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RHOJ encodes one of the many small GTP-binding proteins in the Rho family shown to be associated with focal adhesions in endothelial cells (PMID: 21148427, 22103495). Additionally we are shipping Ras Homolog Gene Family, Member J Antibodies (57) and many more products for this protein.
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Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ signaling halts the growth of BRAF (show BRAF Proteins) mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF (show BRAF Proteins) mutant human melanomas express high levels of RhoJ, these studies nominate the RhoJ-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (show BRAF Proteins) mutant human tumor
These results identify amino acids within the N terminus and a loop region distal to the nucleotide binding pocket of TCL capable of allosterically regulating nucleotide exchange and thus influence membrane association of the protein.
FMNL3 interacts with Cdc42 and RhoJ, two Rho family GTPases known to be required for lumen formation. FMNL3 and RhoJ are concentrated at the early apical surface, or AMIS, and regulate the formation of radiating actin cables from this site.
RhoJ-knockout mice showed reduced tumour growth and diminished tumour vessel density, identifying a role for RhoJ in mediating tumour angiogenesis. Studies give insight into the molecular function of RhoJ in regulating cell motility.
These results identify RhoJ blockade as a selective and effective therapeutic strategy for targeting tumor vasculature with minimal side effects.
These observations identify RHOJ as a melanoma linchpin determinant that regulates both actin cytoskeletal dynamics and chemoresistance by activating PAK1 (show PAK1 Proteins).
Arhgef15 acts as an endothelial cell-specific GEF to mediate VEGF-induced Cdc42 activation and potentiate RhoJ inactivation, thereby promoting actin polymerization and cell motility.
we identified RhoJ and its effector PAK1 (show PAK1 Proteins), as key modulators of melanoma cell sensitivity to DNA damage
Our study supports a novel role for the Rho family member RhoJ in ednothelial cell morphogenesis and in particular in lumen formation
RhoJ is endothelial-expressed in vivo, activated by vascular endothelial growth factor, localizes to focal adhesions, regulates endothelial cell migration and tube formation, and modulates actomyosin contractility and focal adhesion numbers.
The results strongly suggest that TCL/TC10betaL regulates adipocyte differentiation by controlling mitotic clonal expansion and this regulatory effect is closely linked to C/EBPbeta (show CEBPB Proteins) and C/EBPdelta (show CEBPD Proteins) expression.
TCL/TC10betaL has a crucial role in the early stage of adipocyte differentiation, is probably linked to the PPARgamma (show PPARG Proteins) pathway, and up-regulates epression of genes associated with adipogenesis.
Insulin (show INS Proteins) induces phosphatidylinositol 3-phosphate formation through TC10 (show RHOQ Proteins) activation.
This gene encodes one of the many small GTP-binding proteins in the Rho family shown to be associated with focal adhesions in endothelial cells (PMID: 21148427, 22103495). The encoded protein is activated by vascular endothelial growth factor and may regulate angiogenesis.
ras homolog gene family, member J
, TC10-like Rho GTPase
, rho-related GTP-binding protein RhoJ
, RAS-like, family 7, member B
, ras-like protein family member 7B
, tc10-like GTP-binding protein
, tc10-like GTP-binding protein TCL