Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
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RhoC regulates the proliferation of gastric cancer cells through interaction with IQGAP1MicroRNA-21 exhibits antiangiogenic function by targeting RhoB expression in endothelial cellsRac and Rho GTPases in cancer cell motility controlDLC-1 suppresses non-small cell lung cancer growth and invasion by RhoGAP-dependent and independent mechanismsProtein kinase D regulates RhoA activity via rhotekin phosphorylation.ATR/Chk1/Smurf1 pathway determines cell fate after DNA damage by controlling RhoB abundanceA Salmonella typhimurium-translocated glycerophospholipid:cholesterol acyltransferase promotes virulence by binding to the RhoA protein switch regionsMultiple sequence elements facilitate Chp Rho GTPase subcellular location, membrane association, and transforming activityGalphaq directly activates p63RhoGEF and Trio via a conserved extension of the Dbl homology-associated pleckstrin homology domainMetabolic actions of Rho-kinase in periphery and brainSmall G proteins in the cardiovascular system: physiological and pathological aspectsRhoC interacts with integrin α5β1 and enhances its trafficking in migrating pancreatic carcinoma cellsRb suppresses collective invasion, circulation and metastasis of breast cancer cells in CD44-dependent mannerA RhoC biosensor reveals differences in the activation kinetics of RhoA and RhoC in migrating cellsDifferential RhoA dynamics in migratory and stationary cells measured by FRET and automated image analysisFormin-like 2 drives amoeboid invasive cell motility downstream of RhoCROCK1 and ROCK2 are required for non-small cell lung cancer anchorage-independent growth and invasionDLC1 activation requires lipid interaction through a polybasic region preceding the RhoGAP domainDLC1 tumor suppressor gene inhibits migration and invasion of multiple myeloma cells through RhoA GTPase pathwayMyxoma virus oncolytic efficiency can be enhanced through chemical or genetic disruption of the actin cytoskeletonExtracting Diffusive States of Rho GTPase in Live Cells: Towards In Vivo BiochemistryKalirin promotes neointimal hyperplasia by activating Rac in smooth muscle cellsRhoC Promotes Metastasis via Activation of the Pyk2 Pathway in Prostate CancerRhoC Is an Unexpected Target of RhoGDI2 in Prevention of Lung Colonization of Bladder Cancer.Integrin α6β4 cooperates with LPA signaling to stimulate Rac through AKAP-Lbc-mediated RhoA activation.Activation of Rac by Asef2 promotes myosin II-dependent contractility to inhibit cell migration on type I collagenARF1 regulates the Rho/MLC pathway to control EGF-dependent breast cancer cell invasionMouse macrophages completely lacking Rho subfamily GTPases (RhoA, RhoB, and RhoC) have severe lamellipodial retraction defects, but robust chemotactic navigation and altered motility.ALK1 signalling analysis identifies angiogenesis related genes and reveals disparity between TGF-beta and constitutively active receptor induced gene expressionRhoD Inhibits RhoC-ROCK-Dependent Cell Contraction via PAK6.Clostridium difficile toxin B differentially affects GPCR-stimulated Ca2+ responses in macrophages: independent roles for Rho and PLA2.Downregulation of the Rho GTPase signaling pathway is involved in the microRNA-138-mediated inhibition of cell migration and invasion in tongue squamous cell carcinoma.Keeping in touch with contact inhibition of locomotion.8-Oxoguanine DNA glycosylase-1-mediated DNA repair is associated with Rho GTPase activation and α-smooth muscle actin polymerization.Urotensin II alters vascular reactivity in animals subjected to volume overload.ROCK is involved in vasculogenic mimicry formation in hepatocellular carcinoma cell lineRhoA and RhoC are both required for the ROCK II-dependent promotion of centrosome duplication.Rho/ROCK signaling in motility and metastasis of gastric cancerRhoB differentially controls Akt function in tumor cells and stromal endothelial cells during breast tumorigenesisRhoC impacts the metastatic potential and abundance of breast cancer stem cells.
P2860
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P2860
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
description
2004 nî lūn-bûn
@nan
2004 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
name
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@ast
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@en
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@nl
type
label
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@ast
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@en
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@nl
prefLabel
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@ast
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@en
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@nl
P3181
P1476
Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility
@en
P3181
P356
10.1016/J.YEXCR.2004.08.012
P407
P577
2004-11-15T00:00:00Z