. It binds to carbohydrate groups on invading pathogens and plays a key role in the MANNOSE-BINDING LECTIN COMPLEMENT PATHWAY.DNA: A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Immunoglobulins: Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.Complement C3 Nephritic Factor: An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.Haptoglobins: Plasma glycoproteins that form a stable complex with hemoglobin to aid the recycling of heme iron. They are encoded in man by a gene on the short arm of chromosome 16.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Surface Plasmon Resonance: A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.Gene Dosage: The number of copies of a given gene present in the cell of an organism. An increase in gene dosage (by GENE DUPLICATION for example) can result in higher levels of gene product formation. GENE DOSAGE COMPENSATION mechanisms result in adjustments to the level GENE EXPRESSION when there are changes or differences in gene dosage.Lupus Nephritis: Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).Peptides, Cyclic: Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).Antibodies, Antinuclear: Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.Cosmids: Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Homozygote: An individual in which both alleles at a given locus are identical.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Bacterial Proteins: Proteins found in any species of bacterium.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Species Specificity: The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Mannose-Binding Protein-Associated Serine Proteases: Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system.ZymosanPedigree: The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.HLA Antigens: Antigens determined by leukocyte loci found on chromosome 6, the major histocompatibility loci in humans. They are polypeptides or glycoproteins found on most nucleated cells and platelets, determine tissue types for transplantation, and are associated with certain diseases.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Sequence Homology, Nucleic Acid: The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. Sequence homology is an indication of the genetic relatedness of different organisms and gene function.Kinetics: The rate dynamics in chemical or physical systems.Exons: The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Molecular Weight: The sum of the weight of all the atoms in a molecule.Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.B-Lymphocytes: Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.Restriction Mapping: Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.Antibody Formation: The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Genes: A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.Streptococcus pneumoniae: A gram-positive organism found in the upper respiratory tract, inflammatory exudates, and various body fluids of normal and/or diseased humans and, rarely, domestic animals.Collectins: A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.Blotting, Southern: A method (first developed by E.M. Southern) for detection of DNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.DNA, Complementary: Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Blotting, Northern: Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Polymorphism, Restriction Fragment Length: Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Protein PrecursorsLipopolysaccharides: Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.Steroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.Macular Degeneration: Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.Chromosome Mapping: Any method used for determining the location of and relative distances between genes on a chromosome.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization: A mass spectrometric technique that is used for the analysis of large biomolecules. Analyte molecules are embedded in an excess matrix of small organic molecules that show a high resonant absorption at the laser wavelength used. The matrix absorbs the laser energy, thus inducing a soft disintegration of the sample-matrix mixture into free (gas phase) matrix and analyte molecules and molecular ions. In general, only molecular ions of the analyte molecules are produced, and almost no fragmentation occurs. This makes the method well suited for molecular weight determinations and mixture analysis.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Immune Adherence Reaction: A method for the detection of very small quantities of antibody in which the antigen-antibody-complement complex adheres to indicator cells, usually primate erythrocytes or nonprimate blood platelets. The reaction is dependent on the number of bound C3 molecules on the C3b receptor sites of the indicator cell.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Mice, Inbred DBAAntibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.Arthritis, Rheumatoid: A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.Staphylococcus aureus: Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Escherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.Fluorescent Antibody Technique: Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Proteomics: The systematic study of the complete complement of proteins (PROTEOME) of organisms.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Gene Library: A large collection of DNA fragments cloned (CLONING, MOLECULAR) from a given organism, tissue, organ, or cell type. It may contain complete genomic sequences (GENOMIC LIBRARY) or complementary DNA sequences, the latter being formed from messenger RNA and lacking intron sequences.Interleukin-6: A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.

C1qRP is a heavily O-glycosylated cell surface protein involved in the regulation of phagocytic activity. (1/737)

C1q, mannose-binding lectin (MBL), and pulmonary surfactant protein A (SPA) interact with human monocytes and macrophages, resulting in the enhancement of phagocytosis of suboptimally opsonized targets. mAbs that recognize a cell surface molecule of 126,000 Mr, designated C1qRP, have been shown to inhibit C1q- and MBL-mediated enhancement of phagocytosis. Similar inhibition of the SPA-mediated enhancement of phagocytosis by these mAbs now suggests that C1qRP is a common component of a receptor for these macromolecules. Ligation of human monocytes with immobilized R3, a IgM mAb recognizing C1qRP, also triggers enhanced phagocytic capacity of these cells in the absence of ligand, verifying the direct involvement of this polypeptide in the regulation of phagocytosis. While the cDNA for C1qRP encodes a 631 amino acid membrane protein, Chinese hamster ovary cells transfected with the cDNA of the C1qRP coding region express a surface glycoprotein with the identical 126,000 Mr in SDS-PAGE as the native C1qRP. Use of glycosylation inhibitors, cleavage of the mature C1qRP with specific glycosidases, and in vitro translation of C1qRP cDNA demonstrated that both posttranslational glycosylation and the nature of the amino acid sequence of the protein contribute to the difference between its predicted m.w. and its migration on SDS-PAGE. These results verify that the cDNA cloned codes for the mature C1qRP, that C1qRP contains a relatively high degree of O-linked glycoslyation, and that C1qRP cross-linked directly by monoclonal anti-C1qRP or engaged as a result of cell surface ligation of SPA, as well as C1q and MBL, enhances phagocytosis.  (+info)

Alzheimer's beta-amyloid peptides can activate the early components of complement classical pathway in a C1q-independent manner. (2/737)

beta-Amyloid (beta-A) accumulates in the brain of patients with Alzheimer's disease (AD) and is presumably involved in the pathogenesis of this disease, on account of its neurotoxicity and complement-activating ability. Although assembly of beta-A in particular aggregates seems to be crucial, soluble non-fibrillar beta-A may also be involved. Non-fibrillar beta-A does not bind C1q, so we investigated alternative mechanisms of beta-A-dependent complement activation in vitro. On incubation with normal human plasma, non-fibrillar beta-A 1-42, and truncated peptide 1-28, induced dose-dependent activation of C1s and C4, sparing C3, as assessed by densitometric analysis of immunostained membrane after SDS-PAGE and Western blotting. The mechanism of C4 activation was not dependent on C1q, because non-fibrillar beta-A can still activate C1s and C4 in plasma genetically deficient in C1q (C1qd). In Factor XII-deficient plasma (F.XIId) the amount of cleaved C4 was about 5-10% less that in C1qd and in normal EDTA plasma; the reconstitution of F.XIId plasma with physiologic concentrations of F.XII resulted in an increased (8-15%) beta-A-dependent cleavage of C4. Thus our results indicate that the C1q-independent activation of C1 and C4 can be partially mediated by the activation products of contact system. Since the activation of contact system and of C4 leads to generation of several humoral inflammatory peptides, non-fibrillar beta-A might play a role in initiating the early inflammatory reactions leading to a multistep cascade contributing to neuronal and clinical dysfunction of AD brain.  (+info)

C1q binding to liposomes is surface charge dependent and is inhibited by peptides consisting of residues 14-26 of the human C1qA chain in a sequence independent manner. (3/737)

Complement activation by anionic liposomes proceeds by antibody-independent, C1q-initiated activation of the classical pathway. Purified C1q bound to anionic liposomes in an acidic lipid concentration-dependent manner. Saturation binding, but not the apparent association constant, was enhanced by increasing the cardiolipin content of the liposomes or decreasing either the pH or ionic strength of the reaction mixture. These observations indicate the involvement of electrostatic factors in the binding. A highly cationic region in the collagen-like domain of C1q comprised of residues 14-26 of the C1qA polypeptide chain was assessed for involvement in liposome binding. This region has previously been shown to mediate C1q binding to other immunoglobulin-independent activators of the classical pathway of complement. Peptides containing residues 14-26 of C1qA, denoted C1qA14-26, inhibited C1q binding to and complement activation by anionic liposomes. The inhibitory capacity of these cationic peptides had no sequence or conformation specificity. Rather, the amount of positive charge on the peptides was the determining factor. When present in excess, peptides with five cationic residues inhibited C1q binding and complement activation; however, C1q peptides with only two cationic residues did not. In addition to the C1qA14-26 region, other parts of C1q that contain cationic residues may also be involved in C1q binding to anionic liposomes.  (+info)

Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation. (4/737)

C1q-deficient (C1qa-/-) mice develop antinuclear Abs and glomerulonephritis (GN) characterized by multiple apoptotic bodies. To explore the contribution of C3 activation to the induction of spontaneous GN, C1qa-/- mice were crossed with factor B- and C2-deficient (H2-Bf/C2-/-) mice. GN was present in 64% of the 45 C1qa/H2-Bf/C2-/- mice compared with 8% of the 65 H2-Bf/C2-/- mice and none of the 24 wild-type controls. IgG was detected in the glomeruli of diseased C1qa/H2-Bf/C2-/- kidneys. However, glomerular staining for C3 was absent. Increased numbers of glomerular apoptotic bodies were detected in undiseased C1qa/H2-Bf/C2-/- kidneys. These findings support the hypothesis that C1q may play a role in the clearance of apoptotic cells without the necessity for C3 activation and demonstrate that the activation of C3 is not essential for the development of GN in this spontaneous model of lupus-like disease.  (+info)

EMILIN, a component of the elastic fiber and a new member of the C1q/tumor necrosis factor superfamily of proteins. (5/737)

EMILIN (elastin microfibril interface located protein) is an extracellular matrix glycoprotein abundantly expressed in elastin-rich tissues such as blood vessels, skin, heart, and lung. It occurs associated with elastic fibers at the interface between amorphous elastin and microfibrils. Avian EMILIN was extracted from 19-day-old embryonic chick aortas and associated blood vessels and purified by ion-exchange chromatography and gel filtration. Tryptic peptides were generated from EMILIN and sequenced, and degenerate inosine-containing oligonucleotide primers were designed from some peptides. A set of primers allowed the amplification of a 360-base pair reverse transcription polymerase chain reaction product from chick aorta mRNA. A probe based on a human homologue selected by comparison of the chick sequence with EST data base was used to select overlapping clones from both human aorta and kidney cDNA libraries. Here we present the cDNA sequence of the entire coding region of human EMILIN encompassing an open reading frame of 1016 amino acid residues. There was a high degree of homology (76% identity and 88% similarity) between the chick C terminus and the human sequence as well as between the N terminus of the mature chick protein where 10 of 12 residues, as determined by N-terminal sequencing, were identical or similar to the deduced N terminus of human EMILIN. The domain organization of human EMILIN includes a C1q-like globular domain at the C terminus, a collagenous stalk, and a longer segment in which at least four heptad repeats and a leucine zipper can be identified with a high potential for forming coiled-coil alpha helices. At the N terminus there is a cysteine-rich sequence stretch similar to a region of multimerin, a platelet and endothelial cell component, containing a partial epidermal growth factor-like motif. The native state of the recombinantly expressed EMILIN C1q-like domain to be used in cell adhesion was determined by CD spectra analysis, which indicated a high value of beta-sheet conformation. The EMILIN C1q-like domain promoted a high cell adhesion of the leiomyosarcoma cell line SK-UT-1, whereas the fibrosarcoma cell line HT1080 was negative.  (+info)

Antibody-independent classical complement pathway activation and homologous C3 deposition in xeroderma pigmentosum cell lines. (6/737)

Of human malignantly transformed cell lines, xeroderma pigmentosum (XP) cell lines were found to be highly susceptible to homologous complement (C): cells were opsonized by C3 fragments on incubation with diluted normal human serum. C3 fragment deposition on XP cells was Ca2+-dependent and occurred on live cells but not UV-irradiated apoptotic cells. (Ca2+ is required for activation of the classical C pathway via C1q and the lactin pathway via mannose binding lectin (MBL), and the surface of apoptotic cells usually activates the alternative C pathway.) In this study we tested which of the pathways participates in XP cell C3 deposition. In seven cell lines that allowed C3 deposition (i), Clq was shown to be essential but MBL played no role in C activation, (ii) Cls but not MASP bound XP cells for activation, (iii) no antibodies recognizing XP cells were required for homologous C3 deposition, and (iv) the alternative pathway barely participated in C3 deposition. Furthermore, the levels of C-regulatory proteins for host cell protection against C, decay-accelerating factor (DAF, CD55) and membrane cofactor protein (MCP, CD46), were found to be relatively low in almost all XP cell lines compared with normal cells. These results indicate that XP cells activate the classical C pathway in an antibody-independent manner through the expression of a molecule which directly attracts C1q in a C-activating form, and that relatively low levels of DAF and MCP on XP cells facilitate effective C3 deposition. The possible relationship between the pathogenesis of XP and our findings is discussed.  (+info)

Neuronal protection in stroke by an sLex-glycosylated complement inhibitory protein. (7/737)

Glycoprotein adhesion receptors such as selectins contribute to tissue injury in stroke. Ischemic neurons strongly expressed C1q, which may target them for complement-mediated attack or C1qRp-mediated clearance. A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion. The extracellular domain of soluble complement receptor-1 (sCR1) was sialyl Lewis x glycosylated (sCR1sLex) to inhibit complement activation and endothelial-platelet-leukocyte interactions. sCR1 and sCR1sLex colocalized to ischemic cerebral microvessels and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes. Additional benefit was conferred by sialyl Lewis x glycosylation of the unmodified parent sCR1 molecule.  (+info)

Role of complement component C1q in the IgG-independent opsonophagocytosis of group B streptococcus. (8/737)

We investigated the role of complement component C1q in the IgG-independent opsonophagocytosis of type III group B Streptococcus (GBS) by peripheral blood leukocytes. We report that C1q binds to type III GBS both in normal human serum deficient in IgG specific for type III capsular polysaccharide and in a low-ionic strength buffer. The dissociation constant Kd ranged from 2.0 to 5.5 nM, and the number of binding sites Bmax ranged from 630 to 1360 molecules of C1q per bacterium (CFU). An acapsular mutant strain of GBS bound C1q even better than the wild type, indicating that the polysaccharide capsule is not the receptor for C1q. In serum, binding of C1q to GBS was associated with activation of the classical complement pathway. However, normal human serum retained significant opsonic activity after complete depletion of C1q, suggesting that the serum contains a molecule that is able to replace C1q in opsonization and/or complement activation. Mannan-binding lectin, known to share some functions with C1q, appeared not to be involved, since its depletion from serum had little effect on opsonic activity. Excess soluble C1q or its collagen-like fragment inhibited phagocytosis mediated by normal human serum, suggesting that C1q may compete with other opsonins for binding to receptor(s) on phagocytes. We conclude that, although C1q binds directly to GBS, C1q binding is neither necessary nor sufficient for IgG-independent opsonophagocytosis. The results raise the possibility that additional unknown serum factor(s) may contribute to opsonization of GBS directly or via a novel mechanism of complement activation.  (+info)

C1q, the first component of the classical pathway of the complement system, interacts with various cell types and triggers a variety of cell-specific cellular responses, such as oxidative burst, chemotaxis, phagocytosis, etc. Different biological responses are attributed to the interaction of C1q with more than one putative cell-surface C1q receptor/C1q-binding protein. Previously, it has been shown that C1q-mediated oxidative burst by neutrophils is not linked to G-protein-coupled fMet-Leu-Phe-mediated response. In the present study, we have investigated neutrophil migration brought about by C1q and tried to identify the signal-transduction pathways involved in the chemotactic response. We found that C1q stimulated neutrophil migration in a dose-dependent manner, primarily by enhancing chemotaxis (directed movement) rather than chemokinesis (random movement). This C1q-induced chemotaxis could be abolished by an inhibitor of G-proteins (pertussis toxin) and PtdIns(3,4,5)P3 kinase (wortmannin and ...
Abstract: Recent studies have focused on elucidating the contribution of individual complement proteins to post-ischemic cellular injury. As the timing of complement activation and deposition after cerebral ischemia is not well understood, our study investigates the temporal pattern of C1q accumulation after experimental murine stroke. Brains were harvested from mice subjected to transient focal cerebral ischemia at 3, 6, 12, and 24 hr post reperfusion. Western blotting and light microscopy were employed to determine the temporal course of C1q protein accumulation and correlate this sequence with infarct evolution observed with TTC staining. Confocal microscopy was utilized to further characterize the cellular localization and characteristics of C1q deposition. Western Blot analysis showed that C1q protein begins to accumulate in the ischemic hemisphere between 3 and 6 hr post-ischemia. Light microscopy confirmed these findings, showing concurrent C1q protein staining of neurons. Confocal ...
The invention provides a series of G.alpha..sub.q protein variants that functionally couple to sensory cell receptors such as taste GPCRs (TRs) and olfactory GPCRs (ORs) in an overly promiscuous manner. According to the invention, the functional coupling can be determined, for example, by measuring changes in intracellular IP3, or calcium. In a particular embodiment, the G.alpha..sub.q protein variants can be expressed in mammalian cell lines or Xenopus oocytes, and then evaluated using calcium fluorescence imaging and electrophysiological recording.
Influence of the Gαq-protein on myocardial infarct size of the bone marrow-engrafted Gαq-knockout-mouse in a ischemia/reperfusion-model Platelets play a key role in the pathogenesis of an acute myocardial infarction. Thrombus formation, which is mediated by the activation of platelets, results in the occlusion of the coronary artery. On the other hand, agglutinated platelets in the small myocardial vessels impair the myocardial microcirculation. Due to their pro-inflammatory effects, platelets also contribute to the pathogenesis of ischemia/reperfusion injury. The myocardium of Gαq-deficient mice showed a reduced susceptibility to ischemia and reperfusion compared to that of wild-type mice (HEUER, in preparation). Activation of platelets lacking the Gαq-protein is markedly impaired, resulting not only in an increased haemophilia but also in a decreased thrombophilia of Gαq-deficient mice. A bone marrow transplantation was performed to investigate whether the impaired platelet-activation is ...
In a previous study we isolated a series of rat monoclonal antibodies to the human leukocyte common (LC) antigen and demonstrated that synergistic complement lysis was possible between IgG2b antibodies which recognised different epitopes. In this report we have examined the mechanisms that were involved in synergistic lysis. We found that the number of C1q binding sites increased from 30,000 to 40,000/cell using a single antibody to 90,000/cell when two IgG2b antibodies to different epitopes were used together. The affinity of C1q binding also increased approx. 3-fold for the synergistic pair, and there was a similar increase in the rate of C1 activation. Combinations of an IgG2b with IgG1 or IgG2a gave much smaller increases in the amount of C1q bound and in the rate of C1 activation. Despite the large number of C1q molecules bound with the optimal synergistic pair and the increased rate of C1 activation, lysis was inefficient in serum depleted of Factor D, suggesting a requirement for the alternative
Combining with the C1q component of the classical complement cascade and transmitting the signal from one side of the membrane to the other to initiate a change in cell activity.
In addition to binding to cadherins, Gα12 and Gα13 were found to play important roles in other adhesion molecule-dependent cellular functions. In platelets lacking Gαq, coactivation of the Gαq- and Gα12/13-coupled thromboxane A2 receptor and the Gαi-coupled ADP receptor P2Y12 resulted in irreversible integrin αIIbβ3-mediated platelet aggregation (Nieswandt et al., 2002). Because Gαq-deficient platelets fail to respond to thromboxane A2 in αIIbβ3 activation assay, the study demonstrates converging signaling of Gα12/13 and Gαi, which is sufficient to overcome Gαq deficiency for αIIbβ3 activation. A recent study provided evidence for a role of the G12 subfamily in integrin signaling by demonstrating a direct interaction of Gα13 with the cytoplasmic domain of the β3 integrin (Gong et al., 2010). Ligand binding to the integrin αIIbβ3, as well as GTP loading of Gα13, promotes this interaction, supporting an "outside-in" signaling mechanism that favors cell spreading through the ...
* found in: Quartz (particle size), SIGMA Quercetin-3-D-xyloside |=97.0% (HPLC), Quercetin =95% (HPLC), solid, QuadraPure™ TU, 400-600 micron, metal..
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Complete information for MIR548Q gene (RNA Gene), MicroRNA 548q, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
It has been suggested that the human C1qRp is a receptor for the complement component C1q; however, there is no direct evidence for an interaction between C1q and C1qRp. In this study, we demonstrate that C1q does not show enhanced binding to C1qRp-transfected cells compared with control cells. Furthermore, a soluble recombinant C1qRp-Fc chimera failed to interact with immobilized C1q. The proposed role of C1qRp in the phagocytic response in vivo is also unsupported in that we demonstrate that this molecule is not expressed by macrophages in a variety of human tissues and the predominant site of expression is on endothelial cells. Studies on the rodent homolog of C1qRp, known as AA4, have suggested that this molecule may function as an intercellular adhesion molecule. Here we show that C1qRp is the Ag recognized by several previously described mAbs, mNI-11 and two anti-CD93 Abs (clones X2 and VIMD2b). Interestingly, mNI-11 (Fab) has been shown to promote monocyte-monocyte and ...
Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions ...
Lamont & Tonelli talked to Mr. Skin for his weekly fun bags forecast, including the return of "The L Word: Generation Q" on Showtime, a nude photo of Amy Schumer on her Instagram. Plus, Jennifer Lopez and Lizzo wearing thongs in their movie "Hustlers.". ...
ASSIGNMENT STATEMENTS * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1762:E10b] IS (3) OR ([Q1763:E10c] IS (1 OR DK OR RF) AND [Q1762:E10b] IS (A)) OR [Q1765:E10Y1b1] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1767] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1760:E10] IS (A) AND [Q1760:E10] IS (NE DK AND NE RF) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1766] IS (3 OR 5) OR ([Q1761:E10a] IS (3) OR ([Q1762:E10b] IS (1 OR DK OR RF) AND [Q1761:E10a] IS (A))) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1764:E10b1] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1763:E10c] IS (3) OR [Q1764:E10b1] IS (1 OR DK OR RF) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1:PR1] IS (GE 0 OR LE 0) * if [Q1800] IS (A) AND [Q1800] IS (NE DK AND NE RF) then [R1843.E24Y2.ASSIGN DR/OUTPATIENT $] = system calculation: 1800 * if [Q1804] IS (3 OR 5) then [R1843.E24Y2.ASSIGN DR/OUTPATIENT $] = 20000 * if [Q1803] IS (3) OR [Q1804] IS (1 OR DK OR RF) ...
XY, +20, dup(1)(q21q42), der(2)t(2;14)(q37;q24)t(14;18)(q32;q21), t(8;22)(q24;q11.2), der(14)t(X;14)(p21;p13)t(14;18)(q32;q21), dup(17)(q11q22), der(18)t(14;18)(q32;q21); ...
C5b-9小鼠单克隆抗体[aE11](ab66768)可与马, 人, 猪, 猴, 狒狒样本反应并经ELISA, IHC, Flow Cyt, ICC/IF实验严格验证,被7篇文献引用并得到1个独立的用户反馈。
C9小鼠单克隆抗体[aE11](ab90801)可与马, 人, 猪样本反应并经ELISA, IHC, FuncS, Flow Cyt实验严格验证,被5篇文献引用。所有产品均提供质保服务,中国75%以上现货。
NUMBER OF TESTS TAKEN: 210 (no excused absences) Q2Q1 Q2Q2 Q2Q3 Q2Q4 Quiz2 AVERAGE 9.8 7.6 8.9 10.5 36.8 STDEV 2.9 3.2 1.5 2.9 7.3 AVEDEV 2.3 2.6 1.2 2.2 5.9 MINIMUM 1.0 0.0 2.0 2.5 13.0 MAXIMUM 15.0 10.0 10.0 15.0 49.0 Max. Possible 10.0 10.0 10.0 10.0 50.0 ...
XY, +5, +5, +6, -8, +mar, der(5)t(5;6)(q35;p21), t(5;6)(q35;p21), add(10)(q23-24), der(13)t(1;13)(q32;p11)t(1;13)(q21;q34), add(16)(q23), add(19)(p13), 33% - 74(74- ...
All your questions about OldPain2Go answered in this Q and A. Q. Does it work? A. A. Yes it can with a client who is positively wanting to be pain-free.
过了due date宝宝依然没有出动的样子。 爷爷奶奶也因签证到期不得不回国了。 遗憾没能见到小孙女。. 最后一两周Q小某天天在我耳边叨叨让我多走路,帮助顺产。 我也尽力走啊~ 那时候真的走一会就累得想坐下休息。 生前的一晚Q小某还对肚子说,Charlotte你快出来吧。你如果今晚出动,等你一岁生日时爸爸给你买个大hello kitty猫。 结果Charlotte还真听话。 清晨太阳还没升起时,我在睡梦中忽然感觉水破了。 我也没有洗澡,叫Q小某起床准备去医院。我父母刚好在,也马上起来给我做了碗面汤,急急忙忙吃后我和Q小某就去医院了。 7AM左右就到了医院。 就不细写产经了。总而言之,催产催不出来,下午五点就刨了(5:15pm 宝宝的出生时间,to be exact)。 ...
Dietary Supplement Sugar, Salt and Starch Free Vision Support Supplement Facts Serving Size 1 Tablet Amount Per Serving - % Daily Value VitaminA (asretinolpalmitate) 5000 IU 100% VitaminC (asL-ascorbicacid) 10 mg 17% Calcium (asdicalciumphosphate) 55 mg 6% Other Ingredients: Dicalcium Phosphate, Microcrystalline Cellulose, Silica, Vegetable Cellulose, Vegetable Magnesium Stearate. IMPORTANT INFORMATION: Long term intake of high levels of Vitamin A (excluding that sourced from beta-carotene) may increase the risk of osteoporosis in postmenopausal women. Do not take this product if taking other Vitamin A (retinol form) supplements. Not for chronic use. Not formulated for use in children. If you are pregnant, nursing, taking any medication or have a medical condition, please consult your medical practitioner before taking any dietary supplement. Solgars Dry Vitamin A Tablets
In invertebrates, the medicinal leech is considered to be an interesting and appropriate model to study neuroimmune mechanisms. Indeed, this non-vertebrate animal can restore normal function of its central nervous system (CNS) after injury. Microglia accumulation at the damage site has been shown to be required for axon sprouting and for efficient regeneration. We characterized HmC1q as a novel chemotactic factor for leech microglial cell recruitment. In mammals, a C1q-binding protein (C1qBP alias gC1qR), which interacts with the globular head of C1q, has been reported to participate in C1q-mediated chemotaxis of blood immune cells. In this study, we evaluated the chemotactic activities of a recombinant form of HmC1q and its interaction with a newly characterized leech C1qBP that acts as its potential ligand. Recombinant HmC1q (rHmC1q) was produced in the yeast Pichia pastoris. Chemotaxis assays were performed to investigate rHmC1q-dependent microglia migration. The involvement of a C1qBP-related
Results Anti-C1q antibodies were more prevalent than anti-ds DNA (n=41,93.2%)in pSLE patients of the current study, which correlated significantly with proteinuria and decreased complement levels (p,0.05). Anti-C1q levels were significantly elevated in patients with class III/IV nephritis compared II/V nephritis. pSLE patients with active nephritis at the time of sample collection demonstrated significantly elevated levels of anti-C1q antibodies compared to those without active nephritis. Anti-C1q antibodies were more sensitive and specific than anti-dsDNA in pSLE patients ...
Highlights: • A human monoclonal antibody against influenza virus was produced from a volunteer. • The antibody was generated from the PBMCs of the volunteer using the fusion method. • The antibody neutralized heterosubtypically group 1 influenza A viruses (H1 and H9). • The antibody targeted a novel epitope in globular head region of the hemagglutinin. • Sequences of the identified epitope are highly conserved among H1 and H9 subtypes. - Abstract: Most neutralizing antibodies elicited during influenza virus infection or by vaccination have a narrow spectrum because they usually target variable epitopes in the globular head region of hemagglutinin (HA). In this study, we describe a human monoclonal antibody (HuMAb), 5D7, that was prepared from the peripheral blood lymphocytes of a vaccinated volunteer using the fusion method. The HuMAb heterosubtypically neutralizes group 1 influenza A viruses, including seasonal H1N1, 2009 pandemic H1N1 (H1N1pdm) and avian H9N2, with a strong ...
We are interested in interactions between the two fundamental cell types of the nervous system, neurons and glia. My laboratory seeks to understand how neuron-glia communication facilitates the formation, elimination and plasticity of synapses-the points of communication between neurons-during both healthy development and disease.. We focus on the role of neuron-glia and neural-immune interactions in the patterning of neural circuits. We and our collaborators have identified an unexpected role for glia and components of the innate immune system in synaptic pruning. We find that astrocytes induce neuronal expression of complement C1q, the initiating protein of the classical complement cascade (which tags unwanted cells and debris for elimination in the immune system). C1q and downstream complement proteins target synapses and are required for synapse elimination in the developing visual system. Importantly, we find that C1q becomes aberrantly upregulated and is relocalized to synapses in the ...
To evaluate whether ischemic myocardium releases molecules that react with the first component of complement, we studied cardiac lymph from eight dogs before and at intervals after coronary artery occlusion and reperfusion. Before occlusion, the dogs were injected intravenously with radiolabeled human C1q. Labeled C1q could be detected in the cardiac lymph within minutes following injection. Rabbit antisera, prepared against substances precipitated from postreprefusion cardiac lymph by anti-human C1q, also reacted with specific constituents of isolated cardiac sarcoplasmic reticulum and mitochondria. To evaluate whether mitochondria are the source of these C1q-binding proteins, we isolated intramyofibrillar and subsarcolemmal mitochondria from canine heart and incubated sonicates of these with purified C1q, immobilized on nitrocellulose. Molecules bound to the immobilized C1q were removed with 0.1% sodium dodecyl sulfate, fractionated under reducing conditions by polyacrylamide gel ...
The C-reactive protein (CRP) is a cyclic pentameric pentraxin family acute phase protein compound of five identical noncovalently bound nonglycosylated subunits (each subunit 24 kDa; physiologic CRP molecule 117,5 kDa). CRP is produced by the liver and its plasma levels rise dramatically during inflammatory processes occuring in the body. CRP is an initiator of classical complement cascade, binds to several nuclear components (chromatin, histones, etc.) and is also believed to play an important role in innate immunity. Patients with elevated basal levels of CRP are at increased risk for hypertension and cardiovascular disease ...
Previous studies have shown that complement opsonization is required for efficient phagocytosis of dying cells in vitro (6, 7) and that uptake of these opsonized cells is associated with expression of the antiinflammatory cytokine, TGF-β (6). Three observations, namely that C1q binds to apoptotic cells in vitro (10), that apoptotic cells accumulate in the kidneys of mice deficient in C1q (4), and that complement activation on apoptotic cells promotes phagocytosis of these cells by macrophages in vitro, suggest a pivotal role for complement in noninflammatory clearance of dying cells. Here, we report that IgM antibodies in normal individuals are quantitatively most important for C1q binding and C3b/bi activation on the apoptotic cell surface and that these natural antibodies bind to lysophosphorylcholine that is exposed on cells undergoing apoptosis.. Since IgM bound to apoptotic cells by the Fab, rather than the Fc, portion of the Ig, binding could be attributed to antibody recognition of an ...
KUALA LUMPUR (Aug 30): DutaLand Bhd returned to the black in the fourth quarter ended June 30, 2017 (4QFY17) with a net profit of RM15.08 million vers...
effect. Instead of specifying gamma directly, we select two quantities that are more intuitive and together define gamma. The first is theta, a threshold value that defines a high-impact mutation . The second is q, the fraction of mutations that exceed this threshold in their effect. For example, a user can first define a high-impact mutation as one that results in 10% or more change in fitness (theta = 0.1) relative to the scale factor and then specify that 0.001 of all mutations (q = 0.001) be in this category. Inside the code the value of is computed that satisfies these requirements. We reiterate that Mendel uses the same value for gamma, and thus the same values for theta and q, for both favorable and deleterious mutations. Figure 3.1 shows the effect of the parameter q on the shape of the distribution of fitness effect. Note that for each of the cases displayed the large majority of mutations are nearly neutral, that is, they have very small effects. Since a utation s effect on fitness can ...
Kur një rrëfim na merr me vete, përvetësojmë identitetin e personazhit dhe e stimulojmë përvojën e tij në jetën reale Shumë shpesh na ndodh që gjatë leximit të një libri, të apasionohemi aq shumë pas historisë, sa të fillojmë të identifikohemi me protagonistin e saj duke kërkuar pika të përbashkëta me të ose të kopjojmë sjelljen dhe mendimet e tij. Sipas një studimi të Universitetit shtetëror të Ohajos, ky është një proces shumë normal që studiuesit e kanë quajtur "përvetësimi i përvojës", ose procesi spontan që çon në përvetësimin e identitetit të një personazhi në një rrëfim të shkruar në një libër dhe më pas stimulimi i përvojës së tij në jetën reale. Pra, në një farë mënyrë, jeni duke humbur brenda historisë së shkruar (në mënyrë letrare) dhe e gjeni veten si pa kuptuar duke vepruar dhe menduar njësoj si protagonisti i romanit, për të arritur deri atje sa të modifikoni sjelljen tuaj në mënyrë që të jetë e ...
I regularly use resource Q on FPLC and the loaded protein always has imidazole. In fact I plan to hook up an anion exchange column in series with the Ni-NTA column and do both the purifications together to save time ...
Complete information for C1QBPP3 gene (Pseudogene), Complement C1q Binding Protein Pseudogene 3, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
46,Y,t(X;14;7)(q11;p11;q?21),t(1;8)(q21;p21),t(2;20)(p13;q13),t(5;16) (p13;q12),der(15)t(15;18)(q15;p11),der(17)t(17;18)(q23;q21),der(18)t (15;18)t(17;18)/46,Y,t(X;10)(p22;q21),t(2;5)(p23;q11),t(6;12)(q23;q21)/46, XY,der(1)t(1;17)(p31;q11)del(1)(q23),dup(1)(q21q?41),?add(6)(q25),t(7;8) (p11;q24),t(10;11)(p11;q23),?t(11;18)(p14;p11),?t(13;16)(q32;q22),t(14;22) (q22;q11),der(17)t(1;17)(p31;q11)/46,XY,inv(6)(p11p21),t(14;15)(p11;q22), inv(17)(q11q25)/46,XY,t(1;3)(q21;p21),t(1;5;13)(q21;q22;q22),t(2;16) (p13;q13),t(11;18)(q21;q21),del(15)(q24 ...
RS6B_SCHPO (Q9C0Z7 ), RS6B_YEAST (P0CX38 ), RS6E_AERPE (Q9Y9B6 ), RS6E_ARCFU (O29739 ), RS6E_CALMQ (A8MA52 ), RS6E_HALLT (B9LR51 ), RS6E_HALMA (P21509 ), RS6E_HALS3 (B0R815 ), RS6E_HALSA (Q9HMJ5 ), RS6E_HALWD (Q18DP5 ), RS6E_HYPBU (A2BJZ7 ), RS6E_METAC (Q8TQL4 ), RS6E_METAR (Q0W8B4 ), RS6E_METBF (Q466D6 ), RS6E_METBU (Q12Z92 ), RS6E_METJA (P54067 ), RS6E_METKA (Q8TVE6 ), RS6E_METMA (Q8PU79 ), RS6E_METS5 (A4YIY0 ), RS6E_METST (Q2NGM7 ), RS6E_METTH (O26360 ), RS6E_NANEQ (Q74MJ5 ), RS6E_NATPD (Q3ISW0 ), RS6E_NITMS (A9A110 ), RS6E_PYRAB (Q9UYS3 ), RS6E_PYRAE (Q8ZX25 ), RS6E_PYRAR (A4WIK0 ), RS6E_PYRCJ (A3MUD0 ), RS6E_PYRFU (Q8U3H8 ), RS6E_PYRHO (O58349 ), RS6E_PYRIL (A1RUW1 ), RS6E_PYRNV (B1YCP4 ), RS6E_STAMF (A3DMS1 ), RS6E_SULIA (C3MZ52 ), RS6E_SULIK (C4KID0 ), RS6E_SULIL (C3MR04 ), RS6E_SULIM (C3MWZ2 ), RS6E_SULIY (C3N772 ), RS6E_SULSO (Q980A6 ), RS6E_SULTO (Q975N7 ), RS6E_THEKO (Q5JDK8 ), RS6E_THEON (B6YW70 ), RS6E_THESM (C6A2D7 ), RS6_AEDAE (Q9U761 ), RS6_AEDAL (Q9U762 ), RS6_APLCA (Q9BMX5 ), ...
GLHA2_ONCKE (P69063 ), GLHA2_ONCTS (P69062 ), GLHA_ACALA (P30970 ), GLHA_AILFU (Q8HZS0 ), GLHA_AILME (Q8WN20 ), GLHA_ANGAN (P27794 ), GLHA_AOTNA (Q3HRV5 ), GLHA_BALAC (P37036 ), GLHA_BOSMU (Q19PY8 ), GLHA_BOVIN (P01217 ), GLHA_BUBBU (Q9GL36 ), GLHA_CALJA (P51499 ), GLHA_CANLF (Q9XSW8 ), GLHA_CAPHI (Q8WMW8 ), GLHA_CAVPO (Q9JK68 ), GLHA_CERNI (Q8WMR3 ), GLHA_CLAGA (P53542 ), GLHA_COTJA (P68242 ), GLHA_CTEID (P30983 ), GLHA_EQUAS (Q28365 ), GLHA_EQUBU (O46642 ), GLHA_FELCA (Q52R91 ), GLHA_FUNHE (P47744 ), GLHA_HORSE (P01220 ), GLHA_HUMAN (P01215 ), GLHA_HYPMO (P37037 ), GLHA_ICTPU (Q9YGP3 ), GLHA_LITCT (P80051 ), GLHA_MACFA (Q9BEH3 ), GLHA_MACMU (P22762 ), GLHA_MACRU (P68267 ), GLHA_MASCO (Q9ERG4 ), GLHA_MELGA (P68241 ), GLHA_MERUN (Q9ERJ6 ), GLHA_MESAU (Q9ERG5 ), GLHA_MICMO (Q9ERG3 ), GLHA_MONDO (Q6YNX4 ), GLHA_MORSA (Q91119 ), GLHA_MOUSE (P01216 ), GLHA_MURCI (P12836 ), GLHA_NIPNI (Q8JIE9 ), GLHA_PANTA (Q9BDI8 ), GLHA_PHYCD (P25329 ), GLHA_PIG (P01219 ), GLHA_RABIT (P07474 ), GLHA_RAT (P11962 ), ...
マウス・モノクローナル抗体 ab17931 交差種: Hu 適用: WB,ELISA,IHC-P,Flow Cyt…C9抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
D123E, I135T, R172RK, I178M, E204Q, Q207E, R211K, F214L, V245Q, E248D, A272P, T286V, E291D, I293V, E297V, A327V, Q394L, A400T, E404D, K431T, V435A, A446S, L452K, V466A, V467I, D471E, T477A, H483Q, L491S, E492D, K512Q, S519N, ...
K20R, V35I, E44G, S48F, D123S, K173A, Q174E, I178L, Q207E, E233X, V245Q, E248D, D250E, S251A, A272P, K275Q, T286A, V292I, E297A, L303M, P321S, S322A, D324E, I329V, Q334L, G335D, R356K, M357R, G359S, A360T, T369A, A371V, T377L, F389I, K390R, A400T, E404D, L422M, E432D, V435A, R461K, D471E, Q480H, L491S, S519N, K530R, A534S, A554N ...
Q. Im like Mark Twains quote: Quitting smoking is easy; Ive done it a thousand times. Now, I really would like to quit. Got any suggestions?A. Twain may not have been truly successful in his
Complement component 1 Q subcomponent-binding protein, mitochondrial is a protein that in humans is encoded by the C1QBP gene.[5][6][7] The human complement subcomponent C1q associates with C1r and C1s in order to yield the first component of the serum complement system. The protein encoded by this gene is known to bind to the globular heads of C1q molecules and inhibit C1 activation. This protein has also been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.[7] ...
Microglia, central nervous system (CNS) resident phagocytic cells, persistently police the integrity of CNS tissue and respond to any kind of damage or pathophysiological changes. These cells sense and rapidly respond to danger and inflammatory signals by changing their cell morphology; by release of cytokines, chemokines, or nitric oxide; and by changing their MHC expression profile. We have shown previously that microglial biosynthesis of the complement subcomponent C1q may serve as a reliable marker of microglial activation ranging from undetectable levels of C1q biosynthesis in resting microglia to abundant C1q expression in activated, nonramified microglia. In this study, we demonstrate that cultured microglial cells respond to extrinsic C1q with a marked intracellular Ca2+ increase. A shift toward proinflammatory microglial activation is indicated by the release of interleukin-6, tumor necrosis factor-alpha, and nitric oxide and the oxidative burst in rat primary microglial cells, an ...
Here, we have addressed the role of an impairment of H2S oxidation in the pathogenesis of CoQ deficiency. We demonstrated that CoQ‐deficient fibroblasts carrying mutations in different COQ genes have decreased SQR‐driven respiration, which is associated with variably reduced SQR steady‐state levels, depending on the severity of CoQ deficiency, and subsequent compensatory up‐regulation of the levels of the downstream proteins of the pathway. We hypothesize that if the levels of CoQ are very low, SQR activity is decreased and SQR becomes unstable and is probably degraded. Partial reduction in SQR and/or its activity leads to up‐regulation of the enzymes of the downstream pathway (TST, ETHE1, and SUOX), which is more evident at the translational than at transcriptional level. The molecular abnormalities observed in COQ‐mutant fibroblasts are due to reduced CoQ levels, because they can be rescued by CoQ supplementation and are partially recapitulated by pharmacological inhibition of CoQ ...
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The classical pathway begins with the formation of antigen-antibody complex (immune complex). When an antigen enters the body, the antibody (IgM/IgG) binds to it. This induces conformational changes in the Fc portion of the antibody which exposes a binding site for C1 protein. Hence, the antibody activates the complement system only when bound to an antigen.. C1 is a large, multimeric, protein complex composed of one molecule of C1q and two molecules each of C1r and C1s subunits. C1q binds to the antigen bound antibody (Fc portion). C1r and C1s are proteases which help to cleave C4 and C2.. The immune complex bound to C1 calls another protein C4 which is cleaved into C4a and C4b. C4a goes away whereas activated C4b attaches to the target surface near C1q. Now, C4b attracts C2 which is also cleaved into C2a and C2b. C2a binds C4b forming the C4b2a complex whereas C2b goes away. The active C4bC2a activates C3. The C4b2a complex is also known as C3 convertase as this converts C3 into an active form ...
Went to the Signal Mtn, TN store yesterday. They are doubling to .99!!! They didnt have some of the BOGO deals posted but they did ring up half price (Ragu and Wishbone were the 2 I tried). Customer service said that they didnt get the tags in until yesterday afternoon so they didnt get a chance to put them out yet. A couple things I got not listed above: Uncle Bens whole grain white rice- 1.99 (not on sale), used a .75/1 I printed off their website= .49. Smart Water- 1 liter bottles are 1.00-.75 q(double to 1.00, no overage)= FREE. Bounty Napkins (small package) 1.00, used 1.00/any bounty napkins from P&G= FREE. Found some mushrooms that were BOGO (dont remember seeing that in the ad) and they had the 1.00 store Q on them b/c the date was 6/10, made them like .38!!. I got Glad trash bags- 7.99, used .75/1 and 1.00(from walgreens coupon book)= 5.49 (not great but I needed them). Also, they accepted the coupon from Earthfare for 5 free ears of corn !. One more thing, I asked them about the ...
Stokes M (2007) CST Curation Set: 2262; Year: 2007; Biosample/Treatment: cell line, M059K/UV; Disease: glioblastoma; SILAC: -; Specificities of Antibodies Used to Purify Peptides prior to LCMS: p[ST]Q Antibodies Used to Purify Peptides prior to LCMS: Phospho-(Ser/Thr) ATM/ATR Substrate Antibody Cat#: 2851 ...
Stokes M (2007) CST Curation Set: 2262; Year: 2007; Biosample/Treatment: cell line, M059K/UV; Disease: glioblastoma; SILAC: -; Specificities of Antibodies Used to Purify Peptides prior to LCMS: p[ST]Q Antibodies Used to Purify Peptides prior to LCMS: Phospho-(Ser/Thr) ATM/ATR Substrate Antibody Cat#: 2851 ...
Compare Anti-C9orf156 Antibody Products from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
immunogen = synthetic peptide: N N Q C H S S H K R R T K, representing the internal region of the human protein according to NP_937762.1. ...
True. • False. Answers:. Q1:C, Q2:A, Q3:B, Q4:D, Q5:D, Q6:D, Q7:D, Q8:B, Q9:A, Q10:D, Q11:FALSE, Q12:FALSE, Q13:D, Q14:TRUE and Q15:FALSE.. This information is provided by MedicineNet.. ...
Gentaur molecular products has all kinds of products like :search , AGC \ Cellufine MAX Q-r Media \ 20 500 for more molecular products just contact us
Plasmid C1QBP from Dr. Cheryl Arrowsmiths lab contains the insert C1QBP and is published in Unpublished This plasmid is available through Addgene.
A while ago, I opened up my Snap Chat for a Q&A session, and received an absolutely shocking number of questions. I did my best to answer each one, with all but a few receiving responses. The response was phenomenal! I will definitely be opening up for more of these- with specific topics- in the…
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1. The a- and b-chains of reduced and alkylated human complement subcomponent C1r were separated by high-pressure gel-permeation chromatography and isolated in good yield and in pure form. 2. CNBr cleavage of C1r b-chain yielded eight major peptides, which were purified by gel filtration and high-pressure reversed-phase chromatography. As determined from the sum of their amino acid compositions, these peptides accounted for a minimum molecular weight of 28 000, close to the value 29 100 calculated from the whole b-chain. 3. N-Terminal sequence determinations of C1r b-chain and its CNBr-cleavage peptides allowed the identification of about two-thirds of the amino acids of C1r b-chain. From our results, and on the basis of homology with other serine proteinases, an alignment of the eight CNBr-cleavage peptides from C1r b-chain is proposed. 4. The residues forming the charge-relay system of the active site of serine proteinases (His-57, Asp-102 and Ser-195 in the chymotrypsinogen numbering) are ...
... Exp Neurol. 2017 Jun 07;: Authors: Wyatt SK, Witt T, Barbaro NM, Cohen-Gadol AA, Brewster AL Abstract Microglia-mediated neuroinflammation is widely associated with seizures and epilepsy. Although microglial cells are professional phagocytes, less is known about th...
Autoantibodies against complement C1q (anti-C1q Abs) were shown to strongly correlate with the occurrence of severe nephritis in patients with systemic lupus erythematosus (SLE), suggesting a potential pathogenic role by interfering with the complement cascade. To analyze the humoral immune response against C1q at the molecular level, we screened a bone marrow-derived IgGkappa/IgGlambda Fab phage display library from a SLE patient with high anti-C1q Ab titer against purified human C1q. Six Fabs that exhibited strong binding to C1q in ELISA were isolated. The anti-C1q Fabs recognized neoepitopes that were only exposed on bound C1q and not present on soluble C1q mapping to different regions of the collagen-like region of C1q. Analysis of the genes encoding the variable H and L chains of the IgG-derived anti-C1q Fab revealed that all the variable H and L chain regions were highly mutated, with nucleotide and amino acid homologies to the closest germline in the range of 71-97% (average 85 +/- 4) and ...
Background: In patients (pts) who are highly sensitized, desensitization therapy is commonly applied to reduce antibody (Abs) load and to reduce potential morbidity and mortality following heart transplant (HTx). It is not known as to what level of antibody binding is needed to initiate desensitization therapy. It is believed that high binding Abs may have the ability to fix complement and lead to cytotoxicity.. Methods: Between 2011 and 2012 we assessed 13 highly sensitized pts who were noted to have standardized fluorescence intensity (SFI) ,100,000 pretransplant.. A complement binding assay (C1q binding assay) was then applied to these Abs to assess for a correlation of binding to cytotoxicity. Correlation statistics were used to derive significance between higher antibody binding and capacity to bind complement.. Results: There seems to be no correlation between the different binding strength and C1q positivity. However, when evaluating Luminex 1:8 test, there seems to be correlation between ...
Receptor (or element of a larger receptor complex) for C1q, mannose-binding lectin (MBL2) and pulmonary surfactant protein A (SPA). May mediate the enhancement of phagocytosis in monocytes and macrophages upon interaction with soluble defense collagens. May play a role in intercellular adhesion.
Recombinant Complement Component 1, Q Subcomponent Binding Protein (C1QBP) Protein. Species: Rat (Rattus). Source: Escherichia coli (E. coli). Order product ABIN6305337.
Eleven monoclonal antibodies directed against the subcomponent C1q of the first component of human complement, C1, were prepared and tested for binding to intact C1q and to the collagenous portion, the C1q stalks. All of the monoclonals bound well to the intact C1q. Eight out of the eleven exhibited strong binding to the collagenous stalks, while three bound very weakly, if at all, to the stalks and, thus, were presumed to bind to the pepsin-sensitive region which includes the C1q heads. For one of the latter monoclonals, this was confirmed by electron microscopy. Five of the monoclonals were purified by C1q affinity chromatography. When tested with C1 reassembled from its subunits, two of these purified monoclonal antibodies markedly enhanced the rate of spontaneous activation.
Recombinant Complement Component 1, R Subcomponent A (C1RA) Protein (His tag). Species: Mouse (Murine). Source: Insect Cells. Order product ABIN3125986.
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books.google.com.auhttps://books.google.com.au/books/about/Principles_of_Polymer_Chemistry.html?id=CQ0EbEkT5R0C&q=concentration&utm_source=gb-gplus-sharePrinciples of Polymer Chemistry ...
This report describes a new, rapid, sensitive, and quantitative method for the detection of immune complexes, endotoxins, and other complement activating materials in patients sera utilizing the ability of these substances to react with isolated C1q. The procedure is based on the inhibition of radiolabeled C1q binding to sensitized sheep erythrocytes by C1q-reactive substances in pathological sera. The C1q deviation test may be performed on 50 mu1 of serum, using 1 mug of radiolabeled C1q per sample. The procedure may be completed in 1.5-2 h, it is capable of detecting 5 mug of aggregated human IgG per ml of serum, and its coefficient of variation is 4.2%. Application of the test to the study of 193 sera from 43 patients with Dengue hemorrhagic fever showed a positive correlation between degree of C1q deviation and severity of disease. ...
Fedders Continued: A3Q08F2B A3Q08F2B-B A3Q08F2BG A3Q08F2BG-D A3Q08F2BG-E A3Q08F2BG-F A3Q08F2CG A3Q08F2CG-A A3Q08F2CG-B A3Q08F2CG-C A3Q08F2CG-D A3Q08F2CG-E A3Q08F2CG-F A3Q08F2CG-G A3Q08F2CG-H A3Q08F2CG-J A3Q08F2CG-K A3Q08F2CG-L A3Q08F2CG-M A3Q08F2CG-N A3Q08F2CG-P A3Q08F2CG-Q A3Q08F2CG-R A3Q08F2CG-S A3Q08F2CG-T A3Q08F2CG-U A3Q08F2CG-V A3Q08F2CG-W A3Q08F2CG-X A3Q08F2D-D A3Q08F2D-E A3Q08F2E-A A3Q08F2E-C A3QO8F2CG A3X08F2A-B A3X08F2A-C A6Q08F2A-A A6X08F2A*C A6X08F2A*D A6X08F2A-A A6X08F2A-B A7Q06F2A-A A7Q08F2A*E A7Q08F2A-A A7Q08F2A-AX A7Q08F2A-BX Air Temp: B2A08F2A-J B2Q08F2A-E B2Q08F2A-F B2Q08F2A-G B2Q08F2A-H B3Q08F2A B3Q08F2A-B B3Q08F2A-C B3Q08F2A-D B3Q08F2A-E B3Q08F2A-F B3Q08F2A-G B3Q08F2A-H B3Q08F2B B3Q08F2B-A B3Q08F2B-B B3Q08F2B-D B3Q08F2B-E B3Q08F2B-F B3Q08F2B-G B3Q08F2BG-F B3Q08F2BG-G B3Q08F2B-H B3Q08F2B-J B3Q08F2B-K B3Q08F2B-L B3Q08F2B-M B3Q08F2B-N B3Q08F2B-P B3Q08F2B-Q B3Q08F2B-R B3Q08F2B-S B3Q08F2B-T B3Q08F2B-U B6X08F2A*A B7Q06F2A-A B7Q08F2A-A C3Q08F2A Comfort-aire: CS-81A-B Hampton Bay: ...
Abdullah, M.T., Nepliounev, I., Alfonina, G., Ram, S., Rice, P., Elkins, C. (2005). Killing of dsrA mutants of haemophilus ducreyi by normal human serum occurs via the classical complement pathway and is initiated by immunoglobulin m binding. Infection and Immunity. 73: 3431-3439 ...
In the story, D.Q and Pancho go to Helens estate towards the end of the story. The outside of the house how the narrator describes it that they stopped by a black iron door. Helen pushed a remote control on the visor and the gate swung open. (page 261). By this description given by the narrator the reader is already assuming that Helen is wealthy and has a big house. The garage itself looked like a house large enough for a family to live in. (page 261) If the garage is large enough for a family to live in, then the house must be double or triple the size of the garage. Pancho climbed the three flights of stairs silently with D.Q on his back. (page 295). If some climbed three flights of stairs that means that Helens house is three stories with a gallery room on the third floor ...
C3 antibody (complement component 3) for FACS, IE, ICC/IF, WB. Anti-C3 pAb (GTX72994) is tested in Human, Mouse, Pig, Rat, Baboon, Guinea pig, Hamster, Horse, Rabbit samples. 100% Ab-Assurance.
摘要 利用Bac-to-Bac昆虫杆状病毒表达系统表达具有天然构象的猪Ficolin α。首先构建重组穿梭质粒rBacmid-Ficolin α,转染sf9细胞获得重组杆状病毒rBV-Ficolin α;通过Image J软件对优化表达的Western blot图片进行灰度分析确定较佳表达条件;纯化目的蛋白质后,进一步评价其体外抗病毒活性。Western blot结果显示以7.5 MOI接种量感染的sf9细胞在96 h时获得了较高的表达,同时获得的重组猪Ficolin α具有抗猪繁殖与呼吸综合征病毒(PRRSV)活性。猪Ficolin α在sf9昆虫细胞中获得成功表达,且具有良好的抗PRRSV活性。本研究可以为猪Ficolin α的抗病毒活性及作用机制研究提供物质基础。. ...
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A cooling arrangement is disclosed for a vehicle having a first component, a first duct, and a cooling fan configured to deliver air through the first duct to the first component when the cooling fan
C6ORF64 antibody, C-term (SAYSVFN motif domain containing 1) for WB. Anti-C6ORF64 pAb (GTX46296) is tested in Human samples. 100% Ab-Assurance.
Instrument methods file for use with PyroMark Q24 Advanced Software, PyroMark Q24 Advanced Reagents or PyroMark Q24 Advanced CpG Reagents, and PyroMark Q24 Cartridges marked with method 0011 ...
Instrument methods file for use with PyroMark Q24 Advanced Software, PyroMark Q24 Advanced Reagents or PyroMark Q24 Advanced CpG Reagents, and PyroMark Q24 Cartridges marked with method 0010 ...
When I first unboxed the Motorola Q, I knew I was in for disappointment when I saw how small its brick-of-a-battery was and what Id be expecting the Q to do. To put it bluntly, to own a Q, which should involve taking advantage of some of its most prominent features, Verizon Wireless prices of $199 (requires a two-year and online purchase to get the $100 discount from $299) or $349 for the one-year contract version (no discount available) are misleading and heres why.
LG Saate LG FB-K162Q tootetoe. Laadige alla FB-K162Q kasiraamatud, dokumendid ja tarkvara. Vaadake FB-K162Q garantiiteavet ja ajakohastage teenuseid.
Error in Wikidata: wikidata item rabies (Q39222) property instance of (P31) has a strange value disease (Q12136) (currently accepted values: taxon (Q16521), monotypic taxon (Q310890), fossil taxon (Q23038290), clade (Q713623), species aggregate (Q1297859), Wikimedia category (Q4167836)) ...
Q BioMed Inc. (QBIO) and ASDERA LLC recently announce a licensing agreement that provides Q BioMed with the worldwide exclusive rights to...
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Der Fujitsu ESPRIMO Q920 bietet ausgezeichnete Performance, hohe Energieeffizienz und Manageability im Mini-PC-Format. Die Zero Noise-Funktionalität verhindert störende Geräusche, die geringe Stellfläche sorgt für einen aufgeräumten Arbeitsplatz.
/PRNewswire/ -- Telefônica Brasil - (B3: VIVT3 [Common Shares] / VIVT4 [Preferred Shares]; NYSE: VIV), announces its results for 1Q20. Improved customer base...
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Sou um jogador assiduo de MOHAA, jogo todo dia, dia e noite, e gostaria de conhecer a galerinha q joga tambem, ai vai minha foto, gostaria q as
Neuromyelitis optica (NMO) is an autoimmune CNS disorder mediated by pathogenic aquaporin-4 (AQP4) water channel autoantibodies (AQP4-IgG). Although AQP4-IgG-driven complement-dependent cytotoxicity (CDC) is critical for the formation of NMO lesions, the molecular mechanisms governing optimal classical pathway activation are unknown. We investigated the molecular determinants driving CDC in NMO using recombinant AQP4-specific autoantibodies (AQP4 rAbs) derived from affected patients. We identified a group of AQP4 rAbs targeting a distinct extracellular loop C epitope that demonstrated enhanced CDC on target cells. Targeted mutations of AQP4 rAb Fc domains that enhance or diminish C1q binding or antibody Fc-Fc interactions showed that optimal CDC was driven by the assembly of multimeric rAb platforms that increase multivalent C1q binding and facilitate C1q activation. A peptide that blocks antibody Fc-Fc interaction inhibited CDC induced by AQP4 rAbs and polyclonal NMO patient sera. ...
Neuromyelitis optica (NMO) is an autoimmune CNS disorder mediated by pathogenic aquaporin-4 (AQP4) water channel autoantibodies (AQP4-IgG). Although AQP4-IgG-driven complement-dependent cytotoxicity (CDC) is critical for the formation of NMO lesions, the molecular mechanisms governing optimal classical pathway activation are unknown. We investigated the molecular determinants driving CDC in NMO using recombinant AQP4-specific autoantibodies (AQP4 rAbs) derived from affected patients. We identified a group of AQP4 rAbs targeting a distinct extracellular loop C epitope that demonstrated enhanced CDC on target cells. Targeted mutations of AQP4 rAb Fc domains that enhance or diminish C1q binding or antibody Fc-Fc interactions showed that optimal CDC was driven by the assembly of multimeric rAb platforms that increase multivalent C1q binding and facilitate C1q activation. A peptide that blocks antibody Fc-Fc interaction inhibited CDC induced by AQP4 rAbs and polyclonal NMO patient sera. ...
The depurinating adduct 4-OHE1(E2)-1(α, β)-N7Gua was formed in vitro and in vivo by reaction of E1(E2)-3,4-Q with DNA and after activation of 4-OHE by cytochrome P450 and peroxidases (Tables 3 and 4). CE-Q derived from 4-OHE and 2-OHE react differently with nucleosides and DNA because of their distinctive chemical properties (17). CE-2,3-Q bind to the exocyclic amino groups of dA and dG to form adducts that retain the deoxyribose moiety whereas CE-3,4-Q bind exclusively to the N-7 of Gua, resulting in destabilization of the glycosidic bond and subsequent depurination. CE-2,3-Q form 10-50 times higher levels of stable DNA adducts than CE-3,4-Q (16). CE-3,4-Q, however, give two to three orders of magnitude higher levels of depurinating than stable adducts (Table 3). Thus, CE-2,3-Q produce stable DNA adducts (16), and the corresponding CE do not induce kidney tumors in Syrian golden hamsters (18, 19) whereas CE-3,4-Q form predominantly 4-OHE1(E2)-1(α, β)-N7Gua, and E1-3,4-Q is carcinogenic in ...
Mathias wrote: , Dear ng, , , Im looking for a reference about whether the vestibular system yields , an acceleration and/or velocity signal (e.g. used for the head direction , and place cell system). Googling for this I found a website... , http://paperairplane.mit.edu/16.423J/Space/SBE/neurovestibular/NeuroVestibular/2_Physiology/PhysSub3.html , ... that claims the vestibular system outputs a velocity and not an , acceleration signal over the range of normal head movements. , Unfortunately there is no reference and Im not even certain about which , species they talk. , , Any reference on this topic would be highly appreciated, , Mathias Anderson and Eliasmiths book Neural Engineering: Computation, Representation, and Dynamics in Neurobiological Systems, has a good discussion and several references. You can find information about the book here: http://compneuro.uwaterloo.ca/bookinfo.html A paper available on-line: Eliasmith, C., M. B. Westover, and C. H. Anderson (2002). A general ...
Mouse complement component C1q is a serum glycoprotein which consists of six A chains, six B chains and six C chains. The three polypeptides are 223, 228, and 217 residues long, respectively, and are encoded by three genes. DNA probes for mouse C1q A, B, and C chains were hybridized to Southern blots of DNA obtained from various inbred mouse strains. On the basis of fragment length polymorphisms, two different alleles of each of the genes could be identified. The distribution of these alleles was determined in the BXD and LXPL recombinant inbred strain series. Comparison with previously reported strain distribution patterns shows that the genes encoding mouse C1q map to the same locus on distal chromosome 4. Overlapping clones spanning the entire gene cluster of C1q were isolated from genomic libraries using specific cDNA probes. The three genes C1qA, C1qB, and C1qC are closely arranged on a 19 kilobase stretch of DNA in the 5 to 3 orientation A-C-B. Each gene consists of two exons separated ...
545 the: research A. Courtesy of Wikimedia Commons. 545 soil: ion B. Vaidyanathan S, Selmi F, Abraham KA, et al. 545 Renal advantage energy: use A. 545 Renal bootstrapping edema: basis B. 545 Renal Discussion closure: justification C. Behnes CL, Schlegel C, Shoukier M, et al. 546 Renal project: average A. 546 Renal utilization: beam B. 547 Transitional research behavior: regression A. Geavlete B, Stanescu F, Moldoveanu C, et al. 548 K: receptor B. 549 conduction Swiss collaboration, way A and summation. 549 Renal Basic bank. Health and Human Services and William D. 551 Renal reduced-gravity behaviors: theory C. 552 distribution: education of field. comparable and dry edema, binding simulation. Appleton ions; Lange, 1997: 243. Williams needs, keen information. 563 Spanish-speaking roadslope: cortex A. Cross-section of environmental 2215Q protein. 563 X-linked environment: feedback B. 568 lysine( Mullerian) switching aspects: student A-D. Zafarani F, Haghighi H, et al. New York: McGraw-Hill, 2005: ...
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Learn how uncontrolled or excessive complement activation may play a role in several autoimmune and inflammatory diseases, and why APL-2 (pegcetacoplan) targeting of complement proteins at the level of C3 is being investigated as a treatment.
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The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
A measuring device for determining the relative offset between two components in a z-direction includes two measuring members. A first measuring member is affixable on a first component, and the second measuring member is affixable on a second component. Furthermore, the measuring device includes a sensor device for determining the relative position of the two measuring members. The first measuring member and the second measuring member are affixable on the first components at a rigid angle. At least one of the measuring members is able to be brought into adhesive contact with the first component or the second component. The measuring device includes support members for at least one measuring member so that the measuring member is able to assume a parking or an operating position. The measuring members are precisely and reproducibly aligned in space relative to each other in the parking position.
Overall this protein shows similarity to the complement 1Q factors (C1Q). However, when the 3-dimensional structure of the ... Shapiro L, Scherer PE (March 1998). "The crystal structure of a complement-1q family protein suggests an evolutionary link to ... "A novel serum protein similar to C1q, produced exclusively in adipocytes". The Journal of Biological Chemistry. 270 (45): 26746 ...
Opsonins include Mfge8, Gas6, Protein S, antibodies and complement factors C1q and C3b. Phagoptosis has multiple functions ... Pathogenic cells such as bacteria can be opsonised by antibodies or complement factors, enabling their phagocytosis and ...
C1q associates with C1r and C1s in order to yield the first component of the serum complement system. Deficiency of C1q has ... and C-chains of human complement subcomponent C1q. The complete derived amino acid sequence of human C1q". Biochem. J. 274 (2 ... Complement C1q subcomponent subunit A is a protein that in humans is encoded by the C1QA gene. This gene encodes a major ... 1994). "The envelope glycoprotein of HIV-1 gp120 and human complement protein C1q bind to the same peptides derived from three ...
The human complement subcomponent C1q associates with C1r and C1s in order to yield the first component of the serum complement ... C1QBP, GHABP1, SF2p32, gC1Q-R, gC1qR, p32, complement component 1, q subcomponent binding protein, complement C1q binding ... complement component C1q binding. • adrenergic receptor binding. • translation activator activity. Cellular component. • ... Complement component 1 Q subcomponent-binding protein, mitochondrial is a protein that in humans is encoded by the C1QBP gene.[ ...
... fibromodulin activates the classical pathway of complement by directly binding C1q". The Journal of Biological Chemistry. 280 ( ...
Overall this protein shows similarity to the complement 1Q factors (C1Q). However, when the 3-dimensional structure of the ... Shapiro L, Scherer PE (March 1998). "The crystal structure of a complement-1q family protein suggests an evolutionary link to ... Scherer PE, Williams S, Fogliano M, Baldini G, Lodish HF (November 1995). "A novel serum protein similar to C1q, produced ... ADIPOQ, ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1, GBP28, adiponectin, C1Q and collagen domain containing, Adiponectin. ...
Complement C1q tumor necrosis factor-related protein 1 is a protein that in humans is encoded by the C1QTNF1 gene. C1QTNF1 has ... "Entrez Gene: C1QTNF1 C1q and tumor necrosis factor related protein 1". Innamorati, Giulio; Whang Michael Insuk; Molteni ... Innamorati G, Bianchi E, Whang MI (2006). "An intracellular role for the C1q-globular domain". Cell Signal. 18 (6): 761-70. doi ...
... binds with high affinity to the complement component C1q, the extracellular matrix component TNFα induced protein 6 ( ... In addition, preincubation of apoptotic cells with PTX3 enhances C1q binding and C3 deposition on the cell surface, suggesting ... PTX3 activates the classical pathway of complement activation and facilitates pathogen recognition by macrophages and DCs. ... "Biochemical and functional characterization of the interaction between pentraxin 3 and C1q". Eur. J. Immunol. 33 (2): 465-73. ...
Complement C1q tumor necrosis factor-related protein 3 is a protein that in humans is encoded by the C1QTNF3 gene. GRCh38: ... "Entrez Gene: C1QTNF3 C1q and tumor necrosis factor related protein 3". Human C1QTNF3 genome location and C1QTNF3 gene details ... "Effects of the new C1q/TNF-related protein (CTRP-3) "cartonectin" on the adipocytic secretion of adipokines". Obesity. 16 (7): ...
"Secreted chondroitin sulfate proteoglycan of human B cell lines binds to the complement protein C1q and inhibits complex ... complement binding protein (CBP)-like domains, immunoglobulin folds and proteoglycan tandem repeats. Aggrecan is a critical ...
"Secreted chondroitin sulfate proteoglycan of human B cell lines binds to the complement protein C1q and inhibits complex ...
... globular C1q receptor) on the surface, which binds C1q, and prevents it from initiating complement activation. Due to the ... The C1 complement complex binds to these antibodies resulting in its activation via cross proteolysis. This activated C1 ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... The key to the success of the complement system in clearing antigens is regulating the effects of C3b to pathogens alone and ...
The complement system is a part of the innate immune response. C3b, C4b, and C1q are important complement molecules that serve ... In both cases C1q activates complement, resulting in the cells being marked for phagocytosis by C3b and C4b. C1q is an ... Complement receptor 1 is expressed on all phagocytes and recognizes a number of complement opsonins, including C3b and C4b ... As a part of the alternative complement pathway, the spontaneous activation of a complement cascade converts C3 to C3b, a ...
It is the first component of the classical complement pathway and is composed of the subcomponents C1q, C1r and C1s. The C1 ... Activation of the C1 complex initiates the classical complement pathway. This occurs when C1q binds to antigen-antibody ... Such binding of C1q leads to conformational changes in the C1q molecule, which activates the associated C1r molecules. Active ... The C1 complex (complement component 1, C1) is a protein complex involved in the complement system. ...
... appears to influence fibrillogenesis, and also interacts with fibronectin, thrombospondin, the complement component C1q ... Krumdieck R, Höök M, Rosenberg LC, Volanakis JE (Dec 1992). "The proteoglycan decorin binds C1q and inhibits the activity of ...
... suppress the activation of the classical pathway of complement in vitro by binding to solid-phase or fluid-phase complement C1q ... suppress anti-inflammatory mediators and regulate complement activation argues that defensins upregulate innate host ...
... and one of its two carbohydrate chains still reassembles with C1q and C1r to form a functional C1 complex". Biochemistry. 31 ( ... Complement component 1s (EC 3.4.21.42, C1 esterase, activated complement C1s, complement C overbar 1r, C1s) is a protein ... complement activation, lectin pathway. • complement activation. • regulation of complement activation. Sources:Amigo / QuickGO ... complement activation, classical pathway. • immune system process. • innate immune response. • ...
Complement C1q tumor necrosis factor-related protein 3 C5orf3: encoding protein FAM114A2 C5orf13: Neuronal regeneration related ... excision repair cross-complementing rodent repair deficiency, complementation group 8 FAM71B: encoding protein Family with ...
... while the former is also found in complement protein C1q and collectins, which include mannose-binding lectin and lung ... Matsushita M, Endo Y, Fujita T (2000). "Cutting edge: complement-activating complex of ficolin and mannose-binding lectin- ... binds patterns of acetyl groups and activates complement". Scand. J. Immunol. 62 (5): 462-73. doi:10.1111/j.1365-3083.2005. ...
... in order to activate the complement system via C1q. CRP is synthesized by the liver in response to factors released by ... This activates the complement system, promoting phagocytosis by macrophages, which clears necrotic and apoptotic cells and ... Others have shown that CRP can exacerbate ischemic necrosis in a complement-dependent fashion and that CRP inhibition can be a ... It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis by macrophages (opsonin- ...
... activating the classical pathway of the complement system. The complement cascade system instead binds C1Q complex attached to ... Complement Component receptors CR2, CR3 and CR4 have been found to mediate this Complement -Mediated enhancement of infection. ... ADE in HIV can be complement mediated or Fc receptor mediated. Complements in presence of HIV-1 positive sera have been found ... The infection of HIV-1 leads to activation of complements fragments of these complements can assist viruses with infection by ...
Besides complement particles C1q and C3b which help to opsonize the apoptotic cells, also thrombospondin, pentraxins (C- ... components of complement pathways (e.g. C1q, C3b) and other molecules found in extracellular space. Collectins (e.g. mannose- ... interacts with calreticulin which is a known C1q receptor), or complement receptors (CR3 and CR4). There is a variety of ... C1q and collectins are other PRRs which could potentially recognize both PAMPs and ACAMPs structures. It is necessary to ...
... a human protein identified as a putative C1q receptor. C1q belongs to the complement activation proteins and plays a major role ... 1998). "The C1q and collectin binding site within C1q receptor (cell surface calreticulin)". Immunopharmacology. 38 (1-2): 73- ... 1992). "Short amino acid sequences derived from C1q receptor (C1q-R) show homology with the alpha chains of fibronectin and ... Peerschke EI, Ghebrehiwet B (1990). "Platelet C1q receptor interactions with collagen- and C1q-coated surfaces". J. Immunol. ...
... and epidermal growth factor-like domains and a carboxyl terminus similar to the globular domain of complement C1q and collagens ...
Classical complement pathway C1Q complex - C1R / C1S C4 - C4a C2 Mannan-binding lectin pathway MASP1 / MASP2 Mannan-binding ... system Complement system Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement ... Secreted PRRs Complement system (see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A ( ... Complement receptor CR1 (CD35) CR2 (CD21) CR3 - Heterodimer: CD11b / CD18 CR4 - Heterodimer: CD11c / CD18 CRIg (Complement ...
Zipfel, P. F., Hallström, T., & Riesbeck, K. (2013). Human complement control and complement evasion by pathogenic microbes- ... Klassikalise raja initsiatsioon toimub ainult läbi C1q valgu seondumisele antigeen-antikeha kompleksile näiteks viiruse kestal ... 1,0 1,1 1,2 1,3 Rus, H., Cudrici, C., & Niculescu, F. (2005). The role of the complement system in innate immunity. Immunologic ... 7,0 7,1 Lambris, J. D., Ricklin, D., & Geisbrecht, B. V. (2008). Complement evasion by human pathogens. Nature Reviews. ...
... but not with C1q-depleted serum. Addition of purified C1q protein (100 μg/ml) to C1q-depleted serum restored the activity to ... Complement C1q activates canonical Wnt signaling and promotes aging-related phenotypes.. Naito AT1, Sumida T, Nomura S, Liu ML ... C1q was precipitated by Fz8/Fc, but not by IgG/Fc (F). C1q was precipitated by Fz8 CRD-AP, but not by AP (G).. (H and I) ... Our findings therefore suggest the unexpected role of complement C1q in Wnt signal transduction and modulation of mammalian ...
This brings anti-C1q antibodies into the glomerulus, resulting in sufficient complement activation to result in the generation ... Anti-C1q antibodies (in yellow) such as JL-1 recognize the collagen-like "tails" of C1q in much the same manner as they would ... The administration of C1q and anti-C1q is not sufficient to cause glomerular injury as shown by Trouw et al. (. 6. ). However, ... Patients with lupus nephritis typically have autoantibodies to the complement classical pathway protein C1q. Whether these anti ...
Complement component 1q (C1q). Details. Name. Complement component 1q (C1q). Kind. protein group. Organism. Humans. Proteins. ... Complement C1q subcomponent subunit C. P02747. Details. Drug Relations. Drug Relations. DrugBank ID. Name. Drug group. ... Complement C1q subcomponent subunit B. P02746. Details. ... Complement C1q subcomponent subunit A. P02745. Details. ...
Complement C1q subcomponent subunit A. Details. Name. Complement C1q subcomponent subunit A. Synonyms. *Complement C1q ... and C-chains of human complement subcomponent C1q. The complete derived amino acid sequence of human C1q. Biochem J. 1991 Mar 1 ... C1q (PF00386). Transmembrane Regions. Not Available. Cellular Location. Secreted. Gene sequence. ,lcl,BSEQ0016679,Complement ... C1q associates with the proenzymes C1r and C1s to yield C1, the first component of the serum complement system. The collagen- ...
... for C1q, mannose-binding lectin (MBL2) and pulmonary surfactant protein A (SPA). May mediate the enhancement of phagocytosis in ... Complement component C1q receptorAdd BLAST. 631. Amino acid modifications. Feature key. Position(s). DescriptionActions. ... complement component C1q complex binding Source: UniProtKB ,p>Inferred from Direct Assay,/p> ,p>Used to indicate a direct assay ... complement component C1q complex binding Source: UniProtKBInferred from direct assayi*. Ref.2 ...
C1QBP complement C1q binding protein [Homo sapiens] C1QBP complement C1q binding protein [Homo sapiens]. Gene ID:708 ... The human complement subcomponent C1q associates with C1r and C1s in order to yield the first component of the serum complement ... complement C1q binding proteinprovided by HGNC. Primary source. HGNC:HGNC:1243 See related. Ensembl:ENSG00000108561 MIM:601269 ... complement component 1 Q subcomponent-binding protein, mitochondrial. Names. ASF/SF2-associated protein p32. C1q globular ...
Complement C1q tumor necrosis factor-related protein 6Imported. ,p>Information which has been imported from another database ... tr,F8WC87,F8WC87_HUMAN Complement C1q tumor necrosis factor-related protein 6 OS=Homo sapiens OX=9606 GN=C1QTNF6 PE=1 SV=1 ... C1q and tumor necrosis factor related protein 6, isoform CRA_a. HUMAN ... Complement C1q tumor necrosis factor-related protein 6. MOUSE. 264. Complement C1q tumor necrosis factor-related protein 6. RAT ...
Combining with the C1q component of the classical complement cascade and transmitting the signal from one side of the membrane ...
Complement C1q tumor necrosis factor-related protein 5Add BLAST. 228. Proteomic databases. PaxDb, a database of protein ... sp,Q5FVH0,C1QT5_RAT Complement C1q tumor necrosis factor-related protein 5 OS=Rattus norvegicus OX=10116 GN=C1qtnf5 PE=2 SV=1 ... IPR001073, C1q_dom. IPR008160, Collagen. IPR008983, Tumour_necrosis_fac-like_dom. Pfami. View protein in Pfam. PF00386, ... C1qPROSITE-ProRule annotation. ,p>Manual validated information which has been generated by the UniProtKB automatic annotation ...
Isolation of C1q and C1q fragments. C1q was isolated from human serum as previously described (29) with some modifications. C1q ... Measurement of the association constants of the complement formed between intact C1q or pepsin-treated C1q stalks and the ... quiescent HUVEC were incubated for 48 h with 50 μg/ml intact C1q in the presence of 50 μg/ml C1q globular heads, C1q collagen- ... HUVEC were incubated with C1q in the presence or the absence of the C1q fragments or BSA. Incubation with intact C1q alone ...
Complement c1q tumor necrosis factor-related protein 3 a novel adipokine, protect against diabetes mellitus in young adult ...
Classical Pathway of Complement Activation: Longitudinal Associations of C1q and C1-INH With Cardiovascular Outcomes. The CODAM ... Classical Pathway of Complement Activation: Longitudinal Associations of C1q and C1-INH With Cardiovascular Outcomes ... Classical Pathway of Complement Activation: Longitudinal Associations of C1q and C1-INH With Cardiovascular Outcomes ... Classical Pathway of Complement Activation: Longitudinal Associations of C1q and C1-INH With Cardiovascular Outcomes ...
Complement C1q Tumor Necrosis Factor-Related Protein 1 (CTRP1). CTRP1 (Complement C1q tumor necrosis factor-related protein 1) ... You are here: Home Products by Molecule of Interest Complement C1q Tumor Necrosis Factor-Related Protein 1 (CTRP1) ... C1q-like domain and an N-terminal signal peptide sequence followed by a variable region and hence is predicted to be secreted ...
... is a native C1q complement component composed of 18 polypeptide chains consisting of three nonidentical A, B, C subunits of 29 ... More,, Complement C1q, Human, CAS 80295-33-6, is a native C1q complement component composed of 18 polypeptide chains consisting ... Complement C1q, Human, CAS 80295-33-6, is a native C1q complement component composed of 18 polypeptide chains consisting of ... Complement C1q, Human MSDS (material safety data sheet) or SDS, CoA and CoQ, dossiers, brochures and other available documents. ...
The C1q complement/TNF-related protein (CTRP) superfamily, which includes the adipokine adiponectin, has been shown in animal ... Circulating C1q complement/TNF-related protein (CTRP) 1, CTRP9, CTRP12 and CTRP13 concentrations in Type 2 diabetes mellitus: ...
Binding of the complement component C1q to the CH2 domain of antigen-bound immunoglobulin gamma (IgG) activates the classical ... Binding of the complement component C1q to the CH2 domain of antigen-bound immunoglobulin gamma (IgG) activates the classical ... Fc-Galactosylation of Human Immunoglobulin Gamma Isotypes Improves C1q Binding and Enhances Complement-Dependent Cytotoxicity ... We found that Fc-galactosylation enhances the efficacy of CD20-targeting complement-fixing antibodies for C1q binding and ...
Complement C1q Tumor Necrosis Factor-Related Protein 1 Complement C1q Tumor Necrosis Factor-Related Protein 2 Complement C1q ... Complement C1q Tumor Necrosis Factor-Related Protein 6 Complement C1q Tumor Necrosis Factor-Related Protein 7 Complement C1q ... Complement C1q Tumor Necrosis Factor-Related Protein 1 - Proteins. Product filter Complement C1q Tumor Necrosis Factor-Related ... Complement C1q Tumor Necrosis Factor-Related Protein 9A Connective Tissue Growth Factor Cornifin-B Corticosteroid-Binding ...
Complement C1q Tumor Necrosis Factor-Related Protein 1 - Immunoassays. Product filter Complement C1q Tumor Necrosis Factor- ... Complement C1q Tumor Necrosis Factor-Related Protein 1 Complement C1q Tumor Necrosis Factor-Related Protein 9A Connective ...
C1q) in Human samples. Strip well format. Reagents for up to 96 tests. It is designed for detection of complement C1q in human ... C1q) ELISA Kit employs a quantitative enzyme immunoassay technique that measuresComplement Component 1q ( ... Product Inquiry for Human Complement Component 1q (C1q) ELISA Kit. Name. Email. Phone Number. Message. ... Complement C1q in standards and samples is sandwiched by the immobilized antibody and a biotinylated polyclonal antibody ...
HCA RNA Cell Line for Complement C1q tumor necrosis factor-related protein 3. ...
C1QA; Complement C1q subcomponent subunit A; Complement component 1 q subcomponent A chain; Complement component 1 q ... C1q, a subcomponent of the classical complement pathway, is composed of nine subunits that mediate classical complement ... Anti-C1QA / Complement C1q A-Chain Monoclonal Antibody(Clone: C1QA/2783). Product code: 36-3272. *specify in mg or ml ... designated C1q-A throµgh C1q-C, are disulfide-linked dimers of chain C. Each chain contains an N-terminal collagen-like region ...
Find the test centers and pathology labs for Histopathology Direct Immuno Fluorescence Skin Biopsy Dif Complement C1q test in ... 14 Diagnostic Centers found for HISTOPATHOLOGY, DIRECT IMMUNO-FLUORESCENCE (DIF),SKIN / CONJUNCTIVAL BIOPSY, COMPLEMENT C1q in ...
2009) C1q, the recognition subcomponent of the classical pathway of complement, drives microglial activation. Journal of ... C1q, the recognition subcomponent of the classical pathway of complement, drives microglial activation ... We have shown previously that microglial biosynthesis of the complement subcomponent C1q may serve as a reliable marker of ... Our findings indicate 1) that extrinsic plasma C1q is involved in the initiation of microglial activation in the course of CNS ...
May regulate the number of excitatory synapses that are formed on hippocampus neurons. Has no effect on inhibitory synapses (By similarity). May inhibit adipocyte differentiation at an early stage of the process (By similarity ...
Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns ...
  • Given that loss of C1q function is strongly associated with the development of systemic lupus erythematosus, ARRB2 may act to limit the development of autoimmune disease. (edu.au)
  • Background: The relationship between cell-bound complement activation products (CB-CAPs: EC4d, EC3d), anti-C1q, soluble complement C3/C4 and disease activity in systemic lupus erythematosus (SLE) was evaluated. (elsevier.com)
  • The discovery of C1q interactions with LAIR-1 and LAIR-2 lends much needed insight into molecular mechanisms operating to prevent the loss of tolerance, particularly in systemic lupus erythematosus. (nih.gov)
  • Complement plays a major role in inflammation and thrombosis associated with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). (nih.gov)
  • Complement deficiencies in systemic lupus erythematosus. (medscape.com)
  • In addition to playing an important role in host defense against infection, the complement system is a mediator in both the pathogenesis and prevention of immune complex diseases, such as systemic lupus erythematosus (SLE). (medscape.com)
  • The collagen-like regions of C1q interact with the Ca(2+)-dependent C1r(2)C1s(2) proenzyme complex, and efficient activation of C1 takes place on interaction of the globular heads of C1q with the Fc regions of IgG or IgM antibody present in immune complexes. (drugbank.ca)
  • A polyclonal antibody specific for human complement C1q has been pre-coated onto a 96-well microplate with removable strips. (innov-research.com)
  • Complement C1q in standards and samples is sandwiched by the immobilized antibody and a biotinylated polyclonal antibody specific for human complement C1q, which is recognized by a streptavidin-peroxidase (SP) conjugate. (innov-research.com)
  • Complement C1q, anti_human Species Human Format Biotin_IgG Host Rabbit Polyclonal antibody antibody storage GENTAUR recommends for long therm storage to freeze at -24 C. For short time storage up to 30 days we suggest fridge storage at 1 to 10 C. Prevent multiple freeze taw cycles of Complement C1q, anti_human Species Human Format Biotin_IgG Host Rabbit Polyclonal antibody. (antibody-antibodies.com)
  • Do not freeze taw, rather use Complement C1q, anti_human Species Human Format Biotin_IgG Host Rabbit Polyclonal antibody from the fridge if your use is less than 1 or 2 weeks. (antibody-antibodies.com)
  • Complement C1q, anti_human Species Human Format Biotin_IgG Host Rabbit Polyclonal antibody Human samples 80 % of the research is conducted on human samples. (antibody-antibodies.com)
  • This antibody reacts with human C1q complement. (abcam.com)
  • Complement alone drives efficacy of a chimeric antigonococcal monoclonal antibody. (nih.gov)
  • The anti-C1q antibody, however, is more specific than anti-dsDNA for both active renal and extrarenal lupus. (nih.gov)
  • The combined use of immunoadsorption (IA) and membrane filtration (MF) may markedly enhance removal of IgM and complement component C1q, supporting its use as an element of recipient desensitization in antibody-incompatible transplantation. (nih.gov)
  • C1q can also be activated by mycoplasmal organisms, RNA viruses, bacterial endotoxins, and cell membranes of some organelles without the presence of antibody. (medscape.com)
  • The globular regions of C1q recognize and bind to the Fc region of antibody isotypes IgG or IgM. (wikipedia.org)
  • The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. (wikipedia.org)
  • C3b, the larger fragment, becomes covalently attached to the microbial surface or to the antibody molecules through the thioester domain at the site of complement activation. (wikipedia.org)
  • The production of all factors was inhibited (69 ± 7%) by the collagenous fragments of C1q, while the C1q globular heads only induced 13 ± 11% inhibition. (jimmunol.org)
  • Serum C1q concentration is increased with aging, and Wnt signaling activity is augmented during aging in the serum and in multiple tissues of wild-type mice, but not in those of C1qa-deficient mice. (nih.gov)
  • Macrophages are the primary source of C1q, while anti-inflammatory drµgs as well as cytokines differentially regulate expression of the mRNA as well as the protein. (abeomics.com)
  • Here we show that ARRB2 mRNA and protein expression is enriched in macrophages, and that it regulates complement C1q expression and cell survival. (edu.au)
  • These data imply that ARRB2 acts to limit JNK/ERK activation and survival in macrophages, but is required for basal and TLR-inducible complement C1q expression. (edu.au)
  • Immunofluorescence studies on the subcomponents of the first component of complement (C1): detection of C1q and C1s in different cells of biopsy material and on human as well as on guinea pig peritoneal macrophages. (freepatentsonline.com)
  • C1q is composed of 18 polypeptide chains which include 6 A-chains, 6 B-chains, and 6 C-chains. (genecards.org)
  • Complement C1q is a soluble pattern recognition molecule comprising six heterotrimeric subunits assembled from three polypeptide chains (A-C). Each heterotrimer forms a collagen-like stem prolonged by a globular recognition domain. (univ-grenoble-alpes.fr)
  • The three monomers have been linked in tandem to generate a single continuous polypeptide, based on a strategy previously used for adiponectin, a protein structurally related to C1q. (univ-grenoble-alpes.fr)
  • The spirochetemia of relapsing fever in mice is cleared by a complement-independent, polyclonal IgM response with reactivity to two prominent Ags of 20 and 35 kDa. (jimmunol.org)
  • In this study, we have dissected the polyclonal IgM Ab response against a relapsing fever spirochete to determine the specificity of its complement-independent bactericidal properties. (jimmunol.org)
  • Reid KB: Complete amino acid sequences of the three collagen-like regions present in subcomponent C1q of the first component of human complement. (drugbank.ca)
  • Six of these subunits are disulfide-linked dimers of chains A and B, while three of these subunits, designated C1q-A throµgh C1q-C, are disulfide-linked dimers of chain C. Each chain contains an N-terminal collagen-like region and a C-terminal C1q globular domain. (abeomics.com)
  • Each chain contains an N-terminal collagen-like region and a C-terminal C1q globular domain. (genecards.org)
  • C1q family members include the Adiponectin/ACRP30 (C-terminal TNF-like domain), which regulates metabolism and energy homeostasis [ PMID: 22449980 ], and NC1 (non-collagenous domain 1), the C-terminal TNF-like domain of collagen X, which is crucial for collagen X assembly in bone tissue [ PMID: 11839302 ]. (ebi.ac.uk)
  • Multivalent binding of C1q to its targets triggers immune effector mechanisms mediated via its collagen-like stems. (univ-grenoble-alpes.fr)
  • Both C1q and its collagen tail trigger phosphorylation of LAIR-1 immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in monocytes. (nih.gov)
  • Binding of biotinylated-C1q collagen tail (20 μg/mL) to immobilized LAIR-1 ( E ) or LAIR-2 ( F ). A representative experiment is shown ( n = 3). (nih.gov)
  • These share the same topology, each possessing a small, globular N-terminal domain, a collagen-like Gly/Pro-rich central region, and a conserved C-terminal region, the C1q domain. (wikipedia.org)
  • The C1q protein is produced in collagen-producing cells and shows sequence and structural similarity to collagens VIII and X. It is assumed that the globular ends are the sites for multivalent attachment to the complement fixing sites in immune complexed immunoglobulin. (wikipedia.org)
  • Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions. (nih.gov)
  • The interest of this functional recombinant form of the recognition domains of C1q in basic research and its potential biomedical applications are discussed. (univ-grenoble-alpes.fr)
  • However, our studies have suggested that this SNP appears to be associated with a functional abnormality of C1q expression since its presence correlates inversely with serum levels of C1q antigenic protein in both SCLE patients and normal controls. (cdc.gov)
  • Functional analyses show that C1q-mediated inhibition of monocyte-DC differentiation and C1q-mediated inhibition of IFN-α production by plasmacytoid DCs were both reversed by LAIR-2. (nih.gov)
  • Thus, C1q is a functional ligand for LAIR-1 restricting immune cell differentiation and activation. (nih.gov)
  • In addition, evidence is provided to support a role for cell surface calreticulin (CRT) in (also known as the cC1qR) binding the collagenous tails of C1q and MBL attached to the apoptotic cell. (rupress.org)
  • β-catenin stabilization assay was performed in HEK293 cells 1 hr after C1q stimulation (200 μg/ml). (nih.gov)
  • This assay employs a quantitative sandwich enzyme immunoassay technique that measures human complement C1q in less than 4 hours. (innov-research.com)
  • The recovery of C1q R1 spiked to levels throughout the range of the assay was evaluated. (rndsystems.com)
  • To assess the linearity of the assay, samples containing and/or spiked with high concentrations of C1q R1 were serially diluted with Calibrator Diluent to produce samples with values within the dynamic range of the assay. (rndsystems.com)