Complement factor h. Medical search

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).

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.

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.

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.

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.

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.

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.

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.

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.

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).

A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.

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.

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).

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).

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.

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.

Optic disk bodies composed primarily of acid mucopolysaccharides that may produce pseudopapilledema (elevation of the optic disk without associated INTRACRANIAL HYPERTENSION) and visual field deficits. Drusen may also occur in the retina (see RETINAL DRUSEN). (Miller et al., Clinical Neuro-Ophthalmology, 4th ed, p355)

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.

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.

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.

Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.

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.

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.

A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.

Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.

The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.

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.

Colloid or hyaline bodies lying beneath the retinal pigment epithelium. They may occur either secondary to changes in the choroid that affect the pigment epithelium or as an autosomal dominant disorder of the retinal pigment epithelium.

The thin, highly vascular membrane covering most of the posterior of the eye between the RETINA and SCLERA.

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.

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.

Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.

The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.

A pathological process consisting of the formation of new blood vessels in the CHOROID.

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.

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.

The single layer of pigment-containing epithelial cells in the RETINA, situated closely to the tips (outer segments) of the RETINAL PHOTORECEPTOR CELLS. These epithelial cells are macroglia that perform essential functions for the photoreceptor cells, such as in nutrient transport, phagocytosis of the shed photoreceptor membranes, and ensuring retinal attachment.

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.

A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.

A form of MACULAR DEGENERATION also known as dry macular degeneration marked by occurrence of a well-defined progressive lesion or atrophy in the central part of the RETINA called the MACULA LUTEA. It is distinguishable from WET MACULAR DEGENERATION in that the latter involves neovascular exudates.

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.

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).

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.

Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses.

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.

An individual in which both alleles at a given locus are identical.

A specific pair of human chromosomes in group A (CHROMOSOMES, HUMAN, 1-3) of the human chromosome classification.

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).

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.

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.

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.

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.

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.

The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.

A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.

Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone.

Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.

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.

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.

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.

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.

Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.

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.

A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.

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.

A specific pair of GROUP C CHROMOSOMES of the human chromosome classification.

The layer of pigment-containing epithelial cells in the RETINA; the CILIARY BODY; and the IRIS in the eye.

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.

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.

The parts of a macromolecule that directly participate in its specific combination with another molecule.

The naturally occurring or experimentally induced replacement of one or more AMINO ACIDS in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish, enhance, or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties.

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.

An essential amino acid that is required for the production of HISTAMINE.

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.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

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.

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.

Proteins found in any species of bacterium.

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.

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.

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.

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.

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.

Individuals whose ancestral origins are in the southeastern and eastern areas of the Asian continent.

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.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

A plasma protein that circulates in increased amounts during inflammation and after tissue damage.

Genotypic differences observed among individuals in a population.

Proteins prepared by recombinant DNA technology.

Protein H, an antiphagocytic surface protein in Streptococcus pyogenes. (1/741)

Surface-associated M protein is a major virulence factor in Streptococcus pyogenes which confers bacterial resistance to phagocytosis. However, many S. pyogenes strains also express additional structurally related so-called M-like proteins. The strain studied here is of the clinically important M1 serotype and expresses two structurally related surface proteins, the M1 protein and protein H. Mutants were generated that expressed only one or none of these proteins at the bacterial surface. For survival in human blood either protein H or M1 protein was sufficient, whereas the double mutant was rapidly killed. The protein-binding properties of protein H, M1 protein, and the mutants suggest that bacterial binding of immunoglobulin G and factor H or factor H-like protein 1, which are regulatory proteins in the complement system, contribute to the antiphagocytic property. (+info)

Multicenter trial of the quantitative BTA TRAK assay in the detection of bladder cancer. (2/741)

BACKGROUND: Human complement factor H-related protein (hCFHrp) is produced by several bladder cancer cell lines and may be useful as a cancer marker. The aim of this study was to compare urinary hCFHrp and cytology for the detection of bladder cancer found by cystoscopy in patients with suggestive signs, symptoms, or preliminary test results. METHODS: The BTA TRAK assay, a quantitative enzyme immunoassay for the bladder tumor-associated antigen in urine, was compared with exfoliative cytology in 220 patients (155 men, 65 women; mean age, 64.2 years) presenting with signs, symptoms, or preliminary diagnostic results suggestive of this disease. Cystoscopy was the standard of detection. RESULTS: In the 100 patients found to have bladder cancer, the overall sensitivities of the BTA TRAK assay (at a previously determined decision threshold of 14 kilounits/L) and cytology were 66% (66 of 100) and 33% (33 of 100), respectively (P <0.001). The BTA TRAK assay proved to be statistically more sensitive than cytology for tumor grades I and II and for stage Ta and T1 tumors. In contrast, the overall specificity of the BTA TRAK assay in the 120 patients without cystoscopically confirmed bladder cancer was 69% (83 of 120) and that of cytology was 99% (119 of 120; P <0.001). The specificity of the BTA TRAK assay was higher in patients without benign or malignant genitourinary disease other than bladder cancer (76%; n = 89) than in patients with these conditions. When the BTA TRAK assay and cytology were used together such that a positive result in either test was scored as positive and the results compared with those of the BTA TRAK assay alone, increases in overall sensitivity and equivalent specificity were observed. CONCLUSION: Because of its relatively high sensitivity, the BTA TRAK assay could complement cytology as an adjunct to cystoscopy in the diagnosis and follow-up of most patients with bladder cancer. (+info)

In vitro analysis of complement-dependent HIV-1 cell infection using a model system. (3/741)

Previous studies based on the use of human serum as a source of C have provided evidence for the C-dependent enhancement of cell infection by HIV-1. The present study was undertaken to distinguish C from other serum factors and to identify the proteins and the mechanisms involved in C-dependent cell infection by HIV-1. The classical C activation pathway was reconstituted from the proteins C1q, C1r, C1s, C4, C2, C3, factor H, and factor I; each were purified to homogeneity. A mixture of these proteins at physiological concentrations was shown to reproduce the ability of normal human serum to enhance the infection of MT2 cells by HIV-1 at low doses of virus. This enhancing effect was abolished when heat-inactivated serum and C2- or C3-depleted serum were used, and was restored upon addition of the corresponding purified proteins. A mixture of two synthetic peptides corresponding to positions 10-15 and 90-97 of human C receptor type 2 (CD21) as well as soluble CD4 both inhibited the C-dependent infection process. These data provide unambiguous evidence that HIV-1 triggers a direct activation of the classical C pathway in vitro and thereby facilitates the infection of MT2 cells at low doses of virus. These findings are consistent with a mechanism involving increased interaction between the virus opsonized by C3b-derived fragment(s) and the CD21 cell receptors and subsequent virus entry through CD4 receptors. (+info)

Disruption of disulfide bonds is responsible for impaired secretion in human complement factor H deficiency. (4/741)

Factor H, a secretory glycoprotein composed of 20 short consensus repeat modules, is an inhibitor of the complement system. Previous studies of inherited factor H deficiency revealed single amino acid substitutions at conserved cysteine residues, on one allele arginine for cysteine 518 (C518R) and on the other tyrosine for cysteine 941 (C941Y) (Ault, B. H., Schmidt, B. Z., Fowler, N. L., Kashtan, C. E., Ahmed, A. E., Vogt, B. A., and Colten, H. R. (1997) J. Biol. Chem. 272, 25168-25175). To ascertain if the phenotype, impaired secretion of factor H, is due to the C518R substitution or the C941Y substitution and to ascertain the mechanism by which secretion is impaired, we studied COS-1 and HepG2 cells transfected with wild type and several mutant factor H molecules. The results showed markedly impaired secretion of both C518R and C941Y factor H as well as that of factor H molecules bearing alanine or arginine substitutions at the Cys518-Cys546 disulfide bond (C518A, C546A, C546R, C518A-C546A). In each case, mutant factor H was retained in the endoplasmic reticulum and degraded relatively slowly as compared with most other mutant secretory and membrane proteins that are retained in the endoplasmic reticulum. These data indicate that impaired secretion of the naturally occurring C518R and C941Y mutant factor H proteins is due to disruption of framework-specific disulfide bonds in factor H short consensus repeat modules. (+info)

Hypocomplementemia discloses genetic predisposition to hemolytic uremic syndrome and thrombotic thrombocytopenic purpura: role of factor H abnormalities. Italian Registry of Familial and Recurrent Hemolytic Uremic Syndrome/Thrombotic Thrombocytopenic Purpura. (5/741)

Familial hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) carry a very poor outcome and have been reported in association with decreased serum levels of the third complement component (C3). Uncontrolled consumption in the microcirculation, possibly related to genetically determined deficiency in factor H--a modulator of the alternative pathway of complement activation--may account for decreased C3 serum levels even during disease remission and may predispose to intravascular thrombosis. In a case-control study by multivariate analysis, we correlated putative predisposing conditions, including low C3 serum levels, with history of disease in 15 cases reporting one or more episodes of familial HUS and TTP, in 25 age- and gender-matched healthy controls and in 63 case-relatives and 56 control-relatives, respectively. The relationship between history of disease, low C3, and factor H abnormalities was investigated in all affected families and in 17 controls. Seventy-three percent of cases compared with 16% of controls (P < 0.001), and 24% of case-relatives compared with 5% of control-relatives (P = 0.005) had decreased C3 serum levels. At multivariate analysis, C3 serum level was the only parameter associated with the disease within affected families (P = 0.02) and in the overall study population (P = 0.01). Thus, subjects with decreased C3 serum levels had a relative risk of HUS or TTP of 16.56 (95% confidence interval [CI], 1.66 to 162.39) within families and of 27.77 (95% CI, 2.44 to 314.19) in the overall population, compared to subjects with normal serum levels. Factor H abnormalities were found in four of the cases, compared with three of the healthy family members (P = 0.02) and none of the controls (P = 0.04) and, within families, factor H abnormalities were correlated with C3 reduction (P < 0.05). Reduced C3 clusters in familial HUS and TTP is likely related to a genetically determined deficiency in factor H and may predispose to the disease. Its demonstration may help identify subjects at risk in affected families. (+info)

Familial relapsing haemolytic uraemic syndrome and complement factor H deficiency. (6/741)

BACKGROUND: In a recent study of three families we have found that inherited haemolytic uraemic syndrome (HUS) maps to a region of chromosome 1q containing the gene for complement factor H. In one of these families and also in a case of sporadic D-HUS, we have identified mutations in the factor H gene. A further family with inherited HUS has therefore been investigated. METHODS: DNA extracted from the family members and DNA extracted from archival post-mortem material from a deceased family member, was studied. Review of renal biopsies and study of complement components was also undertaken. RESULTS: This family demonstrates an inherited deficiency of complement factor H. Non-diarrhoeal HUS has affected at least two family members with half normal levels of factor H. CONCLUSION: These findings represent further evidence of the association between factor H dysfunction and HUS. (+info)

Identification of human complement Factor H as a ligand for L-selectin. (7/741)

The selectin family of adhesion molecules (E-, P- and L-selectins) is involved in leukocyte recruitment to sites of inflammation and tissue damage. Recently it has been shown that L-selectin is involved not only in leukocyte tethering and rolling, but also plays an important role in leukocyte activation. For example, glycosylation-dependent cell-adhesion molecule 1 (GlyCAM-1), a known ligand for L-selectin, has been shown to enhance beta2-integrin function. GlyCAM-1 is a secreted protein and is present in mouse serum at a concentration of approx. 1.5 microg/ml. There is no obvious GlyCAM-1 homologue in man and, to date, L-selectin ligand(s) from human serum have not been characterized. Therefore we have used L-selectin affinity chromatography, followed by ion-exchange chromatography, to isolate specific ligand(s) for L-selectin. Using this procedure, we have isolated three major glycoproteins of apparent molecular masses 170 kDa, 70kDa and 50 kDa. The 170 kDa protein band was digested with trypsin and peptides were analysed by delayed extraction matrix-assisted laser desorption ionization MS and protein database searching. The 170 kDa protein was identified as the human complement protein Factor H. Human Factor H, isolated by a different method, was shown to bind specifically to L-selectin in the presence of CaCl2, and binding was inhibited by anti-L-selectin antibodies, fucoidan and lipopolysaccharide. Only a part of the purified Factor H preparation bound to immobilized L-selectin. The interaction of Factor H with leukocyte L-selectin was shown to induce the secretion of tumour necrosis factor-alpha (TNF-alpha). Pretreatment of Factor H with sialidase reduced both the binding of L-selectin to Factor H and the Factor H-induced L-selectin-mediated TNF-alpha secretion by leukocytes. Taken together, these results demonstrate that a post-translationally modified form of human plasma Factor H is a potential physiological ligand for L-selectin. (+info)

Resistance to both complement activation and phagocytosis in type 3 pneumococci is mediated by the binding of complement regulatory protein factor H. (8/741)

To study the role of surface-associated proteins in the virulence of Streptococcus pneumoniae, we used two serotype 3 strains, ATCC 6303 and WU2, and two PspA-negative mutants of WU2, an encapsulated one, JY1123 (Caps(+)/PspA(-)), and an unencapsulated one, DW3.8 (Caps(-)/PspA(-)). ATCC 6303 and WU2 were highly virulent in mice, while the virulence of JY1123 was slightly decreased (50% lethal doses [LD(50)s], 24, 6, and 147 CFU/mouse, respectively); DW3.8 was avirulent (LD(50), 2 x 10(8) CFU). In vitro, ATCC 6303, WU2, and JY1123 (Caps(+)/PspA(-)) strongly resisted complement activation and complement-dependent opsonophagocytosis, whereas DW3.8 (Caps(-)/PspA(-)) was easily phagocytized in fresh serum. Trypsin treatment of ATCC 6303, WU2, and JY1123 (Caps(+)/PspA(-)) resulted in enhanced complement activation and complement-dependent opsonophagocytosis. Trypsin had no deleterious effect on the polysaccharide capsule. In addition, trypsin pretreatment of ATCC 6303 strongly reduced virulence upon intraperitoneal challenge in mice. This indicated that surface proteins play a role in the resistance to complement activation and opsonophagocytosis and contribute to the virulence of type 3 pneumococci. In subsequent experiments, we could show that the modulation of complement activation was associated with surface components that bind complement regulator factor H; binding is trypsin sensitive and independent of prior complement activation. Immunoblotting of cell wall proteins of the virulent strain ATCC 6303 with anti-human factor H antibody revealed three factor H-binding proteins of 88, 150, and 196 kDa. Immunogold electron microscopy showed a close association of factor H-binding components with the outer surface of the cell wall. The role of these factor H-binding surface proteins in the virulence of pneumococci is interesting and warrants further investigation. (+info)

There are two main types of MD:

1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.

The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:

* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision

MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.

There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:

* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.

It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.

The symptoms of HUS include:

* Diarrhea
* Vomiting
* Abdominal pain
* Fatigue
* Weakness
* Shortness of breath
* Pale or yellowish skin
* Easy bruising or bleeding

If you suspect that someone has HUS, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order blood tests to diagnose the condition. Treatment for HUS typically involves addressing the underlying cause of the condition, such as stopping certain medications or treating an infection. In some cases, hospitalization may be necessary to manage complications such as kidney failure.

Preventative measures to reduce the risk of developing HUS include:

* Practicing good hygiene, especially during outbreaks of diarrheal illnesses
* Avoiding certain medications that are known to increase the risk of HUS
* Maintaining a healthy diet and staying hydrated
* Managing any underlying medical conditions such as high blood pressure or diabetes.

Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.

The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.

Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.

The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).

The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.

There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.

The main complications of GNM include:

1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.

It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.

Optic disk drusen (ODD) is a condition that affects the optic nerve and can cause vision loss if left untreated. It is characterized by the accumulation of lipids or other substances on the surface of the optic disk, which is the area where the retinal nerve fibers converge and leave the eye.

The symptoms of ODD can vary in severity and may include:

1. Blurred vision
2. Distorted vision
3. Eye pain or discomfort
4. Sensitivity to light
5. Reduced peripheral vision

If you are experiencing any of these symptoms, it is important to seek medical attention as soon as possible. ODD can be diagnosed through a comprehensive eye exam, which may include imaging tests such as optical coherence tomography (OCT) or visual field testing.

While there is no cure for ODD, there are several treatment options available that can help manage the condition and slow down its progression. These may include:

1. Vitamin supplements: Vitamins A, C, and E, as well as other antioxidants, may help reduce inflammation and slow down the progression of ODD.
2. Anti-inflammatory medications: Corticosteroids or other anti-inflammatory drugs may be prescribed to reduce inflammation and swelling in the eye.
3. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser therapy to reduce inflammation and slow down the progression of ODD.
4. Laser surgery: In severe cases of ODD, laser surgery may be necessary to remove the accumulated lipids or other substances on the surface of the optic disk.

It is important to note that while these treatments can help manage the condition, they may not completely restore vision that has already been lost. Therefore, early detection and treatment are crucial to preventing or slowing down the progression of ODD.

Retinal drusen appear as small, flat spots or patches in the retina and are usually yellow or orange in color. They are made up of lipids (fatty substances) and other waste products that have accumulated in the retina over time. The exact cause of retinal drusen is not known, but they are thought to be related to the natural aging process and the decline in the function of the retina over time.

Retinal drusen can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT). There is no treatment for retinal drusen, but they can be monitored with regular eye exams to ensure that they are not progressing or causing any vision problems.

In some cases, retinal drusen may be a sign of a more serious underlying condition such as macular degeneration, which can cause vision loss if left untreated. It is important for individuals over the age of 50 to have regular comprehensive eye exams to detect any changes in the retina and to prevent vision loss.

In summary, retinal drusen are small deposits that accumulate in the retina and are a common age-related change. They do not cause vision problems on their own but can be an early warning sign of more serious eye diseases such as macular degeneration. Regular comprehensive eye exams can detect any changes in the retina and prevent vision loss.

CNV develops when the underlying choroidal layers experience changes that lead to the growth of new blood vessels, which can leak fluid and cause damage to the retina. This can result in vision distortion, loss of central vision, and even blindness if left untreated.

The formation of CNV is a complex process that involves various cellular and molecular mechanisms. It is thought to be triggered by factors such as oxidative stress, inflammation, and the presence of certain growth factors and proteins.

There are several clinical signs and symptoms associated with CNV, including:

1. Distortion of vision, including metamorphopsia (distorted vision of geometric shapes)
2. Blind spots or scotomas
3. Decreased central vision
4. Difficulty reading or performing other daily tasks
5. Reduced color perception
6. Sensitivity to light and glare

The diagnosis of CNV is typically made based on a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography (OCT).

There are several treatment options for CNV, including:

1. Anti-vascular endothelial growth factor (VEGF) injections: These medications work by blocking the growth of new blood vessels and can help improve vision and reduce the risk of further damage.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser therapy to damage and shrink the abnormal blood vessels.
3. Focal photocoagulation: This involves the use of a high-intensity laser to destroy the abnormal blood vessels in the central retina.
4. Vitrectomy: In severe cases, a vitrectomy may be performed to remove the vitreous gel and blood vessels that are causing the CNV.

It is important to note that these treatments do not cure CNV, but they can help improve vision and slow the progression of the disease. Regular follow-up appointments with an eye care professional are necessary to monitor the condition and adjust treatment as needed.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."

The term "geographic" refers to the characteristic map-like pattern of atrophy that occurs in the retina, with areas of degeneration resembling geographical features such as rivers, lakes, and islands. The progression of GA is typically slower than that of neovascular AMD, but it can still lead to significant vision loss over time.

The exact cause of GA is not fully understood, but it is believed to be related to the aging process and the accumulation of waste material in the retina. Risk factors for developing GA include age, family history, and prior history of AMD. There is currently no cure for GA, but various treatments are being developed to slow its progression and manage symptoms. These may include vitamin supplements, anti-inflammatory medications, and photodynamic therapy. Regular eye exams are important for early detection and monitoring of GA to help preserve vision and quality of life.

The term "serum sickness" was first used in the late 19th century to describe this condition, which was often seen in people who had received serum (a type of blood product) containing antibodies against diseases such as diphtheria or tetanus. Today, the term is still used to describe similar reactions to other substances, including medications and vaccines.

Serum sickness can be mild or severe, and in rare cases, it can lead to serious complications such as kidney failure or inflammation of the heart. Treatment typically involves stopping the use of the offending substance and providing supportive care to manage symptoms. In severe cases, corticosteroids or other medications may be used to reduce inflammation.

While serum sickness is a relatively rare condition, it is important for healthcare providers to be aware of it as a potential complication of medication and vaccine use. This knowledge can help them recognize and manage the condition effectively, reducing the risk of serious complications and improving outcomes for patients.

Factor I deficiency in turn leads to low levels of complement component 3 (C3), factor B, factor H and properdin in blood, due ... Complement factor I (factor I) is a protein of the complement system, first isolated in 1966 in guinea pig serum, that ... Loss of function mutations in the Complement Factor I gene lead to low levels of factor I which results in increased complement ... Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. ...

https://en.wikipedia.org/wiki/Complement_factor_I

... is a protein that in humans is encoded by the CFB gene. This gene encodes complement factor B, a component ... CFB complement factor B". Ambrus JL, Peters MG, Fauci AS, Brown EJ (March 1990). "The Ba fragment of complement factor B ... Christie DL, Gagnon J (January 1983). "Amino acid sequence of the Bb fragment from complement Factor B. Sequence of the major ... Upon activation of the alternative pathway, it is cleaved by complement factor D yielding the noncatalytic chain Ba and the ...

https://en.wikipedia.org/wiki/Complement_factor_B

"The role of complement factor C3 in lipid metabolism". Molecular Immunology. 15th European Meeting on Complement in Human ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ... that allows it to bind to a plasma protein called Factor B. This complex is then cleaved by Factor D, a serine protease, to ... Factor I, a serine protease activated by cofactors, can cleave and C3b and C4b, thus preventing convertase formation. C3 ...

https://en.wikipedia.org/wiki/C3a_(complement)

PSAP Complement component 4, partial deficiency of; 120790; C1NH Complement factor H deficiency; 609814; HF1 Complement factor ... GLA Factor V and factor VIII, combined deficiency of; 227300; MCFD2 Factor V deficiency; 227400; F5 Factor XI deficiency, ... F11 Factor XII deficiency; 234000; F12 Factor XIIIA deficiency; 613225; F13A1 Factor XIIIB deficiency; 613235; F13B Failure of ... LCAT Fletcher factor deficiency; 612423; KLKB1 Focal cortical dysplasia, Taylor balloon cell type; 607341; TSC1 Focal dermal ...

https://en.wikipedia.org/wiki/List_of_OMIM_disorder_codes

"OMIM Entry - * 300383 - COMPLEMENT FACTOR PROPERDIN; CFP". www.omim.org. Retrieved 2022-03-24. editor., Leung, Donald Y. M., ... The gene responsible for the production of properdin, Complement Factor Properdin (CFP), lies on the X-chromosome at the ... Properdin deficiency is a rare X-linked disease in which properdin, an important complement factor responsible for the ... Pertaining to complement deficiencies, there is no cure and the treatments for complement deficiencies vary widely. The best ...

https://en.wikipedia.org/wiki/Properdin_deficiency

Activated C3 can then interact with factor B. Factor B is then activated by factor D, to form Bb. The resultant complex, C3bBb ... "Interactions between human complement components factor H, factor I and C3b". The Biochemical Journal. 326 (2): 553-61. doi: ... c3 may be lost in urine in nephrotic syndrome Complement component 3 has been shown to interact with Factor H. Deficiencies in ... Factor I is the protease cleaves C3b but requires a cofactor (e.g Factor H, CR1, MCP or C4BP) for activity. Several ...

https://en.wikipedia.org/wiki/Complement_component_3

This gene encodes the basic form of complement factor 4, part of the classical activation pathway. The protein is expressed as ... Complement component 4 Complement component 4A HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency ... Aoki H, Takizawa F, Tsuji S, Nagasawa S (Jul 2000). "Elongation factor-1alpha as a homologous complement activator of Jurkat ... Complement component 4B (Chido blood group) is a kind of the Complement component 4 protein that in humans is encoded by the ...

https://en.wikipedia.org/wiki/Complement_component_4B

Like complement factor H, CFHR5 is able to bind to complement C3. A mutation in CHFR5 was found in patients with the disease ... "Entrez Gene: CFHR5 complement factor H-related 5". McRae JL, Duthy TG, Griggs KM, et al. (2005). "Human factor H-related ... 2006). "Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with ... Complement factor H-related protein 5 is a protein that in humans is encoded by the CFHR5 gene. CFHR5 is structurally related ...

https://en.wikipedia.org/wiki/CFHR5

Decay Accelerating Factor, DAF (CD55) Protectin (CD59) Complement C3b/C4b Receptor 1, CR1 (CD35) Complement Regulator of the ... Complement control protein are proteins that interact with components of the complement system. The complement system is ... Complement proteins protect against malignant cells- both by direct complement attack and through initiation of Complement- ... factor H competes with factor B to bind C3b; if it manages to bind, then the convertase is not formed. Factor H can bind C3b ...

https://en.wikipedia.org/wiki/Complement_control_protein

"Cellular adhesion mediated by factor J, a complement inhibitor. Evidence for nucleolin involvement". The Journal of Biological ... Nucleolin is also able to act as a transcriptional coactivator with Chicken Ovalbumin Upstream Promoter Transcription Factor II ...

https://en.wikipedia.org/wiki/Nucleolin

... is produced when complement factor I cleaves C3b. Complement receptors on white blood cells are able to bind iC3b, so iC3b ... thus preventing amplification of the complement cascade through the alternative pathway. Complement factor I can further cleave ... iC3b is a protein fragment that is part of the complement system, a component of the vertebrate immune system. ... v t e (Complement system, All stub articles, Biochemistry stubs). ...

https://en.wikipedia.org/wiki/IC3b

... complement subgroups factor a group into smaller pieces. As previously mentioned, complements need not exist. A p-complement is ... A Frobenius complement is a special type of complement in a Frobenius group. A complemented group is one where every subgroup ... if K is a complement of H, then H is a complement of K. Neither H nor K need be a normal subgroup of G. Complements need not ... That is, H could have two distinct complements K1 and K2 in G. If there are several complements of a normal subgroup, then they ...

https://en.wikipedia.org/wiki/Complement_(group_theory)

Complement factors are decreased in rheumatoid arthritis and lupus arthritis. Microscopic analysis of synovial fluid is ... Jay, GD; Britt, DE; Cha, CJ (March 2000). "Lubricin is a product of megakaryocyte stimulating factor gene expression by human ...

https://en.wikipedia.org/wiki/Synovial_fluid

Calippe, Bertrand; Guillonneau, Xavier; Sennlaub, Florian (March 2014). "Complement factor H and related proteins in age- ... A SNP in the F5 gene causes Factor V Leiden thrombophilia. rs3091244 is an example of a triallelic SNP in the CRP gene on human ... Other factors, like genetic recombination and mutation rate, can also determine SNP density. SNP density can be predicted by ... LD can be affected by two parameters (among other factors, such as population stratification): 1) The distance between the SNPs ...

https://en.wikipedia.org/wiki/Single-nucleotide_polymorphism

Overall this protein shows similarity to the complement 1Q factors (C1Q). However, when the 3-dimensional structure of the ... "The crystal structure of a complement-1q family protein suggests an evolutionary link to tumor necrosis factor". Current ... Renaldi O, Pramono B, Sinorita H, Purnomo LB, Asdie RH, Asdie AH (January 2009). "Hypoadiponectinemia: a risk factor for ... A low level of adiponectin is an independent risk factor for developing: Metabolic syndrome Diabetes mellitus Dyslipidemia ...

https://en.wikipedia.org/wiki/Adiponectin

The Factor H-related protein 1 (FHR1) has been identified as a novel inhibitor of the complement pathway. FHR1 blocks C5 ... Apparently Factor H and FHR1 control complement activation in a sequential manner. In hemolytic uremic syndrome (HUS), the ... 2009). "Factor H-related protein 1 (FHR-1) inhibits complement C5 convertase activity and terminal complex formation". Blood. ... Factor B then binds to C3b and is cleaved by a plasma serine protease Factor D. The C3bBb complex (= alternative pathway C3 ...

https://en.wikipedia.org/wiki/C5-convertase

Malhotra R, Ward M, Sim RB, Bird MI (July 1999). "Identification of human complement Factor H as a ligand for L-selectin". The ... The embryo secretes human chorionic gonadotropin (hCG), which downregulates anti-adhesion factor, MUC-1, located on the uterine ... Human sell consists of 10 exons and its transcription factor is FOXO 1, on the other hand the mouse sell gene is composed of 9 ... an adjacent epidermal growth factor-like domain, two to the consensus repeat units homologous to those found in C3/C4-binding ...

https://en.wikipedia.org/wiki/L-selectin

April 2005). "Complement factor H variant increases the risk of age-related macular degeneration". Science. 308 (5720): 419-21 ... Some of the factors that should be considered are the level of efficacy of various genetic tests in the general population, ... Combining molecular scale information with macro-scale clinical data, such as patients' tumor type and other risk factors, ... 2 July 2015). "Race/Ethnic Differences in the Associations of the Framingham Risk Factors with Carotid IMT and Cardiovascular ...

https://en.wikipedia.org/wiki/Personalized_medicine

Diaz-Guillen MA, Rodriguez de Cordoba S, Heine-Suner D (Jul 1999). "A radiation hybrid map of complement factor H and factor H- ... CFHR4 complement factor H-related 4". Hageman GS, Hancox LS, Taiber AJ, et al. (2007). "Extended Haplotypes in the Complement ... Complement factor H-related protein 4 is a protein that in humans is encoded by the CFHR4 gene. GRCh38: Ensembl release 89: ... 2000). "Functional properties of complement factor H-related proteins FHR-3 and FHR-4: binding to the C3d region of C3b and ...

https://en.wikipedia.org/wiki/CFHR4

Complement factor H-related protein 2) at the PDBe-KB. Zipfel PF, Skerka C (1994). "Complement factor H and related proteins: ... Díaz-Guillén MA, Rodríguez de Córdoba S, Heine-Suñer D (1999). "A radiation hybrid map of complement factor H and factor H- ... "Two additional human serum proteins structurally related to complement factor H. Evidence for a family of factor H-related ... Complement factor H-related protein 2 is a protein that in humans is encoded by the CFHR2 gene. GRCh38: Ensembl release 89: ...

https://en.wikipedia.org/wiki/CFHR2

BCX9930, an oral Factor D inhibitor for the treatment of complement-mediated diseases. FDA has granted Fast Track designation ...

https://en.wikipedia.org/wiki/BioCryst_Pharmaceuticals

Opsonins include Mfge8, Gas6, Protein S, antibodies and complement factors C1q and C3b. Phagoptosis has multiple functions ... Pathogenic cells such as bacteria can be opsonised by antibodies or complement factors, enabling their phagocytosis and ...

https://en.wikipedia.org/wiki/Phagoptosis

1989). "20 KDa homologous restriction factor of complement resembles T cell activating protein". Biochem. Biophys. Res. Commun ... When complement activation leads to deposition of C5b678 on host cells, CD59 can prevent C9 from polymerizing and forming the ... Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... 1992). "Complement regulatory proteins at the feto-maternal interface during human placental development: distribution of CD59 ...

https://en.wikipedia.org/wiki/CD59

... factor H, factor HR1 or HR3, membrane cofactor protein, factor I, factor B, complement C3, and thrombomodulin). This results in ... The complement system activation may be due to mutations in the complement regulatory proteins (factor H, factor I, or membrane ... of complement can result from production of anti-factor H autoantibodies or from genetic mutations in any of several complement ... "Platelet-associated complement factor H in healthy persons and patients with atypical HUS". Blood. 114 (20): 4538-4545. doi: ...

https://en.wikipedia.org/wiki/Atypical_hemolytic_uremic_syndrome

Lee FJ, Moss J, Vaughan M (1992). "Human and Giardia ADP-ribosylation factors (ARFs) complement ARF function in Saccharomyces ... ADP-ribosylation factor 5 is a protein that in humans is encoded by the ARF5 gene. ADP-ribosylation factor 5 (ARF5) is a member ... Shin, O H; Exton J H (August 2001). "Differential binding of arfaptin 2/POR1 to ADP-ribosylation factors and Rac1". Biochem. ... Tsuchiya M, Price SR, Tsai SC, Moss J, Vaughan M (March 1991). "Molecular identification of ADP-ribosylation factor mRNAs and ...

https://en.wikipedia.org/wiki/ARF5

"Entrez Gene: CFHR3 complement factor H-related 3". Zipfel PF, Skerka C (1994). "Complement factor H and related proteins: an ... Diaz-Guillen MA, Rodriguez de Cordoba S, Heine-Suner D (Jul 1999). "A radiation hybrid map of complement factor H and factor H- ... Complement factor H-related protein 3 is a protein that in humans is encoded by the CFHR3 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 ...

https://en.wikipedia.org/wiki/CFHR3

Lee FJ, Moss J, Vaughan M (1992). "Human and Giardia ADP-ribosylation factors (ARFs) complement ARF function in Saccharomyces ... ADP-ribosylation factor 4 is a protein that in humans is encoded by the ARF4 gene. ADP-ribosylation factor 4 (ARF4) is a member ... "ADP-ribosylation factor 4 small GTPase mediates epidermal growth factor receptor-dependent phospholipase D2 activation". J. ... "ADP-ribosylation factor 4 small GTPase mediates epidermal growth factor receptor-dependent phospholipase D2 activation". J. ...

https://en.wikipedia.org/wiki/ARF4

Complement factor H-related protein 5 (CFHR5) nephropathy is a form of inherited kidney disease which is endemic in Cyprus and ... 26 August 2010). "Identification of a mutation in complement factor H-related protein 5 in patients of Cypriot origin with ... "Recurrence of Complement Factor H-Related Protein 5 Nephropathy in a Renal Transplant". American Journal of Transplantation. 11 ... This is evidence that the disease is caused by a problem with alternative complement pathway regulation, rather than activation ...

https://en.wikipedia.org/wiki/CFHR5_nephropathy

Lee FJ, Moss J, Vaughan M (1992). "Human and Giardia ADP-ribosylation factors (ARFs) complement ARF function in Saccharomyces ... ADP-ribosylation factor 3 is a protein that in humans is encoded by the ARF3 gene. ADP-ribosylation factor 3 (ARF3) is a member ... Williger BT, Provost JJ, Ho WT, Milstine J, Exton JH (July 1999). "Arfaptin 1 forms a complex with ADP-ribosylation factor and ... Lee CM, Haun RS, Tsai SC, Moss J, Vaughan M (1992). "Characterization of the human gene encoding ADP-ribosylation factor 1, a ...

https://en.wikipedia.org/wiki/ARF3

Wu LC, Morley BJ, Campbell RD (Jan 1987). "Cell-specific expression of the human complement protein factor B gene: evidence for ... Gagnon J (Sep 1984). "Structure and activation of complement components C2 and factor B". Philosophical Transactions of the ... "The reaction of iodine and thiol-blocking reagents with human complement components C2 and factor B. Purification and N- ... Complement C2 is a protein that in humans is encoded by the C2 gene. The protein encoded by this gene is part of the classical ...

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Another factor contributing to the trends of this period was the "post-industrial boom" that helped to generate wealth in the ... Furthermore, bold headbands were often worn to complement women's customarily shorter hair lengths. Since a lot of women's ...

https://en.wikipedia.org/wiki/Women's_oversized_fashion_in_the_United_States_since_the_1920s

... announced in May 2017 that it will increase its usage of renewable natural gas (RNG) by a factor of three ... thereby complementing its initiative to expand its recycling capabilities. As of November 2016, Republic Services operated a ... Kadleck, Chrissy (17 December 2015). "How the Solid Waste Industry Factors into the Circular Economy". Waste 360. Retrieved 21 ...

https://en.wikipedia.org/wiki/Republic_Services

... with the same scaling factor; or a fraction of half-turn between −1.0 (inclusive) and +1.0 (exclusive) with scaling factor 1/2n ... in the two's complement convention. They can also be interpreted as a fraction of a full turn between −0.5 (inclusive) and +0.5 ... represented in binary fixed-point format with a scaling factor of 1/2n. Multiplying that fraction by 360° or 2π gives the angle ...

https://en.wikipedia.org/wiki/Binary_angular_measurement

Each commanding officer outfitted armaments to his liking, taking into consideration factors such as the overall weight of ... stores, complement of personnel aboard, and planned routes to be sailed. Consequently, the armaments on ships changed often ...

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This factor further highlights the need to reevaluate Tolkowsky's results, and to recalculate the effects of a diamond's ... A slightly steep pavilion angle can sometimes be complemented by a shallower crown angle, and vice versa. Other proportions ...

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215-. ISBN 978-0-521-87927-9. "Conversion Factors for Controlled Substances". Diversion Control Division. U.S. Department of ... and mutually complements the analgesic effect of its NMDA receptor antagonism. Levorphanol shows a high rate of psychotomimetic ...

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Factor Mfge produced in lymphoid tissues mainly by FDCs is known to enhance engulfment of apoptotic cells. Deficit of this ... Follicular DCs have high expression of complement receptors CR1 and CR2 (CD 35 and CD 21 respectively) and Fc-receptor FcγRIIb ... Follicular DCs receptors CR1, CR2 and FcγRIIb trap antigen opsonized by complement or antibodies. These antigens are then taken ... By secreting the bridging factor MFGE8, which crosslinks apoptotic cells and phagocytes, FDCs promote selective debris removal ...

https://en.wikipedia.org/wiki/Follicular_dendritic_cells

This circumstance, combined with Wright's tendency to live beyond his means (and other factors), led to great financial ... because the designs complemented the land around Chicago.[citation needed] Prairie Style houses often have a combination of ...

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In late January 2019, the New York Times reported rising housing prices to be a major factor in the increasing homelessness in ... This funding complements the Government's Housing First programme. Homelessness in Australia Housing in New Zealand " ...

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It is complemented by the Aquaventure water park and the Lost Chambers Aquarium, home to over 65,000 marine animals. The ... In 2009, an episode of The X Factor was partially filmed at the hotel, with Dannii Minogue using it to choose which female ...

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As a basic trainer, the M-345 is designed to complement the Aermacchi M-346 advanced jet trainer. It has been designed with a ... Aermacchi's competitive analysis director Sergio Coniglio stated low maintenance costs shall be a decisive factor in the M- ...

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The complement of the Cantor ternary set is an example of a fractal string. In arithmetical terms, the Cantor set consists of ... It is self-similar, because it is equal to two copies of itself, if each copy is shrunk by a factor of 3 and translated. More ... Every point of the Cantor set is also an accumulation point of the complement of the Cantor set. For any two points in the ... Since the Cantor set is the complement of a union of open sets, it itself is a closed subset of the reals, and therefore a ...

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The higher the Q factor of the capacitor, the closer it approaches the behavior of an ideal capacitor. The Q factor of a ... by Bell Laboratories in the early 1950s as a miniaturized and more reliable low-voltage support capacitor to complement their ... The quality factor (or Q) of a capacitor is the ratio of its reactance to its resistance at a given frequency, and is a measure ... Factors such as voltage and chassis material are of secondary consideration, which are more related to how easily a shock can ...

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Tashilhunpo was destined to become 'Southern Tibet's greatest monastic university' with a complement of 3,000 monks. Gendun ... "Despite the complex historical, religious and political factors surrounding the selection of incarnate masters in the exiled ...

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Cells containing the protein complement desired are grown. Proteins are then extracted from the mixture and digested with a ... including low-abundance proteins like transcription factors and protein kinases. They were also able to identify 131 proteins ... uses shotgun proteomics to implicate protease inhibition and complement activation in the antiinflammatory properties of high- ... March 2007). "Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of ...

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Thus oxidative damage to mtDNA of motor neurons may be a significant factor in the etiology of ALS. Over the past decade, an ... Lehmann G, Segal E, Muradian KK, Fraifeld VE (April 2008). "Do mitochondrial DNA and metabolic rate complement each other in ... It has been proposed that aged mitochondria is the critical factor in the origin of neurodegeneration in Alzheimer's disease. ... the expression of the mitochondrial genes may be strongly regulated by external factors, apparently to enhance the synthesis of ...

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Factor V and Factor VIII, gastrin, the leech enzyme hirudin, fibrinogen, Complement component 4, follicle-stimulating hormone ... Based on crystal structure of TPST-2 with C4 complement and PAP, an SN2-like in-line displacement mechanism has been proposed. ...

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Ones Complement Accumulator 7020 - CML - Complement L Bit 7001 - IAC - Increment 7010 - RAR - Rotate Right 7004 - RAL - Rotate ... The Memory Extension Controller expands the addressable memory by a factor of 8, to a total of 32,768 words. This expansion was ... the twos-complement negation. Since there is no subtraction instruction, only the twos-complement add (TAD), computing the ... 001 - TAD - Two's complement ADd the memory operand to (a 12 bit signed value (AC) w. carry in L). 010 - ISZ - Increment the ...

https://en.wikipedia.org/wiki/PDP-8

Another key factor is the existence of the Jesuitical architecture, also called "plain style" (Estilo Chão or Estilo Plano) ... The gardens were designed by André Le Nôtre specifically to complement and amplify the architecture. The Galerie des Glaces ( ... It is conditioned by several political, artistic, and economic factors, that originate several phases, and different kinds of ...

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Manner is the category that assesses the way in which a speaker presents their material and usually includes factors such as ... held on different days over a longer period of time have Short Preparation debates in one or more of the rounds to complement ... Method is category that assesses the way in which a speaker structures their speech and includes factors such as dynamics (the ...

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J Biol Chem 279:8181-8189 (2004) Myeloid Leukemia Factor 1 associates with a novel heterogeneous nuclear ribonucleoprotein U- ... Nature 507:462-470 (2014) Complementing tissue characterisation by integrating transcriptome profiling from the Human Protein ...

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The factor by which a future income is reduced is known as the 'discount rate'. Thus, $1.00 received a year from now is worth $ ... it is non-interactive it does not exceed the sound recording performance complement it is accompanied by information on the ... The actual discount factor used depends on the risk assumed by the principal gainer in the transaction. For instance, a mature ... The rate of royalty applied in a given case is determined by various factors, the most notable of which are: Market drivers and ...

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... such as the journal impact factor. The impact factor, which is often used as a proxy of prestige, can influence revenues, ... Elsevier has incorporated other businesses that were either complementing or competing in the field of research and publishing ... Nine Elsevier journals, which exhibited unusual levels of self-citation, had their journal impact factor of 2019 suspended from ... "Use of the Journal Impact Factor in academic review, promotion, and tenure evaluations". eLife. 8. doi:10.7287/peerj.preprints. ...

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Later it can be complemented with standardised ETCS information. This is the same migration path as chosen in Italy (SCMT) or ... Both factors led to efforts to reduce the time and cost of cross-border traffic. On 4 and 5 December 1989, a working group ... In Belgium, the TBL 1 crocodiles were complemented with Eurobalises in the TBL 1+ operation scheme. The TBL 1+ definition ...

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In essence, they are virulence factors, factors that make the bacteria harmful and infective to the host organism. TAAs are ... They do this by aiding complement resistance. The stalk protein domain is also alternatively named the internal passenger ... This may be due to BadA's inducing the transcription of proangiogenic factors, as it activates of NF-κB as well as hypoxia- ... All Trimeric Autotransporter Adhesins are crucial virulence factors that cause serious disease in humans. The most-studied and ...

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In La Palma they were preserved by these environmental factors and in La Gomera, and El Hierro the existence of mummification ... These armaments were commonly complemented with an obsidian knife known as Tabona. Dwellings were situated in natural or ... no real intention to mummify the deceased and that the good conservation of some of them is due rather to environmental factors ...

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Another contributing factor to her controversial image were tabloid rumors of incest that began when Jolie, upon winning her ... PSVI was established to complement wider UK government work by raising awareness and promoting international co-operation. ...

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It also created a voluntary insurance policy that would complement the mandatory coverage each citizen received. After 2002, ... Noting that such factors as the country's aging and the generous benefits established since 1993 threatened the fund's ...

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He was preparing to depart for England to take delivery of the unit's planned complement of Short Sunderland flying boats when ... Despite claiming that employing women in the Air Force was an important factor in reducing "antagonism and prejudice" against ...

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ISBN 978-0-393-04729-5. Brlek, Srećko (1989). "Enumeration of Factors in the Thue-Morse Word". Discrete Applied Mathematics. 24 ... and two's complement arithmetic so that when n == 0, x is odd (e.g. 31 or 63) x = indexOfHighestOneBit(n ^ (n - 1)) if ((x & 1 ... obtained by starting with 0 and successively appending the Boolean complement of the sequence obtained thus far. The first few ...

https://en.wikipedia.org/wiki/Thue–Morse_sequence

Complement factor I deficiency is a disorder that affects the immune system. Explore symptoms, inheritance, genetics of this ... or absent complement factor I. The lack (deficiency) of functional complement factor I protein allows uncontrolled activation ... medlineplus.gov/genetics/condition/complement-factor-i-deficiency/ Complement factor I deficiency. ... Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when ...

https://medlineplus.gov/genetics/condition/complement-factor-i-deficiency/

JavaScript is disabled for your browser. Some features of this site may not work without it ...

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Complement profiling of the patient showed decreased C3 and FB levels, with elevated levels of the terminal membrane attack ... Complement profiling of the patient showed decreased C3 and FB levels, with elevated levels of the terminal membrane attack ... Complement components analysis using specific immunoassays was performed on frozen plasma samples from the patient and mother. ... Complement components analysis using specific immunoassays and Western blotting was performed on frozen plasma samples from the ...

https://www.frontiersin.org/articles/10.3389/fimmu.2021.608604/full?utm_source=S-TWT&utm_medium=SNET&utm_campaign=ECO_FIMMU_XXXXXXXX_auto-dlvrit

Complement Factor H--genetics. Macular Degeneration--etiology. Macular Degeneration--genetics. Risk Factors ... NEI symposium : age-related macular degeneration (AMD) and complement factor H / Michael Pangburn and Paul Sieving. ... presenting their data on the discovery of the association of AMD and complement factor H (CFH). It also features Michael ...

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Factor H is a key regulator of the alternative pathway of complement, and genetic or acquired impairments in Factor H are ... Complement activation at a particular location is determined by the balance of activating and inhibitory proteins. ... Factor H is a key regulator of the alternative pathway of complement, and genetic or acquired impairments in Factor H are ... Factor H related proteins modulate complement activation on kidney cells Brandon Renner 1 , Jennifer Laskowski 1 , Felix ...

https://pubmed.ncbi.nlm.nih.gov/36063874/

Of the 5 AMD-associated complement genes, complement factor H (CFH) and CFI exhibit a significant rare variant burd … ... complement factor H (CFH) and CFI exhibit a significant rare variant burden implicating a major contribution of the complement ... Ultra-rare complement factor 8 coding variants in families with age-related macular degeneration Lina Zelinger 1 , Tammy M ... we report the identification of ultra-rare variants in complement factors 8A and 8B, two components of the terminal complement ...

https://www.ncbi.nlm.nih.gov/pubmed/?term=37153444

Here we discuss how expertise in Human Factors can complement engineering expertise in a variety of civil litigation cases. We ... For this reason and others, Human Factors is a growing scientific field that addresses how people interact with equipment, ... Chase Coelho is a human factors, technical safety, and risk management professional with experience in aviation, aerospace, ... On Demand: How Human Factors Can Complement Engineering in Civil Litigation: Principles and Case Studies. Start Date: 3/4/2021 ...

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Osteopontin, Macrophage Migration Inhibitory Factor and Anti-Interleukin-8 Autoantibodies Complement CA125 for Detection of ... Osteopontin, Macrophage Migration Inhibitory Factor and Anti-Interleukin-8 Autoantibodies Complement CA125 for Detection of ... A four-biomarker panel (CA125, osteopontin (OPN), macrophage inhibitory factor (MIF), and anti-IL-8 autoantibodies) detected 82 ...

https://edrn.nci.nih.gov/data-and-resources/publications/31035430-2648-osteopontin-macrophage-migration-inhibitory-factor-and-anti-interleukin-8-autoantibodies-complement-ca125-for-detection-of-early-stage-ovarian-cancer/

The alternative pathway of complement represents an important humoral component of natural defense against microbial attack. ... The human complement factor D ELISA kit is to be used for the in vitro quantitative determination of human complement factor D ... versus the corresponding concentrations of the human complement factor D standards (log). The human complement factor D ... Factor D is highly specific and cleaves factor B bound to C3b, generating the C3bBb enzyme. Factor D is the rate-linking C3 ...

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Purchase Recombinant Rat Complement factor D(Cfd). It is produced in Mammalian cell. High purity. Good price. ... Recombinant Rat Complement factor D (Cfd) ( Mammalian cell-CSB-MP005271RA ). *Recombinant Rat Complement factor D(Cfd) ( E.coli ... Factor D cleaves factor B when the latter is complexed with factor C3b, activating the C3bbb complex, which then becomes the C3 ... Complement factor D; EC 3.4.21.46; Adipsin; C3 convertase activator; Endogenous vascular elastase; Properdin factor D ...

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... Review Article (Web of Science) ...

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Factors affecting IgG4-mediated complement activation.. Oskam, Nienke; Damelang, Timon; Streutker, Marij; Ooijevaar-de Heer, ... Lastly, we show that bispecific, monovalent IgG4 resulting from Fab arm exchange is a less potent activator of complement than ... We show that IgG4 can activate complement only at high antigen and antibody concentrations, via the classical pathway. Moreover ... Taken together, these results imply that involvement of IgG4-mediated complement activation in pathology is possible but ...

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View Full Project Details for COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS ...

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Human CFH(Complement Factor H) ELISA Kit. Human CFH(Complement Factor H) ELISA Kit. To Order: [email protected] ... Description: A sandwich quantitative ELISA assay kit for detection of Mouse Complement Factor H (CFH) in samples from serum, ... Description: A sandwich quantitative ELISA assay kit for detection of Mouse Complement Factor H (CFH) in samples from serum, ... Description: This is Competitive Enzyme-linked immunosorbent assay for detection of Rat Complement Factor H (CFH) in serum, ...

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Complement Factor D/CFD. Synonyms. Adipsin; C3 convertase activator; Complement factor D; CFD; PFD; DF; ADN; FACTOR D; AMBP-1; ... Recombinant Mouse Complement Factor D/CFD Protein is expressed from HEK293 with hFc tag at the C-terminal.It contains Ile26- ... Mouse Complement Factor D on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.. ... The purity of Mouse Complement Factor D is greater than 95% as determined by SEC-HPLC.. ...

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Factor How. Welcome to Factor How The goal of Factor How is to give you the absolute best news sources for any topic! Our ... "But the complement trade focuses on one. Our physique, although is unimaginable subtle, and is aware of find out how to use the ... Over ten years in the past, she had the concept of a food-based complement firm, Wild Diet. She began it in her backyard shed; ... Utilizing Money Again Playing cards (or Factors Playing cards) for Simple Month-to-month Passive Earnings 3 months ago ...

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Characterisation of a heparin binding domain in complement factor H Clark SJ., Higman VA., Fernando A., Mulloy B., Perkins SJ ...

https://www.immunology.ox.ac.uk/publications/11832?a302ea9e-0301-11ee-8001-061b866677b4

All photos and videos on this site belong to the National Eye Institute (NEI). Please credit ©NEI when you use any image or video from the library ...

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Active immunization against complement factor C5a: a new therapeutic approach for Alzheimers disease BIBLIOGRAPHIC THERAPEUTIC ... Notably, the pro-inflammatory complement factor C5a and its receptor have been found to be up-regulated in microglia in the ... The authors speculate that active immunotherapy against complement factor C5a may be a new and effective approach for the ... Inflammatory processes in AD are primarily triggered by the up-regulation of the complement system in response to misfolded and ...

https://alzped.nia.nih.gov/node/4921/printable/print

... associated with low serum Factor I (FI) levels, are strong risk factors for developing the advanced stages of Age-Related ... Rare variants in the Complement Factor I (CFI) gene, ... Age-Related Macular Degeneration, Complement Factor I, Factor I ... Rare variants in the Complement Factor I (CFI) gene, associated with low serum Factor I (FI) levels, are strong risk factors ... Prevalence and Phenotype Associations of Complement Factor I Mutations in Geographic Atrophy. ...

https://www.stemcells.ox.ac.uk/publications/1184112?20889254-0102-11ee-9c13-0a3af28e70c2

The complement system plays an important part in defense against pyogenic organisms. ... The complement system is part of the innate immune system. ... Molecular basis of complement factor I deficiency in Tunisian ... complement receptor 2 (CR2), and decay accelerating factor (DAF). A North African study of molecular basis of complement factor ... Cases of complement deficiency have helped defined the role of complement in host defense. [4] A registry of complement ...

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Primary: complement. Persistent complement, properdin, or Factor B deficiency. None. Pneumococcal. Meningococcal. Hib (children ... Persons with functional or anatomic asplenia (including sickle cell disease), HIV infection and persistent complement component ... Persons with functional or anatomic asplenia (including sickle cell disease) and persistent complement component deficiency ( ... Other immunosuppressive medications include human immune mediators like interleukins and colony-stimulating factors, immune ...

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... rheumatoid factor, complement C3 and C4 levels). If joint inflammation is suspected, joint ultrasound is indicated (or simple ... Other factors (loss of physical condition, psychological factors) should be evaluated if not. ... Prognostic factors in Spanish COVID-19 patients: A case series from Barcelona. PLoS ONE 2020, 15, e0237960. [Google Scholar] [ ... Information on factors that may identify populations most at risk of long COVID-19 is very scarce. A prepress study suggests an ...

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Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor D in samples from blood, plasma, serum, ... Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor D in samples from blood, plasma, serum, ... Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor H in samples from blood, plasma, serum, ... Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor H in samples from blood, plasma, serum, ...

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Complement-mediated. Autoantibody inhibition of complement factor H activity. Acute kidney injury. ... Complement-mediated. Mutations in complement genes causing uncontrolled activation of alternative complement pathway. Usually ... Our patient had no anti-intrinsic factor antibodies, but she did have antiparietal cell antibodies, which suggests but is not ... Hemoglobin 68 g/L; platelets 70 × 109/L; homocysteine 16.2 μmol/L; positive anti-intrinsic factor antibodies 4 patients (67%). ...

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Low complement factor H (i.e., ,70%). 3/69 (4.3). Low complement factor I (i.e., ,70%). 1/69 (1.4). ... Frémeaux-Bacchi V, Sellier-Leclerc A-L, Vieira-Martins P, Limou S, Kwon T, Lahoche A, et al. Complement gene variants and Shiga ... Wong CS, Mooney JC, Brandt JR, Staples AO, Jelacic S, Boster DR, et al. Risk factors for the hemolytic uremic syndrome in ... characterization of isolates and identification of risk factors for haemolytic uremic syndrome. BMC Infect Dis. 2015;15:324. ...

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Atypical Hemolytic-uremic Syndrome with Postrenal Transplant Recurrence Due to a Novel Frameshift Variant in Complement Factor ...

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Human complement factor H related protein test for monitoring bladder cancer. Raitanen, M.P., Marttila, T., Nurmi, M., Ala-Opas ... Human complement factor H related protein test for monitoring bladder cancer.. PURPOSE: The BTA stat test is a rapid, ... human complement factor H related protein) in urine. We compared BTA stat test to voided urine cytology in patients monitored ...

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Complement InhibitorsPegcetacoplan binds to complement protein C3 and its activation fragment C3b, thereby regulating cleavage ... Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005 Apr 15. 308(5720):419-21. [ ... Complement factor H polymorphism and age-related macular degeneration. Science. 2005 Apr 15. 308(5720):421-4. [Medline]. ... Complement factor H variant Y402H is a major risk determinant for geographic atrophy and choroidal neovascularization in ...

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Clinical significance of complement deficiencies. (medlineplus.gov)
Deficiencies in the complement cascade can lead to overwhelming infection and sepsis. (medscape.com)
Complement deficiencies are said to comprise between 1 and 10% of all primary immunodeficiencies. (medscape.com)
[ 4 ] A registry of complement deficiencies has been established as a means to promote joint projects on treatment and prevention of diseases associated with defective complement function. (medscape.com)
This article outlines some of the disease states associated with complement deficiencies and their clinical implications. (medscape.com)
Complement pathways and deficiencies. (medscape.com)
Deficiencies in complement predispose patients to infection via 2 mechanisms: (1) ineffective opsonization and (2) defects in lytic activity (defects in MAC). (medscape.com)
Specific complement deficiencies are also associated with an increased risk of developing autoimmune disease, such as SLE. (medscape.com)
Complement factor deficiencies are absent, only zinc need routinely be given in alternating fashion. (aaan.org)

These multicomponent enzymes assemble on the surface of alternative pathway of complement activators and are stabilized by properdin (P). The participation of the alternative pathway of complement has been implicated in the pathogenesis of a wide variety of human diseases. (hycultbiotech.com)
Properdin can bind C3b and activate the alternative complement pathway and also stabilizes the C3bBb alternative pathway C3 convertase enzyme, thereby directing the deposition of C3 fragments to the cell surface and driving the amplification loop ( 17 - 19 ). (frontiersin.org)

This gene provides instructions for making a protein called complement factor I. This protein helps regulate a part of the body's immune response known as the complement system . (medlineplus.gov)
Mutations in the CFI gene that cause complement factor I deficiency result in abnormal, nonfunctional, or absent complement factor I. The lack (deficiency) of functional complement factor I protein allows uncontrolled activation of the complement system. (medlineplus.gov)
The unregulated activity of the complement system decreases blood levels of another complement protein called C3, reducing the immune system's ability to fight infections. (medlineplus.gov)
Furthermore, factor D plays a role in fatty tissue distinct from its role as a complement protein. (hycultbiotech.com)
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. (cusabio.com)
Recombinant Mouse Complement Factor D/CFD Protein is expressed from HEK293 with hFc tag at the C-terminal.It contains Ile26-Ser259. (kactusbio.com)
Adipsin protein production was analyzed in primary cultured orbital fibroblasts under insulin growth factor (IGF)-1, CD40 ligand ( CD40L ) stimulation, and adipogenesis . (bvsalud.org)
Factor Xa is inactivated by protein Z-dependent protease inhibitor (ZPI), a serine protease inhibitor (serpin). (bionity.com)
The affinity of this protein for factor Xa is increased 1000-fold by the presence of protein Z , while it does not require protein Z for inactivation of factor XI . (bionity.com)
Defects in protein Z lead to increased factor Xa activity and a propensity for thrombosis. (bionity.com)
Other homologous domains occur in related receptors, including the very low-density lipoprotein receptor and the LDL receptor-related protein/alpha 2-macroglobulin receptor, and in proteins which are functionally unrelated, such as the C9 component of complement. (embl.de)
Notably, these pentraxins may also recruit soluble complement regulators, such as factor H (FH) and C4b-binding protein (C4BP), which in turn limit excessive complement activation on the surface ( 11 - 14 ). (frontiersin.org)

Complement factor I deficiency is a disorder that affects the immune system. (medlineplus.gov)
Some people with complement factor I deficiency have a kidney disorder called glomerulonephritis with isolated C3 deposits. (medlineplus.gov)
Complement factor I deficiency can also be associated with autoimmune disorders such as rheumatoid arthritis or systemic lupus erythematosus (SLE). (medlineplus.gov)
Complement factor I deficiency is caused by mutations in the CFI gene. (medlineplus.gov)
Baracho GV, Nudelman V, Isaac L. Molecular characterization of homozygous hereditary factor I deficiency. (medlineplus.gov)
Grumach AS, Leitao MF, Arruk VG, Kirschfink M, Condino-Neto A. Recurrent infections in partial complement factor I deficiency: evaluation of three generations of a Brazilian family. (medlineplus.gov)
Ponce-Castro IM, Gonzalez-Rubio C, Delgado-Cervino EM, Abarrategui-Garrido C, Fontan G, Sanchez-Corral P, Lopez-Trascasa M. Molecular characterization of Complement Factor I deficiency in two Spanish families. (medlineplus.gov)
The molecular basis of hereditary complement factor I deficiency. (medlineplus.gov)
Cases of complement deficiency have helped defined the role of complement in host defense. (medscape.com)
A North African study of molecular basis of complement factor I deficiency in atypical hemolytic and uremic syndrome patients suggested that the Ile357Met mutation may be a founding effect. (medscape.com)
Inborn deficiency of factor X is very uncommon (1:500,000), and may present with epistaxis (nosebleeds), hemarthrosis (bleeding into joints) and gastrointestinal blood loss. (bionity.com)
Apart from congenital deficiency, low factor X levels may occur occasionally in a number of disease states. (bionity.com)
Deficiency of vitamin K or antagonism by warfarin (or similar medication) leads to the production of an inactive factor X. In warfarin therapy, this is desirable to prevent thrombosis . (bionity.com)
American and British scientists described deficiency of factor X independently in 1953 and 1956, respectively. (bionity.com)
1997). "Inherited factor X deficiency: molecular genetics and pathophysiology. (bionity.com)

The Role of Adipsin, Complement Factor D, in the Pathogenesis of Graves' Orbitopathy. (bvsalud.org)
We investigated the pathogenic role of a specific adipokine , adipsin , known as complement factor D in Graves' orbital fibroblasts . (bvsalud.org)

Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when it is not needed. (medlineplus.gov)
The interaction of the proteins C3, factor B, and factor D results in the formation of the alternative C3- and C5-convertases, i.e. (hycultbiotech.com)
Genes that encode the proteins of complement components or their isotypes are distributed throughout different chromosomes, with 19 genes comprising 3 significant complement gene clusters in the human genome. (medscape.com)
The important components of this system are various cell membrane-associated proteins such as complement receptor 1 (CR1), complement receptor 2 (CR2), and decay accelerating factor (DAF). (medscape.com)
The FH-related (FHR) proteins share common ligands with FH, due to their homology with this complement regulator, but they lack the domains that mediate the complement inhibitory activity of FH. (frontiersin.org)

Samples and standards are incubated in microtiter wells coated with antibodies recognizing human complement factor D. Biotinylated tracer antibody will bind to the captured human complement factor D. Streptavidin-peroxidase conjugate will bind to the biotinylated tracer antibody. (hycultbiotech.com)
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Complement Factor H (CFH) in serum, plasma and other biological fluids. (elisastrip.com)
Lectins activate the lectin pathway in a manner similar to the antibody interaction with complement in the classical pathway. (medscape.com)
Human IgG antibody Laboratories manufactures the monkey complement elisa kit reagents distributed by Genprice. (aabioetica.org)
InflaRx N.V. is testing IFX-1, a monoclonal anti-human complement factor C5a antibody currently under development as treatment for inflammatory conditions and COVID-19 pneumonia. (who.int)

Because of its significance as an threat to both human and related ungulates, such as cow, its genome was sequenced and still being studied to gain more insight into the virulence factor and to develop treatments and preventive prophylactic antibodies. (kenyon.edu)

The human complement factor D ELISA kit is to be used for the in vitro quantitative determination of human complement factor D in serum, plasma and urine samples. (hycultbiotech.com)
Description: A sandwich quantitative ELISA assay kit for detection of Mouse Complement Factor H (CFH) in samples from serum, plasma or other biological fluids. (elisastrip.com)
The Monkey Complement Elisa Kit reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (aabioetica.org)
Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor D in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (aabioetica.org)
Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor H in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (aabioetica.org)
Interactions of the FHRs with pentraxins resulted in enhanced activation of both the classical and the alternative complement pathways on dead cells when exposed to human serum. (frontiersin.org)
The effects of settled grain dust on the human serum complement cascade were investigated. (cdc.gov)

Some new clinical entities are linked with partial complement defects. (medscape.com)

This result, combined with a normal total complement test, allowed us to conclude that a diagnosis of autoimmune hemolytic anemia was unlikely. (cmaj.ca)
Immurological behavior (IgG, lgM, lgA) and total complement (CH50) of newborns infants with risk factors for early onset sepsis. (bvsalud.org)

The alternative pathway of complement represents an important humoral component of natural defense against microbial attack. (hycultbiotech.com)
The complement system is a key humoral component of innate immunity, and in addition to its many other functions, it is involved in the clearance of waste material, such as immune complexes and apoptotic and necrotic cells ( 1 , 2 ). (frontiersin.org)

Factor D is the rate-linking C3 convertase enzyme of the alternative pathway. (hycultbiotech.com)
Factor D cleaves factor B when the latter is complexed with factor C3b, activating the C3bbb complex, which then becomes the C3 convertase of the alternate pathway. (cusabio.com)

The human complement factor D ELISA is a ready-to-use solid-phase enzyme-linked immunosorbent assay based on the sandwich principle with a working time of 3½ hours. (hycultbiotech.com)

In addition to playing an important role in host defense against infection, the complement system is a mediator in both the pathogenesis and prevention of immune complex diseases, such as systemic lupus erythematosus (SLE). (medscape.com)

The complement cascade consists of 3 separate pathways that converge in a final common pathway. (medscape.com)
Dying cells also expose ligands that bind initiator molecules of the various complement pathways, so that complement activation and opsonin deposition on the dead cell surface may enhance phagocytotic clearance ( 1 , 8 ). (frontiersin.org)

Factor H (FH), a major soluble complement inhibitor, binds to dead cells and inhibits excessive complement activation on their surface, preventing lysis, and the release of intracellular material, including DNA. (frontiersin.org)

Both genetics and environmental factors influence the expression of asthma, and not all asthma is the result of a specific immune response to allergen. (cdc.gov)
Both host factors (genetics) and low molecular weight allergens. (cdc.gov)

Mutations of complement factor I and potential mechanisms of neuroinflammation in acute hemorrhagic leukoencephalitis. (upmc.edu)

Aliquots were analyzed for factor-B conversion and hemolytic activity. (cdc.gov)
Factor-B conversion and reductions in hemolytic complement consumption were dose related. (cdc.gov)

The human factor X gene is located on the thirteenth chromosome (13q34). (bionity.com)

Factor D is highly specific and cleaves factor B bound to C3b, generating the C3bBb enzyme. (hycultbiotech.com)
Glicoproteína sérica termolábil rica en glicina que contiene un componente de la CONVERTASA DEL COMPLEMENTO C3 DE LA VÍA ALTERNATIVA (C3bBb). (bvsalud.org)

Examples of high molecular environmental factors are known to influence the development weight occupational allergens include proteases used in the and expression of asthma, and a vast array of triggers of asthma detergent industry, laboratory animal allergens, and ovalbumin have been identified. (cdc.gov)

The complement system is part of the innate immune system. (medscape.com)
Although the complement system is part of the body's innate, relatively nonspecific defense against pathogens, its role is hardly primitive or easily understood. (medscape.com)

Measurable quantities of factor D were detected in urine of 85% of healthy individuals (0.62 ± 0.33 ng/ml). (hycultbiotech.com)

In vitro activation of the alternative pathway of complement by settled grain dust. (cdc.gov)

New studies point to the complex interplay between the complement cascade and adaptive immune response, and complement is also being studied in association with ischemic injury as a target of therapy. (medscape.com)
Factor X , also known by the eponym Stuart-Prower factor or as thrombokinase , is an enzyme ( EC 3.4.21.6) of the coagulation cascade . (bionity.com)

The complement system plays an important part in defense against pyogenic organisms. (medscape.com)

Because their roles in complement regulation is controversial and incompletely understood, we studied the interaction of FHR-1 and FHR-5 with DNA and dead cells and investigated whether they influence the regulatory role of FH and the complement activation on DNA and dead cells. (frontiersin.org)

Factor D, a 24 kD serine protease of the alternative complement pathway, is synthesized as a precursor single-chain molecule. (hycultbiotech.com)
Factor D is unique among serine proteases because it requires neither enzymatic cleavage for expression of proteolytic activity nor activation by a serpin for its control. (hycultbiotech.com)
Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb. (bvsalud.org)

Following these repeats is a 350 residue domain that resembles part of the epidermal growth factor (EGF) precursor. (embl.de)

While HIV infection reports complement other HIV/AIDS studies of HIV infection in a community (5,6), AIDS surveillance and the HIV family of surveys (7) remain the basis for determining the current status and course of HIV infection in the United States. (cdc.gov)

This difference in outcome may indicate that both donor and recipient factors contribute to the development of posttransplant TMA. (hindawi.com)

An intricate system regulates complement activity. (medscape.com)

at the same time, the inflammation promoted by complement activation can result in cellular damage when not kept in check. (medscape.com)
Both FHRs caused increased complement activation on DNA. (frontiersin.org)

Complement plays an essential role in the opsonophagocytic clearance of apoptotic/necrotic cells. (frontiersin.org)

So that suspect case of Ebola disease or suspect case of Ebola disease definition is a person with signs and symptoms compatible with Ebola disease and an epidemiological risk factor within 21 days before the onset of symptoms. (cdc.gov)
environmental factors that can increase agents and of primary interventions the risk of cancer. (who.int)
Testing and reporting may be influenced by factors other than the incidence and prevalence of AIDS, e.g., public awareness of risk factors, confidentiality concerns, and testing accessibility. (cdc.gov)

In healthy individuals factor D is rapidly eliminated via the kidney and neither modified extrarenal catabolism nor changes in synthesis contribute to elevated factor D levels observed in patients with renal failure. (hycultbiotech.com)
Factor X is synthesized in the liver and requires vitamin K for its synthesis. (bionity.com)

These findings underscore the duality of the complement system. (medscape.com)
Knowledge about the complement system is expanding. (medscape.com)

The human complement factor D concentration of samples, which are run concurrently with the standards, can be determined from the standard curve. (hycultbiotech.com)

1991). "Cloning and expression in COS-1 cells of a full-length cDNA encoding human coagulation factor X.". Gene 99 (2): 291-4. (bionity.com)
The regenerative medicine is the combination of cells, material engineering, and biochemical factors to improve or replace the biological functions attempting to promote the medicine advancement. (bvsalud.org)

Anatomy5

Diseases9

Chemicals and Drugs46

Analytical, Diagnostic and Therapeutic Techniques and Equipment7

Phenomena and Processes24

Information Science3

Named Groups1

Health Care2

Protein H, an antiphagocytic surface protein in Streptococcus pyogenes. (1/741)

Multicenter trial of the quantitative BTA TRAK assay in the detection of bladder cancer. (2/741)

In vitro analysis of complement-dependent HIV-1 cell infection using a model system. (3/741)

Disruption of disulfide bonds is responsible for impaired secretion in human complement factor H deficiency. (4/741)

Hypocomplementemia discloses genetic predisposition to hemolytic uremic syndrome and thrombotic thrombocytopenic purpura: role of factor H abnormalities. Italian Registry of Familial and Recurrent Hemolytic Uremic Syndrome/Thrombotic Thrombocytopenic Purpura. (5/741)

Familial relapsing haemolytic uraemic syndrome and complement factor H deficiency. (6/741)

Identification of human complement Factor H as a ligand for L-selectin. (7/741)

Resistance to both complement activation and phagocytosis in type 3 pneumococci is mediated by the binding of complement regulatory protein factor H. (8/741)

No images available that match "complement factor h"

Complement Factor H

Complement Factor B

Complement C3b Inactivator Proteins

Macular Degeneration

Complement Factor I

Complement C3b

Complement C3

Complement Activation

Complement Factor D

Complement System Proteins

Hemolytic-Uremic Syndrome

Complement Pathway, Alternative

Complement C2

Complement C3d

Complement C4

Glomerulonephritis, Membranoproliferative

Optic Disk Drusen

Complement C5

Complement C5a

Complement C3-C5 Convertases

Receptors, Complement

Complement C1q

Complement Membrane Attack Complex

Polymorphism, Single Nucleotide

Blood Proteins

Genotype

Complement Pathway, Classical

Retinal Drusen

Choroid

Complement Inactivator Proteins

Antigens, CD46

Complement Inactivating Agents

Gene Frequency

Choroidal Neovascularization

Complement C9

Complement C3a

Retinal Pigment Epithelium

Complement Hemolytic Activity Assay

Genetic Predisposition to Disease

Geographic Atrophy

Complement Activating Enzymes

Complement C4b

Receptors, Complement 3b

Serum Sickness

Protein Binding

Homozygote

Chromosomes, Human, Pair 1

Complement C4b-Binding Protein

Complement C3 Convertase, Alternative Pathway

Case-Control Studies

Haplotypes

Antigens, CD55

Molecular Sequence Data

Polymorphism, Genetic

Receptor, Anaphylatoxin C5a

Linkage Disequilibrium

Alleles

Amino Acid Sequence

Complement C6

Complement C1

Surface Plasmon Resonance

Serine Endopeptidases

Properdin

Heparin

Complement C3c

Chromosomes, Human, Pair 10

Pigment Epithelium of Eye

Complement Pathway, Mannose-Binding Lectin

Complement C1 Inhibitor Protein

Binding Sites

Amino Acid Substitution

Mutation

Histidine

Complement Fixation Tests

Base Sequence

Blood Bactericidal Activity

Protein Structure, Tertiary

Bacterial Proteins

Enzyme-Linked Immunosorbent Assay

Complement C7