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LncRNA TDRG1 overexpression induced tumor development and RhoC expression.
This article summarizes recent progress on the mechanisms that control the expression of the three members of the Rho-like subfamily (RhoA, RhoB, and RhoC) at the level of gene transcription as well as their post-transcriptional regulation by microRNAs. [review]
a SDF-1/CXCR4-RhoA and RhoC-ROS-cytoskeleton pathway that regulates Jurkat cell migration in response to SDF-1.
Studied the involvement in epithelial ovarian cancer (EOC) of lncRNA ABHD11-AS1 in and the regulation of EOC by RhoC.
Out of multiple members of this family, RhoA and RhoC are important factors. RhoA is supposed to increase tumor proliferation when overexpressed while RhoC is responsible for tumor initiation.
Spatiotemporal analysis of RhoA/RhoB/RhoC activation in primary human endothelial cells has been uncovered.
YMO1 suppresses tumor invasion and metastasis by inhibiting RhoC activity.
this studies show the ability of miR-10b to activate the expression of c-Jun through RhoC and NF1, which represents a novel pathway for promoting migration and invasion of human cancer cells
swapping residue 188 identity effectively flips the membrane binding profile of wild-type RhoA and RhoC through positive arginine contribution rather than negative phosphoserine regulation
HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.
E2F transcription factor 1 (E2F1) downregulated micrRNA miR-519d directly and miR-519d downregulated Ras homolog gene family member C (RhoC) directly.
These results reveal a previously unidentified pathway downstream of RHO that regulates the polarity of migrating cells through Golgi reorientation in a FAM65A-, CCM3- and MST3- and MST4-dependent manner.
During the process of epithelial-mesenchymal transition in A549 cells induced by TGF-beta1, upregulated RhoC protein and RhoC activity were detected, which was associated with the enhanced invasive capability of the cells in vitro.
RhoC downregulation may inhibit the proliferation, drug resistance, invasion and migration of ovarian cancer stem cells.
Downregulation of RHOC inhibited cholangiocellular carcinoma cells invasion and migration partially via inhibition of matrix metalloproteinase 2, 3 and 9 expression. RHOC also modulated the expression of several epithelial-mesenchymal transition (EMT)-associated proteins
RT-PCR and Western blot assays demonstrated that miR-372 transfection reduced the expression of RhoC.
Significant associations between ROCK1, ROCK2, RhoA and RhoC gene polymorphisms and systemic sclerosis were demonstrated.
study has identified several new proteins like RHOC, DLG5, UGDH, TMOD3 in addition to known chemoresistance associated proteins in non-small cell lung carcinoma.
the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in Inflammatory Breast Cancer cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role in cytoskeletal rearrangement.
The knockdown of RhoC protein decreased the proliferation rate of the parental and the IE1-expressing glioblastoma cells.
what was seen for RhoC, mDia1 silencing through RNAi inhibited phagosome formation. Additionally, the coexpression of mDia1 with constitutively active mutant RhoC-G14V or expression of active mutant mDia1-DeltaN3 drastically inhibited the uptake of IgG-Es. These data suggest that RhoC modulates phagosome formation be modifying actin cytoskeletal remodeling via mDia1
RhoC co-localizes with Fam65b in stereocilia and regulates Fam65b oligomerization what is critical for hair cell function.
Inhibition of ovarian epithelial carcinoma tumorigenesis and progression by miR106b proceeds through the RhoC pathway.
RHOC and RAB38 are dispensable for osteoclast function.
A p27(kip1)-binding protein, p27RF-Rho, promotes cancer metastasis via activation of RhoA and RhoC.
We found that both RhoA and RhoC, but not RhoB, were required for initiation of centrosome duplication, and overactivation of RhoA, as well as RhoC, but not RhoB, promoted centrosome duplication and centrosome amplification.
RhoC has a role in metastasis of lung cancer in mice
loss of RhoC does not affect tumor development but decreases tumor cell motility and metastatic cell survival leading to a drastic inhibition of metastasis
RhoC promotes melanoma progression via separate mechanisms that regulate the PI3K/Akt pathway and the ROCK signaling pathway.
This gene encodes a member of the Rho family of small GTPases, which cycle between inactive GDP-bound and active GTP-bound states and function as molecular switches in signal transduction cascades. Rho proteins promote reorganization of the actin cytoskeleton and regulate cell shape, attachment, and motility. The protein encoded by this gene is prenylated at its C-terminus, and localizes to the cytoplasm and plasma membrane. It is thought to be important in cell locomotion. Overexpression of this gene is associated with tumor cell proliferation and metastasis. Multiple alternatively spliced variants, encoding the same protein, have been identified.
ras homolog gene family, member C
, rho-related GTP-binding protein RhoC
, RAS-related homolog 9
, oncogene RHO H9
, rho cDNA clone 9
, rhoC GTPase
, small GTP binding protein RhoC
, aplysia ras-related homolog 9 (RhoC)
, ras homolog 9 (RhoC)
, silica-induced gene 61 protein
, GTP-binding protein
, GTPase cRhoC