RHOB, a member of the Rho GTPase superfamily, functions as a critical molecular switch that regulates diverse cellular processes, including cytoskeletal reorganization, cell migration, proliferation, and apoptosis, by cycling between an active GTP-bound state and an inactive GDP-bound state. As a small G protein, RHOB exerts its effects by interacting with specific downstream effectors such as Rho-associated protein kinase (ROCK) and mDia, thereby modulating actin dynamics to maintain cell morphology and facilitate motility. A distinctive feature of RHOB is its C-terminal prenylation, a post-translational modification that anchors the protein to the plasma membrane, ensuring proper spatial localization for signal transduction. Within the Rho subfamily, RHOB shares the conserved GTP-binding domain and involvement in Rho-ROCK and PAK signaling pathways with homologs like RHOA and RAC1, yet it exhibits unique functional specificity; whereas RHOA is primarily associated with stress fiber formation, RHOB is more closely linked to endosomal transport and cellular stress responses. Biologically, RHOB often acts as a tumor suppressor, as its overexpression can induce cell cycle arrest or apoptosis, whereas its downregulation, frequently observed in cancers such as lung and breast carcinoma, correlates with enhanced cell migration, increased invasiveness, and loss of growth control. Beyond oncology, RHOB plays significant roles in cardiovascular health by regulating vascular smooth muscle contraction and in the nervous system by influencing synaptic plasticity, while its dysregulation can also impact inflammatory responses through pathways such as NF-κB activation, highlighting its complex context-dependent roles in both physiological homeostasis and pathological disease states.
Subcellular localization of RHOB (and its protein):
Gene Ontology (GO) terms for RHOB:
| Interacting Gene | Interaction | Source/Score |
| Name |
|---|
| Axon guidance |
| Developmental Biology |
| G alpha (12/13) signalling events |
| GPCR downstream signaling |
| GPVI-mediated activation cascade |
| Hemostasis |
| Platelet activation, signaling and aggregation |
| Rho GTPase cycle |
| RHO GTPase Effectors |
| RHO GTPases activate CIT |
| RHO GTPases Activate Formins |
| RHO GTPases activate PKNs |
| RHO GTPases Activate Rhotekin and Rhophilins |
| RHO GTPases Activate ROCKs |
| Sema4D in semaphorin signaling |
| Sema4D induced cell migration and growth-cone collapse |
| Semaphorin interactions |
| Signaling by GPCR |
| Signaling by Rho GTPases |
| Disease | Score | NofPmids | NofSnps | Source |
| Systemic Scleroderma | 0.120542884 | 2 | 0 | BeFree_CTD_human |
| melanoma | 0.08 | 1 | 0 | RGD |
| Sarcoma, Avian | 0.08 | 1 | 0 | RGD |
| Degenerative polyarthritis | 0.010182764 | 3 | 0 | GAD_LHGDN |
| Lung Neoplasms | 0.0054487 | 2 | 0 | LHGDN |
| Glioblastoma | 0.00272435 | 1 | 0 | LHGDN |
| Thyroid Neoplasm | 0.00272435 | 1 | 0 | LHGDN |
| Prostatic Neoplasms | 0.00272435 | 1 | 0 | LHGDN |
| Osteoarthritis, Knee | 0.002638474 | 1 | 0 | BeFree_GAD |
| Sclerosis | 0.002367032 | 1 | 1 | GAD |
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