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Ask your administrator if you think this is wrong. ======= C4B ======= == Gene Information == * **<color #00a2e8>Official Symbol</color>**: C4B * **<color #00a2e8>Official Name</color>**: complement C4B (Chido blood group) * **<color #00a2e8>Aliases and Previous Symbols</color>**: N/A * **<color #00a2e8>Entrez ID</color>**: [[https://www.ncbi.nlm.nih.gov/gene/?term=721|721]] * **<color #00a2e8>UniProt</color>**: [[https://www.uniprot.org/uniprot/P0C0L5|P0C0L5]] * **<color #00a2e8>Interactions</color>**: [[https://thebiogrid.org/search.php?search=C4B&organism=9606|BioGRID]] * **<color #00a2e8>PubMed articles</color>**: [[https://www.ncbi.nlm.nih.gov/pubmed/?term=gene%20C4B|Open PubMed]] * **<color #00a2e8>OMIM</color>**: [[https://omim.org/entry/120820|Open OMIM]] == Function Summary == * **<color #00a2e8>Entrez Summary</color>**: This gene encodes the basic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluster exist, such that individuals may have 1, 2, or 3 copies of this gene. In addition, this gene exists as a long form and a short form due to the presence or absence of a 6.4 kb endogenous HERV-K retrovirus in intron 9. [provided by RefSeq, Jul 2008]. * **<color #00a2e8>UniProt Summary</color>**: Non-enzymatic component of the C3 and C5 convertases and thus essential for the propagation of the classical complement pathway. Covalently binds to immunoglobulins and immune complexes and enhances the solubilization of immune aggregates and the clearance of IC through CR1 on erythrocytes. C4A isotype is responsible for effective binding to form amide bonds with immune aggregates or protein antigens, while C4B isotype catalyzes the transacylation of the thioester carbonyl group to form ester bonds with carbohydrate antigens. <button type='primary' size='sm' modal='Pfam_Domains'>Pfam Domains</button> <button type='primary' size='sm' modal='GO_terms'>GO Terms</button> <modal id='Pfam_Domains' size='lg' title='Pfam Domains'> |A2M| |A2M comp| |A2M recep| |NTR| |ANATO| |Thiol-ester cl| |A2M N| |A2M N 2| </modal> <modal id='GO_terms' size='lg' title='GO Terms'> |other organism cell| |complement binding| |positive regulation of apoptotic cell clearance| |opsonization| |regulation of apoptotic cell clearance| |detection of molecule of bacterial origin| |detection of external biotic stimulus| |detection of biotic stimulus| |endopeptidase inhibitor activity| |positive regulation of phagocytosis| |regulation of phagocytosis| |regulation of complement activation| |regulation of humoral immune response| |blood microparticle| |complement activation, classical pathway| |humoral immune response mediated by circulating immunoglobulin| |carbohydrate binding| |complement activation| |immunoglobulin mediated immune response| |B cell mediated immunity| |negative regulation of endopeptidase activity| |negative regulation of peptidase activity| |lymphocyte mediated immunity| |synapse| |adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains| |axon| |response to molecule of bacterial origin| |phagocytosis| |humoral immune response| |negative regulation of proteolysis| |regulation of endopeptidase activity| |dendrite| |regulation of peptidase activity| |negative regulation of hydrolase activity| |regulation of immune effector process| |inflammatory response| |detection of chemical stimulus| |cell junction| |regulation of vesicle-mediated transport| |adaptive immune response| |activation of immune response| |response to bacterium| |detection of stimulus| |regulation of proteolysis| |leukocyte mediated immunity| |innate immune response| |negative regulation of catalytic activity| |positive regulation of immune response| |defense response to other organism| |positive regulation of transport| |negative regulation of cellular protein metabolic process| |immune effector process| |negative regulation of protein metabolic process| |negative regulation of molecular function| |positive regulation of immune system process| |regulation of immune response| |regulation of hydrolase activity| |response to other organism| |response to external biotic stimulus| |response to biotic stimulus| |defense response| |extracellular space| |regulation of immune system process| |regulation of transport| |immune response| |extracellular region| |vesicle-mediated transport| </modal> \\ === CRISPR Data === <button type='default' size='small' modal='Compound_Hit'>Compound Hit</button> <button type='primary' size='small' modal='Most_Correlated_Genes'>Most Correlated Genes in Chemogenomics</button> <button type='primary' size='small' modal='Essential_Avana'>Tissues where Essential in the Avana Dataset (DepMap 20Q1)</button> <modal id='Compound_Hit' size='lg' title='Compound Hit'> No hits were found. </modal> <modal id='Most_Correlated_Genes' size='lg' title='Most Correlated Genes in Chemogenomics'> ^Gene^Correlation^ |[[:human genes:h:hgc6.3|HGC6.3]]|0.401| </modal> <modal id='Essential_Avana' size='lg' title='Tissues where Essential in the Avana Dataset (DepMap 20Q1)'> Global Fraction of Cell Lines Where Essential: N/A ^Tissue^Fraction Of Cell Lines Where Essential^ </modal> == Essentiality in NALM6 == * **<color #00a2e8>Essentiality Rank</color>**: 14970 * **<color #00a2e8>Expression level (log2 read counts)</color>**: 0.52 <button type='primary' size='small' modal='Dist_expr'>Expression Distribution</button> <modal id='Dist_expr' size='lg' title='C4B Expression in NALM6 Cells: 0.52'> {{:chemogenomics:nalm6 dist.png?nolink |}} </modal> Last modified: 2025/12/10 20:19by 127.0.0.1