ARHGDIB
Rho GDP-dissociation inhibitor 2
Also known as: GDIA2, GDID4, GDIR2_HUMAN, Ly-GDI, RAP1GN1, RhoGDI2
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P52566
- Gene
- ARHGDIB
- Ensembl
- ENSG00000111348
- Chromosome
- 12
- Canonical length
- 201 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Cytosol
OverviewNCBI Gene
Members of the Rho (or ARH) protein family (see MIM 165390) and other Ras-related small GTP-binding proteins (see MIM 179520) are involved in diverse cellular events, including cell signaling, proliferation, cytoskeletal organization, and secretion. The GTP-binding proteins are active only in the GTP-bound state. At least 3 classes of proteins tightly regulate cycling between the GTP-bound and GDP-bound states: GTPase-activating proteins (GAPs), guanine nucleotide-releasing factors (GRFs), and GDP-dissociation inhibitors (GDIs). The GDIs, including ARHGDIB, decrease the rate of GDP dissociation from Ras-like GTPases (summary by Scherle et al., 1993 [PubMed 8356058]).[supplied by OMIM, Dec 2010]
Canonical amino-acid sequenceUniProt
201 residues, UniProt reviewed canonical sequence.
>P52566|ARHGDIB
1 MTEKAPEPHV EEDDDDELDS KLNYKPPPQK SLKELQEMDK DDESLIKYKK TLLGDGPVVT
61 DPKAPNVVVT RLTLVCESAP GPITMDLTGD LEALKKETIV LKEGSEYRVK IHFKVNRDIV
121 SGLKYVQHTY RTGVKVDKAT FMVGSYGPRP EEYEFLTPVE EAPKGMLARG TYHNKSFFTD
181 DDKQDHLSWE WNLSIKKEWT ELocalizationUniProt · AlphaFold · HPA
Whether an antibody against ARHGDIB 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)
- 0.34
- Highest tissue expression
- 1,491 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 1,491 nTPM
- thymus: 1,002 nTPM
- tonsil: 971 nTPM
- lymph node: 846 nTPM
- spleen: 608 nTPM
- appendix: 491 nTPM
Single-cell type
- platelets: 1,664 nCPM
- megakaryocytes: 1,335 nCPM
- neutrophils: 1,322 nCPM
- hofbauer cells: 1,168 nCPM
- extravillous trophoblasts: 1,010 nCPM
- neutrophil progenitors: 912 nCPM
Immune cell
- total PBMC: 9,860 nTPM
- eosinophil: 6,481 nTPM
- basophil: 5,911 nTPM
- T-reg: 5,605 nTPM
- neutrophil: 5,446 nTPM
- non-classical monocyte: 3,822 nTPM
Brain region
- white matter: 92 nTPM
- medulla oblongata: 69 nTPM
- thalamus: 64 nTPM
- pons: 61 nTPM
- spinal cord: 54 nTPM
- choroid plexus: 45 nTPM
ReferencesPubMed · IEDB
Publications for ARHGDIB 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
5 publications
- Antibodies against ARHGDIB are associated with long-term kidney graft loss.
2019 · Am J Transplant · RCR 2.7 · 50 citations - Antibodies Against ARHGDIB and ARHGDIB Gene Expression Associate With Kidney Allograft Outcome.
2020 · Transplantation · RCR 2.1 · 35 citations - Proteomics-based identification of human acute leukemia antigens that induce humoral immune response.
2005 · Mol Cell Proteomics · RCR 1.1 · 46 citations - ARHGDIB and AT1R autoantibodies are differentially related to the development and presence of chronic antibody-mediated rejection and fibrosis in kidney allografts.
2021 · Hum Immunol · RCR 0.8 · 11 citations - A Review on the Function and Regulation of ARHGDIB/RhoGDI2 Expression Including the Hypothetical Role of ARHGDIB/RhoGDI2 Autoantibodies in Kidney Transplantation.
2020 · Transplant Direct · RCR 0.7 · 12 citations
Reference: T cellIEDB
1 publication
- CD8+ T Cells Specific to Apoptosis-Associated Antigens Predict the Response to Tumor Necrosis Factor Inhibitor Therapy in Rheumatoid Arthritis.
2015 · PLoS One · RCR 0.6 · 18 citations
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. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). 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)
- 1.3
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.04
- DepMap mean gene effect
- 0.04
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cellular response to redox state
- negative regulation of trophoblast cell migration
- regulation of Rho protein signal transduction
- Rho protein signal transduction
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of ARHGDIB 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 ARHGDIB as an antibody target. Whether an autoantibody or antibody against ARHGDIB could matter depends on whether native ARHGDIB is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ARHGDIB 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 ARHGDIB as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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