Seroatlas · Human Serome Atlas

ARHGDIG

Rho GDP-dissociation inhibitor 3

Also known as: GDIR3_HUMAN, RHOGDI-3

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

Protein identityUniProt · HPA

UniProt accession
Q99819
Gene
ARHGDIG
Ensembl
ENSG00000242173
Chromosome
16
Canonical length
225 aa
Protein class
Predicted intracellular proteins
Subcellular location
Plasma membrane,Cytosol

OverviewNCBI Gene

The GDP-dissociation inhibitors (GDIs) play a primary role in modulating the activation of GTPases by inhibiting the exchange of GDP for GTP. See ARHGDIB (MIM 602843).[supplied by OMIM, Nov 2010]

Canonical amino-acid sequenceUniProt

225 residues, UniProt reviewed canonical sequence.

>Q99819|ARHGDIG
     1  MLGLDACELG AQLLELLRLA LCARVLLADK EGGPPAVDEV LDEAVPEYRA PGRKSLLEIR
    61  QLDPDDRSLA KYKRVLLGPL PPAVDPSLPN VQVTRLTLLS EQAPGPVVMD LTGDLAVLKD
   121  QVFVLKEGVD YRVKISFKVH REIVSGLKCL HHTYRRGLRV DKTVYMVGSY GPSAQEYEFV
   181  TPVEEAPRGA LVRGPYLVVS LFTDDDRTHH LSWEWGLCIC QDWKD

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against ARHGDIG 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)
0.35
Highest tissue expression
246 nTPM

Expression across tissuesHPA

Tissue

  • cerebral cortex: 246 nTPM
  • cerebellum: 202 nTPM
  • amygdala: 189 nTPM
  • hippocampal formation: 142 nTPM
  • hypothalamus: 128 nTPM
  • pancreas: 106 nTPM

Single-cell type

  • other brain neurons: 92 nCPM
  • pancreatic acinar cells: 83 nCPM
  • gastric chief cells: 52 nCPM
  • brain excitatory neurons: 49 nCPM
  • enterocytes: 48 nCPM
  • brain inhibitory neurons: 43 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: 217 nTPM
  • white matter: 179 nTPM
  • basal ganglia: 175 nTPM
  • hypothalamus: 157 nTPM
  • cerebellum: 148 nTPM
  • amygdala: 141 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)
0.37
gnomAD pLI
0.92
gnomAD missense Z
0
DepMap mean gene effect
-0.09
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% 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 ARHGDIG as an antibody target. Whether an autoantibody or antibody against ARHGDIG could matter depends on whether native ARHGDIG is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

ARHGDIG 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 ARHGDIG as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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