Seroatlas · Human Serome Atlas

RARA

Retinoic acid receptor alpha

Also known as: NR1B1, RAR, RAR-alpha, RARA_HUMAN, RARalpha

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

Protein identityUniProt · HPA

UniProt accession
P10276
Gene
RARA
Ensembl
ENSG00000131759
Chromosome
17
Canonical length
462 aa
Protein class
Cancer-related genes, Disease related genes, FDA approved drug targets, Human disease related genes, Nuclear receptors, Plasma proteins, Predicted intracellular proteins, Transcription factors
Subcellular location
Nucleoplasm,Nucleoli,Actin filaments,Cytosol

OverviewNCBI Gene

This gene represents a nuclear retinoic acid receptor. The encoded protein, retinoic acid receptor alpha, regulates transcription in a ligand-dependent manner. This gene has been implicated in regulation of development, differentiation, apoptosis, granulopoeisis, and transcription of clock genes. Translocations between this locus and several other loci have been associated with acute promyelocytic leukemia. Alternatively spliced transcript variants have been found for this locus.[provided by RefSeq, Sep 2010]

Canonical amino-acid sequenceUniProt

462 residues, UniProt reviewed canonical sequence.

>P10276|RARA
     1  MASNSSSCPT PGGGHLNGYP VPPYAFFFPP MLGGLSPPGA LTTLQHQLPV SGYSTPSPAT
    61  IETQSSSSEE IVPSPPSPPP LPRIYKPCFV CQDKSSGYHY GVSACEGCKG FFRRSIQKNM
   121  VYTCHRDKNC IINKVTRNRC QYCRLQKCFE VGMSKESVRN DRNKKKKEVP KPECSESYTL
   181  TPEVGELIEK VRKAHQETFP ALCQLGKYTT NNSSEQRVSL DIDLWDKFSE LSTKCIIKTV
   241  EFAKQLPGFT TLTIADQITL LKAACLDILI LRICTRYTPE QDTMTFSDGL TLNRTQMHNA
   301  GFGPLTDLVF AFANQLLPLE MDDAETGLLS AICLICGDRQ DLEQPDRVDM LQEPLLEALK
   361  VYVRKRRPSR PHMFPKMLMK ITDLRSISAK GAERVITLKM EIPGSMPPLI QEMLENSEGL
   421  DTLSGQPGGG GRDGGGLAPP PGSCSPSLSP SSNRSSPATH SP

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against RARA 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
Intracellular
Secreted
No
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.41
Highest tissue expression
56 nTPM

Expression across tissuesHPA

Tissue

  • bone marrow: 56 nTPM
  • skeletal muscle: 54 nTPM
  • blood vessel: 53 nTPM
  • lung: 52 nTPM
  • adipose tissue: 42 nTPM
  • gallbladder: 39 nTPM

Single-cell type

  • late spermatids: 304 nCPM
  • neutrophils: 281 nCPM
  • early spermatids: 170 nCPM
  • monocytes: 113 nCPM
  • mast cells: 95 nCPM
  • cdc: 93 nCPM

Immune cell

  • neutrophil: 53 nTPM
  • eosinophil: 35 nTPM
  • basophil: 26 nTPM
  • non-classical monocyte: 20 nTPM
  • intermediate monocyte: 15 nTPM
  • myeloid DC: 12 nTPM

Brain region

  • cerebral cortex: 47 nTPM
  • cerebellum: 26 nTPM
  • hippocampal formation: 26 nTPM
  • hypothalamus: 23 nTPM
  • medulla oblongata: 23 nTPM
  • thalamus: 22 nTPM

ReferencesPubMed · IEDB

Publications for RARA from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.

Reference: AutoantibodyPubMed

1 publication

Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.

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)
0.33
gnomAD pLI
0.96
gnomAD missense Z
3.08
DepMap mean gene effect
-0.06
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% 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

InteractionsUniProt · HPA

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

RARA is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.

Annotation status

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

Canonical record: https://seroatlas.com/gene/RARA. 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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