Seroatlas · Human Serome Atlas

IFNA10

Interferon alpha-10

Also known as: IFN-alphaC, IFN10_HUMAN

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
P01566
Gene
IFNA10
Ensembl
ENSG00000186803
Chromosome
9
Canonical length
189 aa
Protein class
Predicted secreted proteins
Secretome location
Secreted to blood

OverviewNCBI Gene

This gene encodes a protein that belongs to the type I interferon family of proteins, and is located in a cluster of alpha interferon genes on chromosome 9. Interferons are small regulatory molecules that function in cell signaling in response to viruses and other pathogens or tumor cells. This gene is intronless and the encoded protein is secreted. [provided by RefSeq, Aug 2013]

Canonical amino-acid sequenceUniProt

189 residues, UniProt reviewed canonical sequence.

>P01566|IFNA10
     1  MALSFSLLMA VLVLSYKSIC SLGCDLPQTH SLGNRRALIL LGQMGRISPF SCLKDRHDFR
    61  IPQEEFDGNQ FQKAQAISVL HEMIQQTFNL FSTEDSSAAW EQSLLEKFST ELYQQLNDLE
   121  ACVIQEVGVE ETPLMNEDSI LAVRKYFQRI TLYLIERKYS PCAWEVVRAE IMRSLSFSTN
   181  LQKRLRRKD

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against IFNA10 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
Secreted
Secreted
Yes
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.3
Highest tissue expression
0 nTPM

Expression across tissuesHPA

Tissue

  • adipose tissue: 0 nTPM
  • adrenal gland: 0 nTPM
  • amygdala: 0 nTPM
  • appendix: 0 nTPM
  • basal ganglia: 0 nTPM
  • blood vessel: 0 nTPM

Single-cell type

  • adipocytes: 0 nCPM
  • adrenal cortex cells: 0 nCPM
  • adrenal medulla cells: 0 nCPM
  • alveolar cells type 1: 0 nCPM
  • alveolar cells type 2: 0 nCPM
  • astrocytes: 0 nCPM

Immune cell

  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • gdT-cell: 0 nTPM
  • intermediate monocyte: 0 nTPM
  • MAIT T-cell: 0 nTPM

Brain region

  • cerebral cortex: 0.2 nTPM
  • white matter: 0.2 nTPM
  • hippocampal formation: 0.1 nTPM
  • medulla oblongata: 0.1 nTPM
  • pons: 0.1 nTPM
  • thalamus: 0.1 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 missense Z
-2.03
DepMap mean gene effect
0.12
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 2% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads IFNA10 as an antibody target. Whether an autoantibody or antibody against IFNA10 could matter depends on whether native IFNA10 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

IFNA10 is annotated as secreted, so native IFNA10 circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.

Annotation status

The present source text does not explicitly label IFNA10 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/IFNA10. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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