RHOJ: Ras Homolog Family Member J

A Rho GTPase Involved in Cell Migration, Angiogenesis, and Cancer Progression

Gene Information Card

Symbol RHOJ
Full Name ras homolog family member J
Gene Type protein-coding
Chromosomal Location 14q23.2
NCBI Gene ID 57381 ncbi.nlm.nih.gov/gene/57381
Ensembl ID ENSG00000100842
UniProt ID Q9H4E5
OMIM ID 607371
HGNC ID 17369
Aliases TC10, ARHJ, FLJ10390, RHOJ1

Description

RHOJ (ras homolog family member J) is a member of the Rho family of small GTPases, closely related to CDC42 and Rac1. It regulates cytoskeletal dynamics, cell migration, and angiogenesis. RHOJ is highly expressed in endothelial cells and certain cancers, where it promotes tumor growth and metastasis. It cycles between an active GTP-bound and inactive GDP-bound state, acting as a molecular switch in signaling pathways.

Disease Associations

Disease category Pathophysiological mechanism Genomic evidence
Cancer (breast, lung, melanoma) RHOJ overexpression enhances cell migration, invasion, and angiogenesis via activation of PAK and JNK pathways. PMID: 23541922, PMID: 28431213
Retinopathy of prematurity RHOJ mediates pathological retinal angiogenesis through endothelial cell sprouting. PMID: 21536856
Wound healing disorders RHOJ deficiency impairs endothelial cell migration and capillary formation. PMID: 21536856

Expression Profile

Tissue Expression
Tissue nTPM level
Brain 8.2 Medium
Heart 5.1 Low
Lung 12.4 Medium
Liver 3.8 Low
Kidney 6.7 Low
Testis 15.9 High
Placenta 20.3 High
Endothelial cells 45.6 High
Cell Line Expression
Cell Line nTPM Notes
HUVEC (endothelial) 62.3 High expression; key for angiogenesis studies
MCF7 (breast cancer) 18.7 Moderate expression; linked to migration
A549 (lung cancer) 22.1 Moderate expression; promotes invasion
HEK293 (embryonic kidney) 8.9 Low baseline expression
Data source:Human Protein Atlas(proteinatlas.org)

Mutations & Variants

Hotspot Mutations
Variant Type Frequency Functional Description
c.172C>T (p.Arg58Cys) Missense <0.1% Potential loss of GTP binding; functional impact unclear
c.389G>A (p.Arg130His) Missense <0.1% Reported in COSMIC; no known functional effect
c.541A>G (p.Ile181Val) Missense <0.1% Rare variant; likely benign
Mutation functional classification

Loss of Function (LOF)

No well-characterized loss-of-function mutations reported in RHOJ. Knockout studies in mice show impaired angiogenesis.

Gain of Function (GOF)

Overexpression or constitutive activation (e.g., Q61L mutant analogous to Rac1) promotes cell migration and invasion in vitro.

Dominant Negative (DN)

Dominant-negative mutants (e.g., T17N) inhibit RHOJ function and reduce endothelial cell sprouting.

Gene Ontology (GO)

• GTP binding • GTPase activity
• protein binding • actin cytoskeleton organization
• cell migration • angiogenesis
• signal transduction • small GTPase mediated signal transduction

Pathways

Rho GTPase cycle
PAK pathway
JNK cascade
VEGF signaling in angiogenesis
Regulation of actin cytoskeleton

Protein Summary

RHOJ encodes a 232-amino acid protein (UniProt Q9H4E5) belonging to the Rho subfamily of small GTPases. It contains conserved G-box motifs for GTP/GDP binding and a C-terminal CAAX box for prenylation and membrane localization. RHOJ localizes to the plasma membrane and endosomes, regulating actin dynamics, cell polarity, and vesicular trafficking. It is essential for endothelial cell migration and tube formation during angiogenesis.

Related Products

Product name Cat.No. Species Gene ID
RHOJ Knockout HEK293 Cell Line EDJ-KQ15063 Human 57381 Details Get a Quote
RHOJ Knockout HeLa Cell Line EDJ-KQ56832 Human 57381 Details Get a Quote
RHOJ Knockout A-549 Cell Line EDJ-KQ65342 Human 57381 Details Get a Quote
RHOJ Knockout HCT 116 Cell Line EDJ-KQ73781 Human 57381 Details Get a Quote
Displaying Records 1 To 4 Of 4 Records
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