ATRAID
All-trans retinoic acid-induced differentiation factor
Also known as: APR3, ARAID_HUMAN, C2orf28, HSPC013, p18
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q6UW56
- Gene
- ATRAID
- Ensembl
- ENSG00000138085
- Chromosome
- 2
- Canonical length
- 229 aa
- Protein class
- Predicted intracellular proteins, Predicted membrane proteins
OverviewNCBI Gene
This gene is thought to be involved in apoptosis, and may also be involved in hematopoietic development and differentiation. The use of alternative splice sites and promotors result in multiple transcript variants encoding different isoforms.[provided by RefSeq, Dec 2009]
Canonical amino-acid sequenceUniProt
229 residues, UniProt reviewed canonical sequence.
>Q6UW56|ATRAID
1 MAPHDPGSLT TLVPWAAALL LALGVERALA LPEICTQCPG SVQNLSKVAF YCKTTRELML
61 HARCCLNQKG TILGLDLQNC SLEDPGPNFH QAHTTVIIDL QANPLKGDLA NTFRGFTQLQ
121 TLILPQHVNC PGGINAWNTI TSYIDNQICQ GQKNLCNNTG DPEMCPENGS CVPDGPGLLQ
181 CVCADGFHGY KCMRQGSFSL LMFFGILGAT TLSVSILLWA TQRRKAKTSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against ATRAID can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 1
- Mean surface accessibility (rSASA)
- 0.38
- Highest tissue expression
- 324 nTPM
Expression across tissuesHPA
Tissue
- epididymis: 324 nTPM
- choroid plexus: 160 nTPM
- heart muscle: 145 nTPM
- ovary: 143 nTPM
- skeletal muscle: 140 nTPM
- tongue: 130 nTPM
Single-cell type
- epididymal principal cells: 618 nCPM
- late primary spermatocytes: 464 nCPM
- extravillous trophoblasts: 440 nCPM
- decidual stromal cells: 413 nCPM
- cytotrophoblasts: 313 nCPM
- late spermatids: 298 nCPM
Immune cell
- total PBMC: 444 nTPM
- plasmacytoid DC: 295 nTPM
- memory B-cell: 280 nTPM
- T-reg: 279 nTPM
- naive B-cell: 273 nTPM
- myeloid DC: 252 nTPM
Brain region
- choroid plexus: 69 nTPM
- white matter: 52 nTPM
- medulla oblongata: 51 nTPM
- cerebellum: 46 nTPM
- hypothalamus: 44 nTPM
- spinal cord: 43 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.12
- gnomAD pLI
- 0
- gnomAD missense Z
- -1.02
- DepMap mean gene effect
- -0.06
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cell differentiation
- negative regulation of osteoblast proliferation
- negative regulation of protein catabolic process
- positive regulation of bone mineralization
- positive regulation of osteoblast differentiation
- regulation of gene expression
- xenobiotic transmembrane transport
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- EGF-like domain
- All-trans retinoic acid-induced differentiation factor
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of ATRAID in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads ATRAID as an antibody target. Whether an autoantibody or antibody against ATRAID could matter depends on whether native ATRAID is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ATRAID is annotated at the cell surface, where native ATRAID is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label ATRAID as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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