Entity Details

Primary name DAF_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionP08174
EntryNameDAF_HUMAN
FullNameComplement decay-accelerating factor
TaxID9606
Evidenceevidence at protein level
Length381
SequenceStatuscomplete
DateCreated1988-08-01
DateModified2021-06-02

Ontological Relatives

GenesCD55

GO terms

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GOName
GO:0000139 Golgi membrane
GO:0001618 virus receptor activity
GO:0002726 positive regulation of T cell cytokine production
GO:0005576 extracellular region
GO:0005886 plasma membrane
GO:0006888 endoplasmic reticulum to Golgi vesicle-mediated transport
GO:0006958 complement activation, classical pathway
GO:0007204 positive regulation of cytosolic calcium ion concentration
GO:0008289 lipid binding
GO:0009986 cell surface
GO:0030133 transport vesicle
GO:0030449 regulation of complement activation
GO:0030667 secretory granule membrane
GO:0031225 anchored component of membrane
GO:0031664 regulation of lipopolysaccharide-mediated signaling pathway
GO:0033116 endoplasmic reticulum-Golgi intermediate compartment membrane
GO:0043312 neutrophil degranulation
GO:0045087 innate immune response
GO:0045121 membrane raft
GO:0045730 respiratory burst
GO:0045916 negative regulation of complement activation
GO:0070062 extracellular exosome
GO:0101003 ficolin-1-rich granule membrane
GO:1903659 regulation of complement-dependent cytotoxicity
GO:2000516 positive regulation of CD4-positive, alpha-beta T cell activation
GO:2000563 positive regulation of CD4-positive, alpha-beta T cell proliferation

Subcellular Location

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Subcellular Location
Cell membrane
Secreted

Domains

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DomainNameCategoryType
IPR000436 Sushi/SCR/CCP domainDomainDomain
IPR035976 Sushi/SCR/CCP superfamilyFamilyHomologous superfamily

Diseases

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Disease IDSourceNameDescription
226300 OMIMComplement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy (CHAPLE)An autosomal recessive disease characterized by abdominal pain and diarrhea, primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease. Patients' T lymphocytes show increased complement activation causing surface deposition of complement and the generation of soluble C5a. The disease is caused by variants affecting the gene represented in this entry. CHAPLE is caused by biallelic mutations in the CD55 gene.

Drugs

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DrugNameSourceType
DB00446 ChloramphenicolDrugbanksmall molecule