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 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 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 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.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.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.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.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 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.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).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 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).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.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.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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.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.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.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.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.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.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.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.)Cell Line: Established cell cultures that have the potential to propagate indefinitely.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.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.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.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.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.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.Mice, Inbred BALB CBinding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Blood 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.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.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.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.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.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).Recombinant Proteins: Proteins prepared by recombinant DNA technology.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.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.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.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.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).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.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).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).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.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.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.Cosmids: Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.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.Bacterial Proteins: Proteins found in any species of bacterium.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.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.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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.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.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.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.Homozygote: An individual in which both alleles at a given locus are identical.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system.ZymosanTime Factors: Elements of limited time intervals, contributing to particular results or situations.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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.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.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.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.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.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.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.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.Molecular Weight: The sum of the weight of all the atoms in a molecule.Kinetics: The rate dynamics in chemical or physical systems.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.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.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.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.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.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.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.Restriction Mapping: Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.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.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.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.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.Lipopolysaccharides: 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)Protein PrecursorsSteroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.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.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.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.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.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.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.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.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.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.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.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Pedigree: 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.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.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.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.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.Mice, Inbred DBAEscherichia 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.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.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.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.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.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.Antibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Proteomics: The systematic study of the complete complement of proteins (PROTEOME) of organisms.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.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.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).Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.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.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.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.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Hemoglobinuria, Paroxysmal: A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.

Immunohistochemical analysis of arterial wall cellular infiltration in Buerger's disease (endarteritis obliterans). (1/363)

PURPOSE: The diagnosis of Buerger's disease has depended on clinical symptoms and angiographic findings, whereas pathologic findings are considered to be of secondary importance. Arteries from patients with Buerger's tissue were analyzed histologically, including immunophenotyping of the infiltrating cells, to elucidate the nature of Buerger's disease as a vasculitis. METHODS: Thirty-three specimens from nine patients, in whom Buerger's disease was diagnosed on the basis of our clinical and angiographic criteria between 1980 and 1995 at Nagoya University Hospital, were studied. Immunohistochemical studies were performed on paraffin-embedded tissue with a labeled streptoavidin-biotin method. RESULTS: The general architecture of vessel walls was well preserved regardless of the stage of disease, and cell infiltration was observed mainly in the thrombus and the intima. Among infiltrating cells, CD3(+) T cells greatly outnumbered CD20(+) B cells. CD68(+) macrophages or S-100(+) dendritic cells were detected, especially in the intima during acute and subacute stages. All cases except one showed infiltration by the human leukocyte antigen-D region (HLA-DR) antigen-bearing macrophages and dendritic cells in the intima. Immunoglobulins G, A, and M (IgG, IgA, IgM) and complement factors 3d and 4c (C3d, C4c) were deposited along the internal elastic lamina. CONCLUSION: Buerger's disease is strictly an endarteritis that is introduced by T-cell mediated cellular immunity and by B-cell mediated humoral immunity associated with activation of macrophages or dendritic cells in the intima.  (+info)

Deficiency of human complement protein C4 due to identical frameshift mutations in the C4A and C4B genes. (2/363)

The complement protein C4, encoded by two genes (C4A and C4B) on chromosome 6p, is the most polymorphic among the MHC III gene products. We investigated the molecular basis of C4 deficiency in a Finnish woman with systemic lupus erythematosus. C4-specific mRNA was present at low concentrations in C4-deficient (C4D) patient fibroblasts, but no pro-C4 protein was detected. This defect in C4 expression was specific in that synthesis of two other complement proteins was normal. Analysis of genomic DNA showed that the proposita had both deleted and nonexpressed C4 genes. Each of her nonexpressed genes, a C4A null gene inherited from the mother, a C4A null gene, and a C4B null gene inherited from the father, all contained an identical 2-bp insertion (TC) after nucleotide 5880 in exon 29, providing the first confirmatory proof of the C4B pseudogene. This mutation has been previously found only in C4A null genes. Although the exon 29/30 junction is spliced accurately, this frameshift mutation generates a premature stop at codon 3 in exon 30. These truncated C4A and C4B gene products were confirmed through RT-PCR and sequence analysis. Among the possible genetic mechanisms that produce identical mutations is both genes, the most likely is a mutation in C4A followed by a gene conversion to generate the mutated C4B allele.  (+info)

Interaction between protein S and complement C4b-binding protein (C4BP). Affinity studies using chimeras containing c4bp beta-chain short consensus repeats. (3/363)

Human C4b-binding protein (C4BP) is a regulator of the complement system and plays an important role in the regulation of the anticoagulant protein C pathway. C4BP can bind anticoagulant protein S, resulting in a decreased cofactor function of protein S for activated protein C. C4BP is a multimeric protein containing several identical alpha-chains and a single beta-chain (C4BPbeta), each chain being composed of short consensus repeats (SCRs). Previous studies have localized the protein S binding site to the NH2-terminal SCR (SCR-1) of C4BPbeta. To further localize the protein S binding site, we constructed chimeras containing C4BPbeta SCR-1, SCR-2, SCR-3, SCR-1+2, SCR-1+3, and SCR-2+3 fused to tissue-type plasminogen activator. Binding assays of protein S with these chimeras indicated that SCR-2 contributes to the interaction of protein S with SCR-1, since the affinity of protein S for SCR-1+2 was up to 5-fold higher compared with SCR-1 and SCR-1+3. Using an assay that measures protein S cofactor activity, we showed that cofactor activity was decreased due to binding to constructs that contain SCR-1. SCR-1+2 inhibited more potently than SCR-1 and SCR-1+3. SCR-3 had no additional effect on SCR-1, and therefore the effect of SCR-2 was specific. In conclusion, beta-chain SCR-2 contributes to the interaction of C4BP with protein S.  (+info)

Consumption of C4b-binding protein (C4BP) during in vivo activation of the classical complement pathway. (4/363)

C4BP has a central role in regulating the classical complement (C') pathway, but it is still uncertain whether or not it is consumed during in vivo complement activation. Attempts to demonstrate changes in C4BP plasma levels in systemic lupus erythematosus and essential mixed cryoglobulinaemia have failed, probably due to up-regulation of this protein during the inflammatory reaction. We have studied one patient with severe post-transfusion complement-mediated anaphylaxis (CMA), and 67 patients with hereditary C1 inhibitor deficiency (hereditary angioedema (HAE)). The first of these two conditions is characterized by the absence of systemic inflammatory reaction and the second by acute and chronic activation of the C' classical pathway. C4BP, C4BP-C4b complex, and soluble terminal C' complex (sC5b-9) were measured in the patients' plasmas by ELISA techniques and C3a and C4a by radioimmunoassays. In CMA, 15 min after the transfusion, there was a massive C' activation, with increases in C4a, C3a, sC5b-9, C4BP-C4b complexes and decreases in C4, C3 and C4BP. All parameters reverted to preinfusion values within 24 h. Depletion of C4 was correlated with that of C4BP. In patients with HAE, the median value of C4BP (83% range 54-165) was significantly lower (P < 0.0001) than in normal controls (99% range 70-159), with no difference between patients in remission or during acute attacks. C4BP-C4b complexes could not be detected in HAE patients. The results of this study indicate that C4BP is consumed in vivo during acute, and possibly during chronic activation of the C' classical pathway, and that this protein, after interaction with C4b, not longer circulates in plasma.  (+info)

Some anticardiolipin antibodies recognize a combination of phospholipids with thrombin-modified antithrombin, complement C4b-binding protein, and lipopolysaccharide binding protein. (5/363)

The standard enzyme-linked immunosorbent assay (ELISA) for anticardiolipin antibodies (ACA) detects a heterogenous group of antibodies against cardiolipin on its own, beta2-glycoprotein I (beta2GPI), and, potentially, other phospholipid-binding plasma proteins from bovine or human origin. In an attempt to identify new proteic targets of ACA, we selected 6 patients who possessed cofactor-dependent ACA but no antibody to human or bovine beta2GPI detectable in the beta2GPI-ELISA. Three of these samples proved to recognize beta2GPI in combination with cardiolipin, but not beta2GPI directly immobilized on gamma-irradiated polystyrene or agarose beads. In the other cases, the component required for ACA binding was purified from adult bovine serum or plasma by means of ammonium sulfate precipitation and chromatography on Phenyl-Sepharose, diethyl aminoethyl (DEAE)-cellulose, heparin-Ultrogel, and Sephacryl S-300 columns. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis coupled to N-terminal amino acid microsequencing identified the cofactors of patients no. 4, 5, and 6 ACA as lipopolysaccharide binding protein (LBP), complement C4b-binding protein (C4BP), and the thrombin-antithrombin (AT) complex, respectively. Adsorption of each of these cofactor preparations with cardiolipin liposomes led to suppression of ACA reactivity, concomitant with the loss of bands from SDS gels corresponding to sequenced material. Bacterial lipopolysaccharide (which forms high-affinity complexes with LBP) specifically neutralized the cofactor activity of the LBP preparation in a concentration-dependent manner. Bovine serum and plasma, as well as the C4BP preparation, optimally supported the binding of a rabbit anti-C4BP antiserum to immobilized cardiolipin. The binding of a rabbit anti-AT antiserum to solid-phase cardiolipin was sustained by the thrombin-AT preparation and bovine serum, but neither by bovine plasma nor by native AT, thus reproducing the behavior of patient no. 6 ACA. Taking advantage of the restricted recognition by the latter ACA of a cofactor from bovine origin appearing upon clotting, we studied the generation of such activity in human plasma supplemented with bovine AT or bovine prothrombin before clotting. In these conditions, patient no. 6 antibody binding to cardiolipin required the addition of bovine AT, whereas addition of bovine prothrombin alone was ineffective. We therefore concluded that those ACA targeted bovine AT once it has been modified/cleaved by thrombin. These findings underline the wide heterogeneity of ACA and the links that may exist between various coagulation pathways, inflammation and the complement system.  (+info)

A cluster of positively charged amino acids in the C4BP alpha-chain is crucial for C4b binding and factor I cofactor function. (6/363)

C4b-binding protein (C4BP) is a regulator of the classical complement pathway, acting as a cofactor to factor I in the degradation of C4b. Computer modeling and structural analysis predicted a cluster of positively charged amino acids at the interface between complement control protein modules 1 and 2 of the C4BP alpha-chain to be involved in C4b binding. Three C4BP mutants, R39Q, R64Q/R66Q, and R39Q/R64Q/R66Q, were expressed and assayed for their ability to bind C4b and to function as factor I cofactors. The apparent affinities of R39Q, R64Q/R66Q, and R39Q/R64Q/R66Q for immobilized C4b were 15-, 50-, and 140-fold lower, respectively, than that of recombinant wild type C4BP. The C4b binding site demonstrated herein was also found to be a specific heparin binding site. In C4b degradation, the mutants demonstrated decreased ability to serve as factor I cofactors. In particular, the R39Q/R64Q/R66Q mutant was inefficient as cofactor for cleavage of the Arg937-Thr938 peptide bond in C4b. In contrast, the factor I mediated cleavage of Arg1317-Asn1318 bond was less affected by the C4BP mutations. In conclusion, we identify a cluster of amino acids that is part of a C4b binding site involved in the regulation of the complement system.  (+info)

Analysis of human C4A and C4B binding to an immune complex in serum. (7/363)

Previous studies using isolated complement proteins have shown that more C4A than C4B binds to certain types of immune complexes. However, the in vivo binding of the C4 isoforms to an immune complex has not been investigated in detail and may differ from events when measured with the isolated proteins. We report here the binding of C4A and C4B to an immune complex of bovine serum albumin (BSA) anti-BSA as it occurs in serum. We found that when using the isolated C4 proteins more C4A than C4B bound to the complex, but in serum similar amounts of C4A and C4B were found to bind. Furthermore, these results were not explainable by a difference in activity between isoforms. In an attempt to explain these results a number of unexpected observations were noted. First C4A, but not C4B, bound specifically to a yet unidentified 38-kD serum protein. Second, when both covalent and non-covalent binding was assessed, we found that as serum concentration increased there followed a concomitant decrease in covalent binding and C4B was more affected than C4A. The potential biological significance of these findings is discussed.  (+info)

Upregulation of ICAM-1 on cardiomyocytes in jeopardized human myocardium during infarction. (8/363)

OBJECTIVE: Impaired perfusion of the myocardium induces a local inflammatory response. In animal models, there is ample evidence that polymorphonuclear leucocytes (PMNs) infiltrating infarcted myocardium contribute significantly to infarct size. METHODS: To explore a possible role for PMNs in the tissue damage of human myocardial infarction, we investigated localization of intercellular adhesion molecule-1 (ICAM-1) and CD66b (previously clustered as CD67), a marker of degranulation of human PMNs, in relation to deposition of complement in tissue specimens of infarcted and healthy parts of the heart obtained from 20 patients, who had died following acute myocardial infarction. RESULTS: ICAM-1 was transiently expressed by endothelium and for a longer period (few days) on myofibers of infarcted myocardium. This expression only occurred in parts that stained positive for complement. PMN infiltration exclusively occurred in areas with ICAM-1 expression, but not every ICAM-1-positive area contained PMN infiltrates. CD66b was found in PMNs but was also fixed to the plasma membrane of myofibers that stained positive for complement and ICAM-1. CONCLUSION: These findings indicate that, in infarcted human myocardium, PMNs are degranulated, possibly upon interaction with ICAM-1 and activated complement.  (+info)

*Complement component 4

... or C4B-C4B) and 31% trimodular configuration (equally split between LLL as C4A-C4A-C4B or LSS as C4A-C4B-C4B). Regarding C4 ... C4b and C2a, from their complex (whereupon C4b can bind another protein C2, and conduct these steps again). Because C4b is ... an effect produced by the effector proteins of the complement system in which the C4 partakes). Complement system Complement ... Law SK, Dodds AW, Porter RR (August 1984). "A comparison of the properties of two classes, C4A and C4B, of the human complement ...

*C4b-binding protein

... (C4BP) is a protein involved in the complement system where it acts as inhibitor. C4BP has an octopus-like ... Complement C4b-Binding Protein at the US National Library of Medicine Medical Subject Headings (MeSH). ... C4BP accelerates decay of C3-convertase and is a cofactor for serine protease factor I which cleaves C4b and C3b. C4BP binds ... The genes coding for C4BP α-chain (C4BPA) and β-chain (C4BPB) are located in the regulators of complement activation (RCA) gene ...

*Borrelia recurrentis

... duttonii acquire complement regulators C4b-binding protein and factor H". Infection and Immunity. 74 (7): 4157-63. doi:10.1128/ ...

*Protein S

In the circulation, Protein S exists in two forms: a free form and a complex form bound to complement protein C4b-binding ... Protein S also binds to the nascent complement complex C5,6,7 and prevents this complex from inserting into a membrane. This ... Dahlbäck B (2007). "The tale of protein S and C4b-binding protein, a story of affection". Thromb. Haemost. 98 (1): 90-6. doi: ... Griffin JH, Gruber A, Fernández JA (1992). "Reevaluation of total, free, and bound protein S and C4b-binding protein levels in ...

*Complement receptor 1

Complement receptor type 1 (CR1) also known as C3b/C4b receptor or CD35 (cluster of differentiation 35) is a protein that in ... LHR-A binds preferentially to the complement component C4b: LHR-B and LHR-C bind to C3b and also, albeit with a lower affinity ... Membrane cofactor protein is a widely distributed C3b/C4b binding regulatory glycoprotein of the complement system; decay- ... "Identification of a partial cDNA clone for the human receptor for complement fragments C3b/C4b". Proc. Natl. Acad. Sci. U.S.A. ...

*C4A

"Importance of the alpha 3-fragment of complement C4 for the binding with C4b-binding protein". FEBS Letters. 271 (1-2): 131-6. ... Complement C4-A is a protein that in humans is encoded by the C4A gene. This gene encodes the acidic form of complement factor ... "Structural basis of the polymorphism of human complement components C4A and C4B: gene size, reactivity and antigenicity". The ... A large intron (6.5 kb) is present in all C4A genes and some C4B genes". Immunogenetics. 25 (5): 299-304. doi:10.1007/ ...

*Protein S deficiency

Protein S circulates in human plasma in two forms: approximately 60 percent is bound to complement component C4b β-chain while ...

*Neisseria meningitidis

Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding ... fHbp protects meningococci from complement-mediated death in human serum experiments, but has also been shown to protect ... Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important ... and complement deficiency. The incubation period is short, from 2 to 10 days. In susceptible individuals, N. meningitidis may ...

*C5-convertase

The classical pathway C5 convertase is composed of the larger fragments of complement proteins, C4b, C2b produced by cleavage ... The complement component C5 can be also activated by fluid phase C5 convertase. C5 is activated by CVFBb in the presence of ... In these respects, the mode of action of C5 is completely analogous to that of the other components of complement. The C5 step ... The binding of C5 is influenced by C6 and C7, components which are thought to act subsequent to it in the complement sequence. ...

*Opsonin

The complement system is a part of the innate immune response. C3b, C4b, and C1q are important complement molecules that serve ... Complement receptor 1 is expressed on all phagocytes and recognizes a number of complement opsonins, including C3b and C4b ... In both cases C1q activates complement, resulting in the cells being marked for phagocytosis by C3b and C4b. C1q is an ... Antibodies can also activate complement via the classical pathway, resulting in deposition of C3b and C4b onto the antigen ...

*Cold agglutinin disease

In lieu of the membrane attack complex, complement proteins (particularly C3b and C4b) are deposited on red blood cells. This ... Binding of antibodies to red blood cells activates the classical pathway of the complement system. If the complement response ... Detection of antibodies (cold or warm) and /or complement system on RBC from the patient is a direct Coombs antiglobulin test ... In the formation of the membrane attack complex, several complement proteins are inserted into the red blood cell membrane, ...

*SKIV2L

"Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the C4B genes ... are present between complement component genes factor B and C4 in the class III region of the HLA". Genomics. 53 (3): 338-47. ... "Features of the two gene pairs RD-SKI2W and DOM3Z-RP1 located between complement component genes factor B and C4 at the MHC ...

*STK19

"Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the C4B genes ... 1996). "Complete sequence of the complement C4 gene from the HLA-A1, B8, C4AQ0, C4B1, DR3 haplotype". Immunogenetics. 43 (4): ... "Entrez Gene: STK19 serine/threonine kinase 19". Yu CY (1991). "The complete exon-intron structure of a human complement ... 1998). "Four ubiquitously expressed genes, RD (D6S45)-SKI2W (SKIV2L)-DOM3Z-RP1 (D6S60E), are present between complement ...

*Complement receptor 2

1987). "A complement receptor locus: genes encoding C3b/C4b receptor and C3d/Epstein-Barr virus receptor map to 1q32". J. ... Complement receptor type 2 (CR2), also known as complement C3d receptor, Epstein-Barr virus receptor, and CD21 (cluster of ... homology with the receptor for fragments C3b and C4b of the third and fourth components of complement". Proc. Natl. Acad. Sci. ... Complement receptor 2 has been shown to interact with CD19. Epstein-Barr virus (EBV) binds to B cells at CR2 during infection ...

*CD46

... of complement components C3b and C4b by serum factor I, which protects the host cell from damage by complement. The protein ... The protein encoded by this gene is a type I membrane protein and is a regulatory part of the complement system. The encoded ... CD46 complement regulatory protein also known as CD46 (cluster of differentiation 46) and Membrane Cofactor Protein is a ... This gene is found in a cluster on chromosome 1q32 with other genes encoding structural components of the complement system. At ...

*Complement factor I

... , also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. Complement ... that regulates complement activation by cleaving cell-bound or fluid phase C3b and C4b. Factor I deficiency in turn leads to ... complement factor I". Goldberger G, Bruns GA, Rits M, Edge MD, Kwiatkowski DJ (Jul 1987). "Human complement factor I: analysis ... Leitão MF, Vilela MM, Rutz R, Grumach AS, Condino-Neto A, Kirschfink M (Dec 1997). "Complement factor I deficiency in a family ...

*C3a (complement)

C1q mediates the classical pathway by activating the C1 complex, which cleaves C4 and C2 into smaller fragments (C4a, C4b, C2a ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ... C3a is one of the proteins formed by the cleavage of complement component 3; the other is C3b. C3a is a 77 residue ... Anaphylatoxins are small complement peptides that induce proinflammatory responses in tissues. C3a is primarily regarded for ...

*Sushi domain

Complement receptor type 1 (C3b/C4b receptor) (Antigen CD35) belongs to the Knops blood group system and is associated with Kn( ... Complement decay-accelerating factor (Antigen CD55) belongs to the Cromer blood group system and is associated with Cr(a), Dr(a ... Complement components may activate B cells through CD21. CD21 is part of a large signal-transduction complex that also involves ... Sushi domains, also known as Complement control protein (CCP) modules, or short consensus repeats (SCR), exist in a wide ...

*Macrophage-1 antigen

It binds to iC3b and C4b. Complement receptor 3 (CR3)(CD11b/CD18) is a human cell surface receptor found on polymorphonuclear ... "Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3". J. ... Wagner C, Hänsch GM, Stegmaier S, Denefleh B, Hug F, Schoels M (April 2001). "The complement receptor 3, CR3 (CD11b/CD18), on T ... Macrophage-1 antigen (or integrin αMβ2 or macrophage integrin or Mac-1) is a complement receptor ("CR3") consisting of CD11b ( ...

*Complement system

In the classical pathway, C4 binds to Ig-associated C1q and C1r2s2 enzyme cleaves C4 to C4b and 4a. C4b binds to C1q, antigen- ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ... The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells ...

*Anaphylatoxin

C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin receptors Anaphylaxis Complement system Inflammation Immune system ... that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are large ... Ogata, R. T.; Rosa, P. A.; Zepf, N. E. (1989). "Sequence of the gene for murine complement component C4". The Journal of ... C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, ...

*C3-convertase

DAF protects host cells from damage by autologous complement. DAF acts on C2b and Bb and dissociates them rapidly from C4b and ... C4b-binding protein inhibits the haemolytic function of cell-bound C4b. C4b-binding protein and C3b inactivator control the C3 ... C3 convertase (EC 3.4.21.43, C42 , C4bC2b, C3bBb, complement C.hivin.4.hivin2, complement C3 convertase) belongs to family of ... complement receptor 1 (CR1), C4b-binding protein and Factor H. Convertase assembly is suppressed by the proteolytic cleavage of ...

*Factor I deficiency

Deficiency in the Complement factor I, also known as C3b/C4b inactivator. ...

*CFHR1

2005). "Interaction between complement regulators and Streptococcus pyogenes: binding of C4b-binding protein and factor H/ ... "Entrez Gene: CFHR1 complement factor H-related 1". Zipfel PF, Skerka C (1994). "Complement factor H and related proteins: an ... Complement factor H-related protein 1 is a protein that in humans is encoded by the CFHR1 gene. GRCh38: Ensembl release 89: ... 2000). "Complement factor H: sequence analysis of 221 kb of human genomic DNA containing the entire fH, fHR-1 and fHR-3 genes ...

*Antibody opsonization

... complex also creates byproducts like C3b and C4b which are important components for the efficient function of the complement ... As well as endocytic PRRs, phagocytes furthermore express opsonin receptors such as Fc receptor and complement receptor 1 (CR1 ... Should the microbe be coated with opsonising antibodies or C3b complement, the co-stimulation of endocytic PRR and opsonin ...

*Pattern recognition receptor

Together, MBL, C4b and C2a are known as the C3 convertase. C3 is cleaved into its a and b subunits, and C3b binds the ... Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... Once bound to the ligands MBL and Ficolin oligomers recruit MASP1 and MASP2 and initiate the lectin pathway of complement ... binding the C4b subunit and releasing C4a into the bloodstream; similarly, binding of C2 causes release of C2b. ...
La physe des fontaines de Banff (Physella johnsoni [Clench, 1926]) est un petit gastéropode aquatique à coquille globulaire, spiralée vers la gauche (senestre) et mesurant jusquà 11 mm de longueur. Des analyses morphologiques et moléculaires donnent à croire quil sagit dune espèce valide, mais le statut de ce taxon ne fait pas lunanimité. La différenciation de cette espèce serait survenue il y a 3 200 à 5 300 ans, ce qui explique la faible divergence génétique observée entre elle et ses ancêtres.
يهيمن المجلس على قواعد الدراسة والامتحانات والمعادلات والممارسة وشهادة اتمام التدريب الاساسى (لا توجد فىمصر حتى الان) ونقاط التنمية المهنية المستدامة ويسجل الاطباء بناء على مؤهل وبرنامج تدريب قومى ويحاسبهم. ينشأ المجلس كليات قومية تجرى امتحانات قومية أيا كان مكان عمل الطبيب وتنميه مهنيا بالتعاون مع الجمعيات العلمية المسجلة (اقترح اعادة تسجيلها نظرا لعددها الحالي غير الواقعي والصراعات بينها) بدلا من تأرجح الطبيب بين شهادات جامعية متفاوتة المستوى فى انحاء مصر وبين قبول تسجيله فى جامعة ما وفيما يطلق عليه زمالة وزارة الصحة التي تطبق علي البعض فقط ...
TY - JOUR. T1 - Histopathology and immunophenotype of the spleen during acute antibody-mediated rejection. T2 - Case report. AU - Kaplan, B.. AU - Jie, Tun. AU - Diana, R.. AU - Renz, J.. AU - Whinery, A.. AU - Stubbs, N.. AU - Bracamonte, E.. AU - Perry, Catherine S. AU - Schubart, P.. AU - Rilo, H.. AU - Gruessner, Rainer W G. PY - 2010/5. Y1 - 2010/5. N2 - Splenectomy has been reported to have a beneficial effect in treating Acute antibody-mediated rejection (ABMR). This reason for this often rapid and profound beneficial effect is not readily apparent from what is known about normal splenic immunoarchitecture. While the spleen is rich in mature B cells, it has not been noted to be a repository for direct antibody-secreting cells. We present a case of a Native American female who received a renal transplant and developed a severe episode of ABMR. The patient was initially refractory to both plasmapheresis and IVIG. The patient underwent an emergent splenectomy with almost immediate ...
Looking for Antibody-Mediated Rejection? Find out information about Antibody-Mediated Rejection. Destruction of a graft by the immune system of the recipient. Rejection in a dream may suggest that there are feelings or situations the dreamer wants to be... Explanation of Antibody-Mediated Rejection
article{b6c22ab7-8314-43e4-a60f-8c80bb2fb02a, author = {Blom, Anna and Kask, Lena and Ramesh, Bala and Hillarp, Andreas}, issn = {0003-9861}, language = {eng}, number = {2}, pages = {108--118}, publisher = {Academic Press}, series = {Archives of Biochemistry and Biophysics}, title = {Effects of zinc on factor I cofactor activity of C4b-binding protein and factor H.}, url = {http://dx.doi.org/10.1016/j.abb.2003.08.018}, volume = {418}, year = {2003 ...
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Buy Tube, capillary,part #C6469501 and ship it today! Our 365-day return policy guarantees youll always get the right part!
TY - JOUR. T1 - The Value of Protocol Biopsies to Identify Patients With De Novo Donor-Specific Antibody at High Risk for Allograft Loss. AU - Schinstock, Carrie. AU - Cosio, Fernando G. AU - Cheungpasitporn, W.. AU - Dadhania, D. M.. AU - Everly, M. J.. AU - Samaniego-Picota, M. D.. AU - Cornell, L.. AU - Stegall, Mark D. PY - 2017/6/1. Y1 - 2017/6/1. N2 - De novo donor-specific antibody (dnDSA) is associated with antibody-mediated rejection (AMR) and allograft loss, yet the allograft histology associated with dnDSA remains unclear. The aim of this study was to examine the allograft histology associated with dnDSA in patients with serial surveillance biopsies. We retrospectively studied adult conventional solitary kidney transplant recipients from October 2007 to May 2014. The definition of dnDSA was new donor-specific antibody (DSA) with mean fluorescence intensity (MFI) ,1000. The incidence of dnDSA was 7.0% (54 of 771) over mean follow-up of 4.2 ± 1.9 years. Patients with dnDSA had reduced ...
La nostra investigació està dedicada a lestudi dels mecanismes moleculars de la mort i la proliferació cel·lular, ja que aquests estan involucrats en el desenvolupament de diferents patologies humanes.. ...
We are pleased to introduce a new application for one of our neural progenitor markers. In this study our Chicken Nestin Antibody is used to stain these progenitors in dissected mouse brains: Gleave JA, Lerch JP, Henkelman RM, Nieman BJ (2013) A Method for 3D Immunostaining and Optical Imaging of the Mouse Brain Demonstrated in Neural Progenitor Cells. PLoS ONE 8(8): e72039. doi:10.1371/journal.pone.0072039. 3D antibody staining of adult mouse brains: 1% PFA perfused adult mouse brains were removed from the skull and then divided by removing the cerebellum and separating the hemispheres if desired. The samples were immediately dehydrated in a gradient of methanol solutions to 100% methanol over the course of one day. Immediate dehydration is important to preserve the cellular morphology of the lightly-fixed brain. The samples then underwent freeze/thaw (one hour at -80°C/one hour at room temperature) four times. The samples were rehydrated in a gradient of methanol solutions to PBS over the ...
Register today for this webinar, part of the AST Timely Topics in Transplantation Webinar Series. All webinars are broadcast live, and the webinar recording is made available on demand after the live air date. View full details and register here: myAST.org/T3.
Mouse Monoclonal Anti-Complement C4d Antibody (C4D204) [DyLight 550]. Acute Humoral Rejection Marker. Validated: ICC/IF, IHC-Fr, IHC-P. Tested Reactivity: Human. 100% Guaranteed.
Mouse Monoclonal Anti-Complement C4b/d Antibody (SPM545) [PerCP]. Acute Humoral Rejection Marker. Validated: ICC/IF, IHC-Fr, IHC-P. Tested Reactivity: Human. 100% Guaranteed.
2QOS: Crystal structure of complement protein C8gamma in complex with a peptide containing the C8gamma binding site on C8alpha: Implications for C8gamma ligand binding.
This work was supported by the Deutsche Forschungsgemeinschaft within FOR1061 to K. You need hosting and domain name. After 5 h, the channel is localized in the lysosomes, as shown by the pronounced QDots staining of these organelles (bottom). With our content marketing and SEO serviceswell get the right kind of visitors frequenting your website. Our people are empowered to go above breaking changes in sql server 2008 beyond to deliver the best experience in hosting. This is typically the easiest to use and will fit your needs as a beginner. After 24-48 hours, your domain name should be point to your changess web hosting service. Three regions with large positive ООCО values indicate the three Овhelices. We are excited to announce that we are migrating our infrastructure and our order management platform to a new state of the art system. Rhino Web Studios also offers SEO, copywriting, photography, animation, web training, and music composing and sound services. They needed a new accounting ...
Electron microscopy shows widening of the subendothelial zone with interposition of cell processes, loose material, and early basement membrane reduplication, findings consistent with transplant glomerulopathy. (Return to Case Page ...
A group O D-positive patient with no prior history of RBC transfusion and whose antibody screen result was negative prior to receivingIV RhIG one day...
De Banff Cocktail is een cocktail met Crème de Grand Marnier uit het "New New York Bartenders Guide" boek. In het recept staat om Canadese whiskey te gebruiken, maar geen rye whiskey. Aangezien mijn Canadese whiskey wel een flinke hoeveelheid rogge bevat heb ik dan maar besloten om Bourbon te gebruiken ...
The Banff Classification is a schema for nomenclature and classification of renal allograft pathology, established in 1991 by Kim Solez and Lorraine C. Racusen in Banff, Canada. The initiative was "inspired by the then recent development of a consensus grading system for diagnosis of rejection in cardiac allografts led by Dr Margaret Billingham, a key participant at the first Banff meeting". Prior the Banff Classification there was no standardized, international classification for renal allograft biopsies, which resulted in considerable heterogeneity among pathologists in characterization of renal allograft biopsies. The first Banff schema was published in 1993, and has since undergone updates at regular intervals. The classification is expanded and updated every two years in meetings organized by the Banff Foundation for Allograft Pathology. An evaluation of the Banff Classification in March 2000 confirmed significant association between the revised Banff 97 classification and graft outcome. ...
Sigma-Aldrich offers abstracts and full-text articles by [Thomas Bachelet, Celine Nodimar, Jean-Luc Taupin, Sebastien Lepreux, Karine Moreau, Delphine Morel, Gwendaline Guidicelli, Lionel Couzi, Pierre Merville].
article{5be1f4a6-d9f6-43e4-84be-f1c903a8b6fe, abstract = {C4b-binding protein (C4BP), an important inhibitor of complement activation, has a unique spider-like shape. It is composed of six to seven identical alpha-chains with or without a single beta-chain, the chains being linked by disulfide bridges in their C-terminal parts. To elucidate the structural requirements for the assembly of the alpha-chains, recombinant C4BP was expressed in HEK 293 cells. The expressed C4BP was found to contain six disulfide-linked alpha-chains. Pulse-chase analysis demonstrated that the recombinant C4BP was rapidly synthesized in the cells and the polymerized C4BP appeared in the medium after 40 min. The alpha-chains were polymerized in the endoplasmic reticulum (ER) already after 5 min chase. The polymerization process was unaffected by blockage of the transport from the ER to the Golgi mediated by brefeldin A or low temperature (10 degrees C). The C-terminal part of the alpha-chain (57 amino acids), containing ...
... SAN FRANCISCO July 30 2014 /-...The study shows that post-transplant treatment with C1-INH results in ... Antibody-mediated rejection is a severe form of rejection that can oc...The placebo-controlled single-center study evaluated 20 highly sensit...,Study,Suggests,C1-INH,May,Aid,in,Prevention,of,Antibody-Mediated,Rejection,Following,Kidney,Transplant,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
Sellarés, J., Reeve, J., Loupy, A., Mengel, M., Sis, B., Skene, A., de Freitas, D. G., Kreepala, C., Hidalgo, L. G., Famulski, K. S. and Halloran, P. F. (2013), Molecular Diagnosis of Antibody-Mediated Rejection in Human Kidney Transplants. American Journal of Transplantation, 13: 971-983. doi: 10.1111/ajt.12150 ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Abcams Complement C4 ELISA Kit (ab108825) suitable for Cell culture supernatant, Saliva, Milk, Urine, Cerebral Spinal Fluid in human. Reliably quantify 0.07…
MONOCYTE/MACROPHAGES AND C4d IN RENAL ALLOGRAFTS. Alex Magil, MD. BACKGROUND. ACUTE HUMORAL REJECTION (AHR) C ´ split factor C4d generated by Ag-Ab reaction C4d binds covalently to PTC endothelium & BM PTC C4d is a putative marker for AHR Associated with poor outcome. Slideshow 3381369 by rufina
Although considered the gold standard, histologic examination of renal transplant biopsies, expert pathologists frequently disagree on their interpretation of the same sample. The authors of this paper have developed criteria for antibody-mediated rejection based on mRNA expression in biopsy samples detected by microarrays. In this study, they validate their previous findings in a cohort of […]. ...
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TY - JOUR. T1 - Isometric tubular epithelial vacuolization in renal allograft biopsy specimens of patients receiving low-dose intravenous immunoglobulin for a positive crossmatch. AU - Haas, Mark. AU - Sonnenday, Christopher J.. AU - Cicone, Jeffrey S.. AU - Rabb, Hamid. AU - Montgomery, Robert A.. PY - 2004/8/27. Y1 - 2004/8/27. N2 - Background. Perioperative treatment with plasmapheresis and intravenous immunoglobulin (IVIG), combined with a tacrolimus-based immunosuppressive regimen, has been used successfully to allow renal transplantations in crossmatch-positive recipients. A common finding in biopsy specimens of these allografts is isometric vacuolization of proximal tubular epithelium. This finding presents a diagnostic dilemma because it may occur secondary to IVIG treatment or tacrolimus nephrotoxicity. Methods. We compared the frequency and severity of isometric tubular vacuolization in renal allograft biopsy specimens obtained during the first 10 days after transplantation in 24 ...
Controversy exists regarding the criteria used for the diagnosis of Antibody-mediated rejection (AMR) and a consensus has not been reached regarding the most appropriate criteria for the diagnosis. Recent data have suggested the use of Immunohistochemistry for the presence of C4d as being adequate for the diagnosis but has not been uniformly accepted. The added utility of C3d staining in addition to C4d is unknown.. METHODS: We evaluated endomyocardial biopsies from consecutive patients collected over a 14 month period. Biopsies were screened for the presence of complement deposition, specifically C4d and C3d. Electronic medical records were reviewed retrospectively for the clinical data and the diagnosis of clinically relevant AMR.. RESULTS: A total of 1511 endomyocardial biopsies were performed on 330 consecutive patients. Eighteen patients were found to have evidence of C4d complement staining and 18 patients with both C4d and C3d staining. Mortality was significantly higher (28% vs 0%, p , ...
Purpose of Review: Over the past two decades, significant strides made in our understanding of the etiology of antibody-mediated rejection (AMR) in transplantation have put the complement system in the spotlight. Here, we review recent progress made in the field of pharmacologic complement inhibition in clinical transplantation and aim to understand the impact of this therapeutic approach on outcomes in transplant recipients. Recent Findings: Encouraged by the success of agents targeting the complement cascade in disorders of unrestrained complement activation like paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), investigators are testing the safety and efficacy of pharmacologic complement blockade in mitigating allograft injury in conditions ranging from AMR to recurrent post-transplant aHUS, C3 glomerulopathies and antiphospholipid anti-body syndrome (APS ...
In this study, the puzzling phenomenon of spontaneous coexistence of D-positive and D-negative RBC subpopulations was investigated. In a representative number of 9 patients with mixed Rh phenotype, the prevailing molecular background of this condition was elucidated. Rh mosaicism involving a hematopoietic stem-cell line with LOH on chromosome 1 was demonstrated to be the key mechanism for the observed RBC phenotype anomalies.. Frequent causes of mixed Rh phenotype, such as RBC transfusion or HSCT, had been ruled out in these patients, which was also confirmed by the fact that Rh and in one case also Fy but not other blood group antigens were affected. In addition, none of the patients displayed congenital or acquired chimerism,4 as evidenced by microsatellite analysis. This result was remarkable, as spontaneous chimerism had been reported to occur quite frequently.5,46. The immunohematologic properties of the D-positive and D-negative RBC subpopulations indicated loss of one complete RH ...
The SCOP classification for the Complement control module/SCR domain family. Additional information, provided for both this family and the superfamily it belongs to, includes SUPERFAMILY links to genome assignments, alignments, domain combinations, taxonomic visualisation and hidden Markov model information.
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A transient decrease in hemoglobin is to be expected following IV RhIG therapy in D-positive patients. In a large study of 272 patients,3 hemolysis wa...
TY - JOUR. T1 - Use of Ultrasound and Cystoscopically Guided Pancreatic Allograft Biopsies and Transabdominal Renal Allograft Biopsies. T2 - Safety and Efficacy in Kidney-Pancreas Transplant Recipients. AU - Kuhr, Christian S.. AU - Davis, Connie L.. AU - Barr, Darlene. AU - McVicar, John. AU - Perkins, James D.. AU - Bachi, Carlos E.. AU - Alpers, Charles E.. AU - Marsh, Christopher L.. PY - 1995. Y1 - 1995. N2 - The use of allograft biopsies to guide treatment after solid organ transplantation is a valuable tool in the detection and treatment of rejection. Prior development and use of the cystoscopically guided pancreatic allograft biopsy have allowed for more accurate and timely diagnosis of pancreatic allograft dysfunction, possibly contributing to our 1-year pancreas graft, renal allograft and patient survival rates of 87.1%, 88.5% and 96.8%, respectively. We reviewed our experience, examining efficacy and complication rates of pancreas and kidney biopsies in 31 cadaveric pancreas or ...
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Mark, L, Spiller, OB, Okroj, M, Chanas, S, Aitken, JA, Wong, SW, Damania, B, Blom, AM and Blackbourn, DJ (2007) Molecular characterization of the rhesus rhadinovirus (RRV) ORF4 gene and the RRV complement control protein it encodes ...
BACKGROUND: Natural killer (NK) cells localize in the microcirculation in antibody-mediated rejection (AMR) and have been postulated to be activated by donor-specific anti-HLA antibodies triggering their CD16a Fc receptors. However, direct evidence for NK cell CD16a triggering in AMR is lacking. We hypothesized that CD16a-inducible NK cell-selective transcripts would be expressed in human AMR biopsies and would offer evidence for CD16a triggering. METHODS: We stimulated human NK cells through CD16a in vitro, characterized CD16a-inducible transcripts, and studied their expression in human kidney transplant biopsies with AMR and in an extended human cell panel to determine their selectivity ...
Immune complexes (ICs) are formed to clear undesired material from the circulation in normal course and are elevated during disease pathologies. Elevated levels of ICs opsonized by complement activation by-products are present during viral infections such as H1N1, HIV, Hepatitis C, autoimmunity, and malignancies as well as during acute humoral rejection. The IC formation and their defective clearance trigger inflammatory response. ICs trigger complement activation and generate inflammatory mediators such as C3a and C5a anaphylotoxins. Complement opsonized ICs deposit at vascular sites, trigger proinflammatory response by releasing cytokines via Fc-receptor and/or complement receptor engagement. Antibodies present in the ICs by bind to activating or inhibitory Fc receptors (FcRs), which trigger effector function and regulate cellular responses. Myeloid cells express both activating and inhibitory FcRs. Complement opsonized ICs interact and regulate B-cell responses. ICs activate macrophages and produce
Your doctor removed a small piece of tissue from your transplanted kidney to examine it for signs of damage or rejection. The results of a transplant biopsy are usually available within a few hours, so if treatment is needed, it can be started as soon as possible.
Subject with a diagnosis of mild-moderate or severe CDAD (first occurrence or first recurrence within 3 months) with: Diarrhea: a change in bowel habits with > 3 liquid or unformed bowel movements (UBM) within 24 hours prior to randomization, AND Positive C. difficile toxin test on a stool sample produced within 72 hours prior to randomization ...
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PURPOSE Recently, bortezomib has been used to treat antibody-mediated rejection (AMR) refractory to conventional treatment such as plasmapheresis, intravenous immunoglobulin, and rituximab. The authors aimed to describe their experiences when bortezomib was used to treat refractory AMR. MATERIALS AND METHODS Eleven refractory AMR episodes treated with bortezomib were included in this study. The patients received one or two cycles of bortezomib (1.3 mg/m²) on days 1, 4, 8, and 11. RESULTS Bortezomib effectively reduced antibodies against various targets, including human leukocyte antigen (HLA) class I and II, ABO blood group antigen, and angiotensin II type 1 receptor. Antibodies were depleted or reduced significantly in eight AMR episodes. Overall, there was a significant improvement in the mean estimated glomerular filtration rate (eGFR) at 3 months after therapy (36.91±22.15 mL/min/1.73 m²) versus eGFR at time of AMR diagnosis (17.00±9.25 mL/min/1.73 m²; p=0.007). All six early-onset AMR
Kim Solez (born 1946) is an American pathologist and co-founder of the Banff Classification, the first standardized international classification for renal allograft biopsies. He is also the founder of the Banff Foundation for Allograft Pathology. Kim Solez obtained his M.D. with AOA honours from the University of Rochester School of Medicine and Dentistry, and trained in pathology at Johns Hopkins Medical Institutions in Baltimore, Maryland where he was mentored in renal pathology by Robert H. Heptinstall. He joined the faculty at Johns Hopkins and in 1987 became chairman of the Department of Pathology at the University of Alberta in Edmonton, Canada. In 1991, he established the Banff Classification, the first standardized, international classification for renal allograft biopsies, with Johns Hopkins pathologist Lorraine Racusen. The Banff Classification, updated in regular intervals, continues to "set standards worldwide for how biopsies from kidney and other solid organ transplants are ...
2016 International Society for Heart and Lung Transplantation. Background The diagnosis of antibody-mediated rejection (AMR) in the lung transplant is still an area under investigation. We performed a blinded multicenter study to determine if any statistically significant histologic findings in transbronchial biopsy specimens from lung transplant patients correlate with the presence of donor-specific antibodies (DSAs). Methods We asked 9 pathologists with experience in lung transplantation to evaluate 161 lung transplant biopsy specimens for various histologic parameters. The findings were correlated with antibody status positive for DSAs, positive for non-DSAs, and no antibodies (NABs) present. The significance of each histologic variable was reviewed. Results We found no statistically significant association with acute cellular rejection, airway inflammation, or bronchiolitis obliterans and the presence or absence of antibodies. However, biopsy specimens with DSAs had a statistically ...
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The human body is a mystery. As much and as fast as were learning, we still know very little. This post is about a recent discovery. I call it a "discovery," because Ive lived out what this theory holds to be true, as have a number of patients I work with, and perhaps some of you reading this. RCCX theory is quite complex. The best I can do is share my personal experience with the hope that doing so will help make this information more accessible. ...
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During the last 12 years 400 renal allograft biopsies have been performed at this institution to facilitate the differential diagnosis of post-transplant renal dysfunction. Of these cases significant urological complications occurred in 3. In 1 patient a caliceal cutaneous fistula developed after an open surgical biopsy, which required nephrostomy drainage for 6 months. The other 2 patients had needle biopsies and, subsequently, anuria occurred from ureteral blood clots. The problem resolved spontaneously after 23 hours in 1 patient and after 30 hours in the other. The complications in these 3 patients are believed to have resulted from a deeper biopsy and consequent damage to the medullary vasculature and the pelviocaliceal collecting system. Because of these and other potential problems, renal transplant biopsies should be performed by experienced staff, after careful consideration of the risk/benefit ratio at each individual setting.
The Major Histocompatibility Complex (MHC) is a gene-dense region located on the short arm of chromosome 6 (6p21.31). This region contains the highly polymorphic HLA genes as well as many other genes with immunological and non-immunological function. The susceptibility genes of many human disorders have been mapped to genes within the MHC. However, the genes themselves and indeed the locations of the genes, for many of the disorders, remain a mystery. This is a result of the high degree of linkage disequilibrium (LD) that exists between loci within the MHC. The high LD is explained by the genomic structure of the MHC. The MHC contains several blocks of DNA within which recombination is extremely rare, whereas the boundaries of the blocks are defined as "hotspots" of recombination. Most disease association studies have used the highly polymorphic HLA class I and class II genes which are separated by an, as yet, undefined number of blocks and several hundred kilobases of DNA. The MHC gamma block ...
definition of ABMR, what does ABMR mean?, meaning of ABMR, Autologous Bone Marrow Reinfusion, ABMR stands for Autologous Bone Marrow Reinfusion
BACKGROUND:. Free protein S (that portion of plasma protein S which is not in complex with C4b binding protein) is a cofactor for the anticoagulant effect of activated protein C. Patients presenting with acute myocardial infarction have significantly reduced levels of free protein S. If the major hypothesis proved correct, patients at high risk of myocardial infarction could be identified and could be targeted for future studies to examine specific intervention therapy.. DESIGN NARRATIVE:. The blinded and prospective study began in 1992, although the grant was first awarded in 1983. The goal was to determine if low levels of free protein S were associated with an increased incidence of myocardial infarction. Plasma samples were obtained yearly from 2,224 men aged 50-59 years who were participants in the Second Northwick Park Heart Study sponsored by the British Medical Research Council Epidemiology and Medical Care Unit. Clinical endpoints for the study were documented fatal and non-fatal ...
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... Prof. Dr. HUDA AL_KHATEEB 2011-2012 Lec.1 The Circulatory System Aim :study the histology of the circulatory system Objectives: 1. Study the layers and the sub-layers of the heart 2. Study the impulse conducting system structure and ultra-structure 3. Study the types of blood vessels 4. Study the classification of the arteries 5. Study the sorting of veins 6. Study the light and electron microscopical features of the capillaries 7. Classification of capillaries according to their ultra structures 8. Throw light on the lymphatic vessel 4 The circulatory system is categorized as: 1. blood vascular system: Consists of: 1. Heart 2. Vessels: A. arteries B. capillaries C. veins 2. Lymph vascular system: Consists of: 1. lymph vessels 2. organs Circulatory system can be divided into: 1. Macro-vasculature (includes vessels with more than 0.1mm in diameter). These vessels are seen grossly. 2. Micro-vasculature (includes arterioles, capillaries and postcapillary venules). These vessels are seen ...
In a paper published online in Nature Communications, a team of SickKids clinician-scientists led by Drs. Aleixo Muise and Walter Kahr report the discovery of a new hereditary condition: ARPC1B deficiency.
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61840DNAVaccinia virus 1tttttattat ttgtacgatg tccaggataa catttttacg gataaataaa tatgaaggtg 60gagagcgtga cgttcctgac attgttggga ataggatgcg ttctatcatg ctgtactatt 120ccgtcacgac ccattaatat gaaatttaag aatagtgtgg agactgatgc taatgctaat 180tacaacatag gagacactat agaatatcta tgtctacctg gatacagaaa gcaaaaaatg 240ggacctatat atgctaaatg tacaggtact ggatggacac tctttaatca atgtattaaa 300cggagatgcc catcgcctcg agatatcgat aatggccaac ttgatattgg tggagtagac 360tttggctcta gtataacgta ctcttgtaat agcggatatc atttgatcgg tgaatctaaa 420tcgtattgtg aattaggatc tactggatct atggtatgga atcccgaggc acctatttgt 480gaatctgtta aatgccaatc ccctccatct atatccaacg gaagacataa cggatacgag 540gatttttata ccgatgggag cgttgtaact tatagttgca atagtggata ttcgttgatt 600ggtaactctg gtgtcctgtg ttcaggagga gaatggtccg atccacccac gtgtcagatt 660gttaaatgtc cacatcctac aatatcaaac ggatacttgt ctagcgggtt taaaagatca 720tactcataca acgacaatgt agactttaag tgcaagtacg gatataaact atctggttcc 780tcatcatcta cttgctctcc aggaaataca tggaagccgg aacttccaaa atgtgtacgc 8402244PRTVaccinia virus ...
Gwinner, W., Suppa, S., Mengel, M., Hoy, L., Kreipe, H. H., Haller, H. and Schwarz, A. (2005), Early Calcification of Renal Allografts Detected by Protocol Biopsies: Causes and Clinical Implications. American Journal of Transplantation, 5: 1934-1941. doi: 10.1111/j.1600-6143.2005.00938.x ...
1G40: Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans.
Visit One Lambdas booth #1022 at ISHLT to discover how we can help improve your standard of care by reducing the risk of Antibody-Mediated Rejection (AMR) with our DSA monitoring products LABScreen™ Single Antigen and non-HLA biomarker assays including AT1R, and complement binding (C1q) antibodies.
It is increasingly evident that the brain is not isolated from events in the peripheral immune system and that innate pathways important in host protection can become dysregulated leading to neuropsychiatric changes. For example, increased copy number of the human complement C4A gene is a major risk factor for Schizophrenia; while in the periphery, it is protective against systemic autoimmunity such as lupus. Elevation in peripheral levels of interferon alpha (IFN-a) such as in viral infection, autoimmunity, interferonopathies or treatment with recombinant cytokine are strongly associated with psychiatric symptoms. We propose that blood-brain barrier entry of inflammatory cytokines such as IFN-a can activate multiple cell types in the brain triggering excess pruning of synapses altering neural circuits critical in executive function and cognitive memory.. ...
https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png 0 0 Daniel Battaglia https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png Daniel Battaglia2018-10-01 20:08:262018-12-11 20:21:53COMPLEMENT C3 ...
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.
The complement inhibitor C4b-binding protein (C4BP) prevents necrotic cells from spilling their pro-inflammatory guts, according to a study on page 1937. Trouw and colleagues now show that C4BP and its binding partner, anticoagulant protein S (PS), cooperate to grab onto necrotic cells and to inhibit the release of cellular DNA.. C4BP short-circuits the complement cascade by binding to the activated complement components C3b and C4b and presenting them to the proteolytic complement inhibitor Factor I for degradation. This inhibitory capacity of C4BP can be coopted by bacterial pathogens, which coat themselves with this protein to avoid complement-mediated destruction by phagocytic cells.. This group recently identified a role for the C4BP-PS complex: it binds to apoptotic cells through the phosphatidylserine-binding domain of PS. This association could prevent the deposition and activation of complement on the surface of the apoptotic cells, allowing the dying cells to be removed without ...
Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the worlds most expensive drugs. However, the mechanism of C5 activation by C5 convertases remains elusive, thus limiting development of therapeutics. Here we identify and characterize a new protein family of tick-derived C5 inhibitors. Structures of C5 in complex with the new inhibitors, the phase I and phase II inhibitor OmCI, or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. The positions of the inhibitor-binding sites and the ability of all three C5-inhibitor complexes to competitively inhibit the C5 convertase conflict with earlier steric-inhibition models, thus suggesting that a priming event is needed for activation.
Classical enzyme kinetic analyses were applied to define the mechanism of the effect of the fourth component (C4) on cleavage of the second component (C2) by the first component (C1) of human complement. The data indicated that the increased rate of cleavage of C2 by C1 in the presence of C4 was due to availability of a site for product deposition; the effect of C4 was reversed by blocking the site on C4 for C2 deposition. C2 cleavage by C1 followed first order kinetics.. In addition, our findings support the hypothesis that there are separate enzymatic sites on the C1 molecule for its natural substrates.. ...
Chris Thornton manages the European Sustainable Phosphorus Platform (ESPP), promoting sustainable phosphorus management in Europe, from agricultural use through the food industry to recycling from waste streams. ESPP is non-profit, funded by members which include water and waste companies, fertilisers, chemicals, recycling technologies, knowledge institutes and public establishments.. Proposed title of talk. Nutrients: the foundation of food sustainability. Synopsis. Nutrients, alongside water and energy, are the basis of farming and the food-industry, and their content in food is vital for health. However, there are also questions about the impacts of current levels of nutrients in Western diets. Phosphorus is thus sometimes positive (c.f. Blédinas Phosphatine) sometimes negative (from phosphate-free detergents to phosphate free ham?). Also, nutrient use in agriculture today is largely linear, with input of chemical fertilisers and losses to waste or the environment. This poses ...
Protein S is a vitamin K dependent cofactor for the anticoagulant activity of activated protein C (APC). Two forms of protein S are present in plasma : free protein S (40%) and protein S linked to the C4b-binding protein (60%). Only the free form has functional cofactor activity. Protein S deficiency may be hereditary or acquired - as in normal pregnancy. It has been associated with a high risk of developing venous thromboembolism especially in young people. As only the free form of Protein S has the cofactor activity it is only this form that is measured. Measurement of Protein S in pregnancy is rarely useful.. ...
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Walk-In Labs complement C3 serum test helps determine causes of recurrent infections, autoimmune disorders & more. A cheap, convenient online blood test.
Auto-Transfers to MAINPORT EPORTFOLIO. Royal College Fellows and MOC Program participants who provided their identification number at the time of registration will have their MOC Section 1 credits automatically transferred to their MAINPORT holding area following the learning activity. To complete the entry participants will be required to record their learning outcomes.. Letter of Invitation. Individuals requiring an official letter of invitation in order to obtain a visa and authorization to attend the Banff Course should contact us by email at [email protected] . The invitation letter will be issued once the registration form and payment has been received by the Banff Course. The letter does not constitute any financial commitment on the part of the Association.. ...
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4. A moles of A reactants react with b moles of B reactants to form c moles of product C. Which of the following is true for rate of ...

Molecular cloning and chromosomal localization of human membrane cofactor protein (MCP). Evidence for inclusion in the...Molecular cloning and chromosomal localization of human membrane cofactor protein (MCP). Evidence for inclusion in the...

... a regulatory molecular of the complement system with cofactor activity for the factor I-mediated inactivation of C3b and C4b, ... as well as several other complement and non-complement proteins. The remainder of the MCP protein consists of 25 amino acids ... Complement-mediated tumor cell damage induced by antibodies against membrane cofactor protein (MCP, CD46). ... This same genetic region contains the multigene family of complement-regulatory proteins, which is thereby enlarged to include ...
more infohttps://rupress.org/jem/article/168/1/181/49547/Molecular-cloning-and-chromosomal-localization-of

complement c4bcomplement c4b

complement c4a*complement c3b*complement c3d*complement factor i*complement c1q*complement c4*complement membrane attack ... complement c4b. Summary. Summary: The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound ... complement factor b*complement receptors*complement factor h*cd55 antigens*mannose binding lectin*complement c2* ... C4B products*C4A products*C3 products*factor I products*CR1 products*C4BPA products*C4B_2 products*COLEC11 products*C4b ...
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Complement C4b RNAi (H00000721-R01): Novus BiologicalsComplement C4b RNAi (H00000721-R01): Novus Biologicals

Complement C4b RNAi. Tested Reactivity: Hu. Validated: RNAi, RNAi SP. Backed by our 100% Guarantee. ... Blogs on Complement C4b. There are no specific blogs for Complement C4b, but you can read our latest blog posts. ... Reviews for Complement C4b RNAi (H00000721-R01) (0) There are no reviews for Complement C4b RNAi (H00000721-R01). By submitting ... Diseases for Complement C4b RNAi (H00000721-R01). Discover more about diseases related to Complement C4b RNAi (H00000721-R01). ...
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Complement C4b, Human | 204897Complement C4b, Human | 204897

... and γ-chains complement component. - Find MSDS or SDS, a COA, data sheets and more information. ... Complement C4b, Human, is a native, 193 kDa glycoprotein composed of the modified C4 α-chain (α) and intact β- ... and γ-chains complement component.. More,, Complement C4b, Human, is a native, 193 kDa glycoprotein composed of the modified C4 ... Native, human C4b complement component. Cleavage of the C4 α-chain at peptide bond 77 by activated C1 enzyme results in the ...
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Complement C4b/d Antibody (SPM545) [PerCP] (NBP2-34421PCP): Novus BiologicalsComplement C4b/d Antibody (SPM545) [PerCP] (NBP2-34421PCP): Novus Biologicals

Mouse Monoclonal Anti-Complement C4b/d Antibody (SPM545) [PerCP]. Acute Humoral Rejection Marker. Validated: ICC/IF, IHC-Fr, ... Additional Complement C4b/d Products. Complement C4b/d NBP2-34421PCP * Complement C4b/d Antibodies ... Home » Complement C4b/d » Complement C4b/d Antibodies » Complement C4b/d Antibody (SPM545) [PerCP] ... Blogs on Complement C4b/d. There are no specific blogs for Complement C4b/d, but you can read our latest blog posts. ...
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Structural requirements for the intracellular subunit polymerization of the complement inhibitor C4b-binding protein.Structural requirements for the intracellular subunit polymerization of the complement inhibitor C4b-binding protein.

Hydrolysis, Protein Conformation, Receptors, Complement : chemistry, Complement : genetics, Complement : isolation & ... C4b-binding protein (C4BP), an important inhibitor of complement activation, has a unique spider-like shape. It is composed of ... C4b-binding protein (C4BP), an important inhibitor of complement activation, has a unique spider-like shape. It is composed of ... Complement : chemistry,Complement : genetics,Complement : isolation & purification,Recombinant Proteins : chemistry,Recombinant ...
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enQuireBio™ Recombinant Human Complement C4-B Protein 200μg enQuireBio™ Recombinant Human Complement C4-B Protein
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Recombinant Human Complement C4-B Protein Proteins A ... Recombinant Human Complement C4-B Protein 200μg enQuireBio™ ... enQuireBio™ Recombinant Human Complement C4-B Protein A DNA sequence encoding the Homo sapiens (Human) Complement C4-B, was ...
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Compound page for L00080 (Complement component C4b): EzCatDBCompound page for L00080 (Complement component C4b): EzCatDB

Compound page for L00080: Complement component C4b. Top page for Compound List ...
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Binding of Flavivirus Nonstructural Protein NS1 to C4b Binding Protein Modulates Complement Activation | The Journal of...Binding of Flavivirus Nonstructural Protein NS1 to C4b Binding Protein Modulates Complement Activation | The Journal of...

Visualization of human C4b-binding protein and its complexes with vitamin K-dependent protein S and complement protein C4b. ... Binding of human complement component C4b-binding protein (C4BP) to Streptococcus pyogenes involves the C4b-binding site. J. ... In some experiments, unlabeled C4b (300 ng) was used instead of biotinylated C4b, and Western blot of C4b fragments was ... C4b-binding protein. In The complement facts book. Morley B. J., M. J. Walport Academic Press, London, p. 161-167. ...
more infohttps://www.jimmunol.org/content/187/1/424?ijkey=f022e8007e1f3acfeaf6be0e0fafbdd0b57ff430&keytype2=tf_ipsecsha

Functions of human complement inhibitor C4b-binding protein in relation to its structure - Archivum Immunologiae et Therapiae...Functions of human complement inhibitor C4b-binding protein in relation to its structure - Archivum Immunologiae et Therapiae...

C4b-binding protein (C4BP) is a potent soluble inhibitor of the classical and lectin pathways of complement. This large (500 ... Functions of human complement inhibitor C4b-binding protein in relation to its structure. ... Considering the destructive potential of the complement cascade, it is no surprise that there are several complement inhibitors ... function relationships have yielded new understanding of the interactions between C4BP and the activated complement factors C4b ...
more infohttp://psjd.icm.edu.pl/psjd/element/bwmeta1.element.element-from-psjc-1da43f29-9a91-3b96-8a86-8b6f28c24015

Human Complement fragment 4b (C4b) ELISA KitHuman Complement fragment 4b (C4b) ELISA Kit

You need info about Human Complement fragment 4b (C4b) ELISA Kit or any other Gentaur produtct? Contact us on Live Chat Our ... Human (Homo sapiens) C4b elisa. Shipping, handling and storage. The kit is shipped on ice packs. Upon receiving it store the ... Detects Human (Homo sapiens) C4b; Additional information. ...
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Genomic Copy Number Variations of the Complement Component C4B Gene Are Associated With Chronic Central Serous...Genomic Copy Number Variations of the Complement Component C4B Gene Are Associated With Chronic Central Serous...

Genomic Copy Number Variations of the Complement Component C4B Gene Are Associated With Chronic Central Serous ... C4B genomic copy numbers differed significantly between cCSC patients and healthy controls (P = 0.0018). Absence of C4B ... To further investigate the role of the complement system in cCSC, the genomic copy number variations in the complement ... This study showed that copy numbers of C4B are significantly associated with cCSC. Carrying no copies of C4B significantly ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=117467

THE ALFA7BETA0 ISOFORM OF THE COMPLEMENT REGULATOR C4B-BINDING PROTEIN INDUCES A SEMIMATURE, ANTI-INFLAMMATORY STATE IN...'THE ALFA7BETA0 ISOFORM OF THE COMPLEMENT REGULATOR C4B-BINDING PROTEIN INDUCES A SEMIMATURE, ANTI-INFLAMMATORY STATE IN...

Home » Publications » THE ALFA7BETA0 ISOFORM OF THE COMPLEMENT REGULATOR C4B-BINDING PROTEIN INDUCES A SEMIMATURE, ANTI- ... THE ALFA7BETA0 ISOFORM OF THE COMPLEMENT REGULATOR C4B-BINDING PROTEIN INDUCES A SEMIMATURE, ANTI-INFLAMMATORY STATE IN ... THE ALFA7BETA0 ISOFORM OF THE COMPLEMENT REGULATOR C4B-BINDING PROTEIN INDUCES A SEMIMATURE, ANTI-INFLAMMATORY STATE IN ...
more infohttps://www.iibb.csic.es/ca/publications/alfa7beta0-isoform-complement-regulator-c4b-binding-protein-induces-semimature-anti

Binding of Complement Inhibitor C4b-binding Protein to a Highly Virulent Streptococcus pyogenes M1 Strain Is Mediated by...Binding of Complement Inhibitor C4b-binding Protein to a Highly Virulent Streptococcus pyogenes M1 Strain Is Mediated by...

Binding of Complement Inhibitor C4b-binding Protein to a Highly Virulent Streptococcus pyogenes M1 Strain Is Mediated by ... Binding of Complement Inhibitor C4b-binding Protein to a Highly Virulent Streptococcus pyogenes M1 Strain Is Mediated by ... uses exclusively protein H to bind the complement inhibitor C4b-binding protein (C4BP). We found a strong correlation between ... Furthermore, C4b deposited from serum onto AP1 bacterial surfaces was processed into C4c/C4d fragments, which did not occur on ...
more infohttps://www.jpt.com/literature/Binding-of-Complement-Inhibitor-C4b-binding-Protein-to-a-Highly-Virulent-Streptococcus-pyogenes-M1-Strain-Is-Mediated-by-Protein-H-and-Enhances-Adhesion-to-and-Invasion-of-Endothelial-Cells/

C4B deficiency: a risk factor for bacteremia with encapsulated organisms.  - PubMed - NCBIC4B deficiency: a risk factor for bacteremia with encapsulated organisms. - PubMed - NCBI

The fourth component of complement (C4) is crucial to the activation of the classical complement pathway, a key defense against ... The two isotypes of C4, C4A and C4B, have very different in vitro activities. An increased incidence of total C4B deficiency ... C4B deficiency: a risk factor for bacteremia with encapsulated organisms.. Bishof NA1, Welch TR, Beischel LS. ... 2% of race-matched controls, P = .02). In black patients, however, there was no difference in incidence of C4B deficiency ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/2355198?dopt=Abstract

Complement component 4 - WikipediaComplement component 4 - Wikipedia

... or C4B-C4B) and 31% trimodular configuration (equally split between LLL as C4A-C4A-C4B or LSS as C4A-C4B-C4B). Regarding C4 ... C4b and C2a, from their complex (whereupon C4b can bind another protein C2, and conduct these steps again). Because C4b is ... an effect produced by the effector proteins of the complement system in which the C4 partakes). Complement system Complement ... Law SK, Dodds AW, Porter RR (August 1984). "A comparison of the properties of two classes, C4A and C4B, of the human complement ...
more infohttps://en.wikipedia.org/wiki/Complement_component_4

C4b-binding protein - WikipediaC4b-binding protein - Wikipedia

C4b-binding protein (C4BP) is a protein involved in the complement system where it acts as inhibitor. C4BP has an octopus-like ... Complement C4b-Binding Protein at the US National Library of Medicine Medical Subject Headings (MeSH). ... C4BP accelerates decay of C3-convertase and is a cofactor for serine protease factor I which cleaves C4b and C3b. C4BP binds ... The genes coding for C4BP α-chain (C4BPA) and β-chain (C4BPB) are located in the regulators of complement activation (RCA) gene ...
more infohttps://en.wikipedia.org/wiki/C4b-binding_protein

Search results for: Cavia porcellusSearch results for: 'Cavia porcellus'

C4B Antibody (OALA02951) Protein Name:Complement C4-B Catalog #:OALA02951 Type: pAb ...
more infohttps://www.avivasysbio.com/en/catalogsearch/result/index/?host=115354&q=Cavia+porcellus

Patent US6891154 - Amino acid sequence pattern matching - Google PatentsPatent US6891154 - Amino acid sequence pattern matching - Google Patents

gi,1314244,gb,AAA997: complement c4b precursor [homo sapiens]. [mass = 188405]. gi,20545719,ref,XP_0: complement component 3 ...
more infohttp://www.google.com/patents/US6891154?dq=6,757,682

MMP-2 expression in renal tissue with different degree  | Open-iMMP-2 expression in renal tissue with different degree | Open-i

Complement C4b/analysis. *Creatinine/blood. *Disease Progression. *Female. *Fibrosis. *Humans. *Immunohistochemistry. *Male ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC3539883_1746-1596-7-141-2&req=4

Serum proteome changes in acromegalic patients following transsphenoidal surgery: novel biomarkers of disease activity.  -...Serum proteome changes in acromegalic patients following transsphenoidal surgery: novel biomarkers of disease activity. -...

... identified as complement C4B precursor, was increased after the surgery.. CONCLUSIONS: Seven serum protein spots were ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/21059862

Autism and Vaccines: A New Look at an Old Story - Diseases and Vaccines - NVICAutism and Vaccines: A New Look at an Old Story - Diseases and Vaccines - NVIC

Increased frequency of the null allele at the complement C4B locus in autism. Clin Exp Immunol 33:438-440.. Warren RP, Yonk J, ... DR-positive Tcells in autism: association with decreased plasma levels of the complement C4B protein. Neuropsychobiology 31:53- ... Decreased plasma concentrations of the C4B complement protein in autism. Archives of Pediatrics & Adolescent Medicine 148:180- ...
more infohttps://www.nvic.org/vaccines-and-diseases/Autism/specialreport.aspx

Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND C4B Gene-Products  - Kingston...Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND C4B Gene-Products - Kingston...

Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND C4B Gene-Products ... Sim, Edith and Law, Sai-Kit A. (1985) Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND ... C4B Gene-Products. FEBS letters, 184(2), pp. 323-327. ISSN (print) 0014-5793 ...
more infohttp://eprints.kingston.ac.uk/19436/

Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells.Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells.

Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of comple ... Complement C4b-Binding Protein. Complement Factor H / metabolism. Complement System Proteins / metabolism*. Endothelial Cells ... 0/Complement C4b-Binding Protein; 0/Histocompatibility Antigens; 80295-65-4/Complement Factor H; 9007-36-7/Complement System ... We further demonstrate that the inhibitory effect of complement proteins is the result of the bound complement inhibitors C4b- ...
more infohttp://www.biomedsearch.com/nih/Effects-complement-regulators-bound-to/18028369.html
  • Among them, β-actin (ACTB), inactivated complement C3b (iC3b), and C4B were elevated significantly in pre-ERT Fabry disease plasma compared with control plasma. (bmj.com)
  • Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. (novusbio.com)
  • C4B deficiency: a risk factor for bacteremia with encapsulated organisms. (nih.gov)
  • An increased incidence of total C4B deficiency was found in white patients with Streptococcus pneumoniae, Haemophilus influenzae, or Neisseria meningitidis infection (14% of bacteremic children vs. 2% of race-matched controls, P = .02). (nih.gov)
  • In black patients, however, there was no difference in incidence of C4B deficiency between bacteremic patients and race-matched controls (7% and 5%, respectively, P greater than .5). (nih.gov)
  • These data suggest that, at least in whites, total C4B deficiency is a risk factor for invasive disease with these three encapsulated organisms. (nih.gov)
  • It inhibits complement activation at the yeast surface and, in addition, mediates adhesion of C. albicans to host endothelial cells. (labome.org)
  • This observation indicates that low C4B copy number is a strong risk factor for short-term mortality after AMI in smoking Icelandic patients, whereas LTA 252 G allele is not a risk factor in Caucasian population. (labome.org)
  • In the same year, studies relatedly identified a 98 kb region of the chromosome the four class III genes (that express C4A, C4B, C2, and factor B) are closely linked, which does not allow for cross-overs to occur. (wikipedia.org)
  • To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. (biomedsearch.com)
  • The presence of high C4A and C4B copy numbers in AD patients could explain the increased C4 protein expression observed in AD patients, thus highlighting a possible role for C4A and C4B copy number variations in the risk of developing AD. (antibodies-online.com)
  • Like C3b, C4b has the transient ability to form a covalent ester bond with a variety of target cell surfaces. (emdmillipore.com)
  • Originally defined in the context of the Chido/Rodgers blood group system, the C4A-C4B genetic model is under investigation for its possible role in schizophrenia risk and development. (wikipedia.org)
  • Beyond its lytic capacity, complement protects against viral infections by priming adaptive B and T cell responses, triggering leukocyte chemotaxis through the release of anaphylatoxins (C3a and C5a),and opsonizing viruses for phagocytosis and destruction by macrophages (reviewed in Refs. (jimmunol.org)
  • C4B genomic copy numbers differed significantly between cCSC patients and healthy controls (P = 0.0018). (cdc.gov)
  • This study showed that copy numbers of C4B are significantly associated with cCSC. (cdc.gov)
  • Carrying no copies of C4B significantly increases the risk of cCSC, whereas carrying three C4B copies is protective. (cdc.gov)
  • C4A and C4B copy numbers were analyzed in 197 cCSC patients and 303 healthy controls by using a Taqman copy number determination assay. (cdc.gov)
  • A logistic regression model was constructed to calculate the odds ratios (ORs) of each of the C4B copy numbers, using two copies as a reference. (cdc.gov)
  • Taken together, these results suggest that E. coli and GBS utilize contrasting mechanisms of complement-mediated interactions with their target cells for successful establishment of disease. (biomedsearch.com)