نتایج جستجو برای: ژن rhob

تعداد نتایج: 16213  

Journal: :Cancer research 2006
Nicolas Skuli Sylvie Monferran Caroline Delmas Isabelle Lajoie-Mazenc Gilles Favre Christine Toulas Elizabeth Cohen-Jonathan-Moyal

Hypoxia is a crucial factor in tumor aggressiveness and resistance to treatment, particularly in glioma. Our previous results have shown that inhibiting the small GTPase RhoB increased oxygenation of U87 human glioblastoma xenografts, in part, by regulating angiogenesis. We investigated here whether RhoB might also control a signaling pathway that would permit glioma cells to adapt to hypoxia. ...

2012
Francisco M. Vega Audrey Colomba Nicolas Reymond Mairian Thomas Anne J. Ridley

The Rho GTPase RhoB has been shown to affect cell migration, but how it does this is not clear. Here we show that cells depleted of RhoB by RNAi are rounded and have defects in Rac-mediated spreading and lamellipodium extension, although they have active membrane ruffling around the periphery. Depletion of the exchange factor GEF-H1 induces a similar phenotype. RhoB-depleted cells migrate faste...

Journal: :Journal of cell science 2012
Daniela Alfano Pia Ragno M Patrizia Stoppelli Anne J Ridley

Urokinase-type plasminogen activator (uPA) and its receptor, uPAR, play important roles in promoting cancer cell adhesion, migration and invasion. Rho GTPases are key coordinators of these processes; the Rho GTPase Rac1 has previously been implicated in uPA- and/or uPAR-induced migratory or morphological cell responses. We used RNAi to deplete 12 different Rho GTPases to screen for effects on u...

2007
Minzhou Huang James B. DuHadaway George C. Prendergast Lisa D. Laury-Kleintop

Objective—RhoB is a small GTPase localized at the plasma membrane and endosomes that participates in the regulation of endocytic trafficking of the epidermal growth factor (EGF) receptor and the nonreceptor kinases Src and Akt. This study was performed to determine whether RhoB plays a critical role in trafficking and signaling by the platelet-derived growth factor receptor(PDGFR) in vascular s...

Journal: :Cancer research 1999
W Du G C Prendergast

Farnesyltransferase inhibitors (FTIs) are in clinical trials, but their mechanism of action is not fully understood. We have shown that FTI treatment rapidly elevates the level of geranylgeranylated RhoB in cells and that this event is sufficient to inhibit cell cycle transit and reverse malignant transformation without affecting normal cells. However, because these observations were made in ro...

2013
Damien Gerald Irit Adini Sharon Shechter Carole Perruzzi Joseph Varnau Benjamin Hopkins Shiva Kazerounian Peter Kurschat Stephanie Blachon Santosh Khedkar Mandrita Bagchi David Sherris George C. Prendergast Michael Klagsbrun Heidi Stuhlmann Alan C. Rigby Janice A. Nagy Laura E. Benjamin

Mechanisms governing the distinct temporal dynamics that characterize post-natal angiogenesis and lymphangiogenesis elicited by cutaneous wounds and inflammation remain unclear. RhoB, a stress-induced small GTPase, modulates cellular responses to growth factors, genotoxic stress and neoplastic transformation. Here we show, using RhoB null mice, that loss of RhoB decreases pathological angiogene...

Journal: :The Journal of pharmacology and experimental therapeutics 2004
Hiroshi Ishida Xieping Zhang Kelly Erickson Prabhati Ray

Botulinum toxin type A (BoNT/A) produced by Clostridium botulinum inhibits Ca2+-dependent acetylcholine (ACh) release (neuroexocytosis) at peripheral neuromuscular junctions, sometimes causing neuromuscular paralysis. This inhibitory effect is attributed to its metalloprotease activity to cleave the 25-kDa synaptosomal-associated protein, which is essential for the exocytotic machinery. However...

Journal: :Molecular cancer research : MCR 2010
Erin C Connolly Koenraad Van Doorslaer Leslie E Rogler Charles E Rogler

Metastasis is a multistep process that involves the deregulation of oncogenes and tumor suppressors beyond changes required for primary tumor formation. RHOB is known to have tumor suppressor activity, and its knockdown is associated with more aggressive tumors as well as changes in cell shape, migration, and adhesion. This study shows that oncogenic microRNA, miR-21, represses RHOB expression ...

2015
Audrey Delmas Julia Cherier Magdalena Pohorecka Claire Medale-Giamarchi Nicolas Meyer Anne Casanova Olivier Sordet Laurence Lamant Ariel Savina Anne Pradines Gilles Favre

The response of BRAF-mutant melanoma patients to BRAF inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. Here, we show that, in BRAF-mutant melanoma cells, inhibition of BRAF or its target MEK induces RHOB expression by a mechanism that depends on the transcription factor c-Jun...

Journal: :Cancer research 2013
Shiva Kazerounian Damien Gerald Minzhou Huang Y Rebecca Chin Durga Udayakumar Ningning Zheng Rebekah K O'Donnell Carole Perruzzi Lee Mangiante Jacob Pourat Thuy L Phung Arturo Bravo-Nuevo Sharon Shechter Stephanie McNamara James B Duhadaway Olivier N Kocher Lawrence F Brown Alex Toker George C Prendergast Laura E Benjamin

Tumors are composed of cancer cells but also a larger number of diverse stromal cells in the tumor microenvironment. Stromal cells provide essential supports to tumor pathophysiology but the distinct characteristics of their signaling networks are not usually considered in developing drugs to target tumors. This oversight potentially confounds proof-of-concept studies and increases drug develop...

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