Search for P0C0L4

Term identified:
Homo sapiens


6 genes available
ENSG00000244731ENSG00000244731 (HGNC: C4A)
ENSG00000206340ENSG00000206340 (HGNC: C4A)
ENSG00000227746ENSG00000227746 (HGNC: C4A)
OTTHUMG00000031186OTTHUMG00000031186 (HGNC: C4A)
LRG_137LRG_137 (HGNC: C4A)
ENSG00000244207ENSG00000244207 (HGNC: C4A)


C4A expression summary

organism part
  • glioma, amyotrophic lateral sclerosis with C9orf72 repeat expansion, autism, tongue squamous cell carcinoma
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cell type
cell line
  • Not studied or no differential expression found for this gene
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Compound treatment
  • 4-hydroxytamoxifen, DMSO, janus kinase 3 inhibitor, EX00000246, vehicle
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developmental stage
  • Not studied or no differential expression found for this gene
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  • Not studied or no differential expression found for this gene
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  • senescent cell, induced into senescence
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  • Data source: Expression Atlas (12-11-2013).
  • Expression Atlas is a semantically enriched database of publicly available gene and transcript expression data. The data is re-analysed in-house to detect genes showing interesting baseline and differential expression patterns under the conditions of the original experiment.
  • About Expression Atlas


Complement C4-A

  • Non-enzymatic component of 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.
  • Derived from proteolytic degradation of complement C4, C4a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
Subcellular Location
  • Complement component 4A deficiency (C4AD) [MIM:614380]: A rare defect of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus with or without associated glomerulonephritis. Note=The disease is caused by mutations affecting the gene represented in this entry.
  • Systemic lupus erythematosus (SLE) [MIM:152700]: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry. Interindividual copy-number variation (CNV) of complement component C4 and associated polymorphisms result in different susceptibilities to SLE. The risk of SLE susceptibility has been shown to be significantly increased among subjects with only two copies of total C4. A high copy number is a protective factor against SLE.
GO Cellular Component
GO Molecular Function
  • complement component C1q binding; endopeptidase inhibitor activity; serine-type endopeptidase activity
  • View all in UniProt
GO Biological Process
  • complement activation; complement activation, classical pathway; inflammatory response; (3 more)
  • View all in UniProt
Protein Existence
  • Evidence at protein level
  • UniProt Data Source, 2016_09
  • UniProt is a comprehensive, high-quality and freely accessible resource for protein sequences and functional information.
  • View more information in UniProt

Protein Structure

3 protein structures available
4fxgComplement C4 in complex with MASP-2
4fxkHuman complement C4