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Protein / target

Transforming protein RhoA

Encoded byRHOAP61586Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
2
Research papers

Protein at a glance

Biological role

Protein kinase binding

Strongest disease association

Burkitt Lymphoma

Via encoding gene RHOA · Somatic mutation evidence · score 0.53

Research activity

Emerging research

2 papers · latest 2025

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state.

View complete UniProt function annotation

Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. Mainly associated with cytoskeleton organization, in active state binds to a variety of effector proteins to regulate cellular responses such as cytoskeletal dynamics, cell migration and cell cycle (PubMed:23871831). Regulates a signal transduction pathway linking plasma membrane receptors to the assembly of focal adhesions and actin stress fibers (PubMed:31570889, PubMed:8910519, PubMed:9121475). Involved in a microtubule-dependent signal that is required for the myosin contractile ring formation during cell cycle cytokinesis (PubMed:12900402, PubMed:16236794). Plays an essential role in cleavage furrow formation. Required for the apical junction formation of keratinocyte cell-cell adhesion (PubMed:20974804, PubMed:23940119). Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly (PubMed:19934221). The MEMO1-RHOA-DIAPH1 signaling pathway plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex. It controls the localization of APC and CLASP2 to the cell membrane, via the regulation of GSK3B activity. In turn, membrane-bound APC allows the localization of the MACF1 to the cell membrane, which is required for microtubule capture and stabilization (PubMed:20937854). Involved in the reorientation of endothelial cells and their actin stress fibers in response to cellular mechantransduction-mediated activation by ARHGEF40 (By similarity). Regulates KCNA2 potassium channel activity by reducing its location at the cell surface in response to CHRM1 activation; promotes KCNA2 endocytosis (PubMed:19403695, PubMed:9635436). Acts as an allosteric activator of guanine nucleotide exchange factor ECT2 by binding in its activated GTP-bound form to the PH domain of ECT2 which stimulates the release of PH inhibition and promotes the binding of substrate RHOA to the ECT2 catalytic center (PubMed:31888991). May be an activator of PLCE1 (PubMed:16103226). In neurons, involved in the inhibition of the initial spine growth. Upon activation by CaMKII, modulates dendritic spine structural plasticity by relaying CaMKII transient activation to synapse-specific, long-term signaling (By similarity). Acts as a regulator of platelet alpha-granule release during activation and aggregation of platelets (By similarity). When activated by DAAM1 may signal centrosome maturation and chromosomal segregation during cell division. May also be involved in contractile ring formation during cytokinesis

Subcellular location

Cell membraneCytoplasm, cytoskeletonCleavage furrowCytoplasm, cell cortexMidbodyCell projection, lamellipodiumCell projection, dendriteNucleusCytoplasm
Domains and Gene Ontology detail (81)

Gene Ontology

  • Capical junction complex
  • Ccell cortex
  • Ccell junction
  • Ccell periphery
  • Ccleavage furrow
  • Ccytoplasmic side of plasma membrane
  • Ccytoskeleton
  • Ccytosol
  • Cdendritic spine
  • Cendoplasmic reticulum membrane
  • Cendosome
  • Cextracellular exosome

193 aa · 22 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Synaptic signallingUniProt · GOCell migrationUniProt · GOReceptor tyrosine kinase signallingUniProtLipid & lipoprotein metabolismGOImmune signallingUniProt · GOCell adhesionUniProt · GO
View supporting evidence

Synaptic signalling

  • ·Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. M…
  • ·glutamatergic synapse
  • ·postsynapse
  • ·regulation of modification of postsynaptic actin cytoskeleton

Cell migration

  • ·Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. M…
  • ·cell migration
  • ·endothelial cell migration
  • ·negative chemotaxis

Receptor tyrosine kinase signalling

  • ·Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. M…

Lipid & lipoprotein metabolism

  • ·apolipoprotein A-I-mediated signaling pathway

Immune signalling

  • ·Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. M…
  • ·alpha-beta T cell lineage commitment
  • ·cellular response to cytokine stimulus
  • ·positive regulation of alpha-beta T cell differentiation

Cell adhesion

  • ·Small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. M…
  • ·cell junction
  • ·cell junction assembly

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene RHOA

Gene-level evidence surfaced through the gene RHOAthat encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Urinary Bladder Neoplasms
0.50Moderately supported

Somatic mutation evidence dominant · Open Targets 0.47

Burkitt Lymphoma
0.49Limited support

Somatic mutation evidence dominant · Open Targets 0.53

Gastric adenocarcinoma
0.45Limited support

Somatic mutation evidence dominant · Open Targets 0.51

Gastric carcinoma
0.42Limited support

Somatic mutation evidence dominant · Open Targets 0.38

peripheral T-cell lymphoma, not otherwise specified
0.41Limited support

Somatic mutation evidence dominant · Open Targets 0.37

View evidence synthesis (5)
Urinary Bladder NeoplasmsModerately supported
0.50
agreement 0.340.67
Somatic mutation96%Literature4%

Open Targets aggregate 0.47 · 2 independent evidence families

Burkitt LymphomaLimited support
0.49
agreement 0.330.66
Somatic mutation84%Literature16%

Open Targets aggregate 0.53 · 2 independent evidence families

Gastric adenocarcinomaLimited support
0.45
agreement 0.280.61
Somatic mutation94%Literature6%

Open Targets aggregate 0.51 · 2 independent evidence families

Gastric carcinomaLimited support
0.42
agreement 0.260.58
Somatic mutation90%Literature11%

Open Targets aggregate 0.38 · 2 independent evidence families

peripheral T-cell lymphoma, not otherwise specifiedLimited support
0.41
agreement 0.250.57
Somatic mutation95%Literature5%

Open Targets aggregate 0.37 · 2 independent evidence families

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Burkitt Lymphoma0.53
Gastric adenocarcinoma0.51
Urinary Bladder Neoplasms0.47
Gastric carcinoma0.38
peripheral T-cell lymphoma, not otherwise specified0.37

Tractability

Small moleculesEmerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

AntibodiesEmerging

Feasibility evidence (go cc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (9)
SM · Structure with LigandSM · High-Quality LigandAB · GO CC high confAB · UniProt loc med confAB · Human Protein Atlas locPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2025

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Recent

Europe PMC papers linked directly to this protein.