ABRA
Actin-binding Rho-activating protein
Also known as: ABRA_HUMAN, STARS
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8N0Z2
- Gene
- ABRA
- Ensembl
- ENSG00000174429
- Chromosome
- 8
- Canonical length
- 381 aa
- Protein class
- Predicted intracellular proteins
OverviewNCBI Gene
Predicted to enable actin binding activity. Predicted to be involved in actin cytoskeleton organization; positive regulation of Rho protein signal transduction; and positive regulation of transcription by RNA polymerase II. Predicted to act upstream of or within positive regulation of DNA-templated transcription and protein import into nucleus. Located in plasma membrane. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
381 residues, UniProt reviewed canonical sequence.
>Q8N0Z2|ABRA
1 MAPGEKESGE GPAKSALRKI RTATLVISLA RGWQQWANEN SIRQAQEPTG WLPGGTQDSP
61 QAPKPITPPT SHQKAQSAPK SPPRLPEGHG DGQSSEKAPE VSHIKKKEVS KTVVSKTYER
121 GGDVSHLSHR YERDAGVLEP GQPENDIDRI LHSHGSPTRR RKCANLVSEL TKGWRVMEQE
181 EPTWRSDSVD TEDSGYGGEA EERPEQDGVQ VAVVRIKRPL PSQVNRFTEK LNCKAQQKYS
241 PVGNLKGRWQ QWADEHIQSQ KLNPFSEEFD YELAMSTRLH KGDEGYGRPK EGTKTAERAK
301 RAEEHIYREM MDMCFIICTM ARHRRDGKIQ VTFGDLFDRY VRISDKVVGI LMRARKHGLV
361 DFEGEMLWQG RDDHVVITLL KLocalizationUniProt · AlphaFold · HPA
Whether an antibody against ABRA 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)
- 0.55
- Highest tissue expression
- 136 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 136 nTPM
- tongue: 60 nTPM
- heart muscle: 30 nTPM
- esophagus: 2.8 nTPM
- blood vessel: 2.1 nTPM
- testis: 2 nTPM
Single-cell type
- late primary spermatocytes: 158 nCPM
- thymic myoid cells: 135 nCPM
- myonuclei: 122 nCPM
- early spermatids: 79 nCPM
- cardiomyocytes: 22 nCPM
- epicardial cells: 16 nCPM
Immune cell
- eosinophil: 0.2 nTPM
- neutrophil: 0.1 nTPM
- non-classical monocyte: 0.1 nTPM
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- gdT-cell: 0 nTPM
Brain region
- cerebellum: 5.9 nTPM
- white matter: 2.7 nTPM
- cerebral cortex: 2.4 nTPM
- pons: 1.6 nTPM
- basal ganglia: 1.5 nTPM
- medulla oblongata: 1.5 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)
- 1.17
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.15
- DepMap mean gene effect
- 0
- DepMap dependency class
- selective
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
- actin cytoskeleton organization
- positive regulation of Rho protein signal transduction
- positive regulation of transcription by RNA polymerase II
- protein import into nucleus
- transcription by RNA polymerase II
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Costars domain
- Costars domain superfamily
- Costars
- Actin-binding Rho-activating protein
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of ABRA 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 ABRA as an antibody target. Whether an autoantibody or antibody against ABRA could matter depends on whether native ABRA is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ABRA 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 ABRA as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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