PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism - Test2 - elhamkhani - TriplyDB

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

http://www.wikidata.org/entity/Q24536252

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Essential role of PDK1 in regulating cell size and development in mice PPARδ activation acts cooperatively with 3-phosphoinositide-dependent protein kinase-1 to enhance mammary tumorigenesis High resolution crystal structure of the human PDK1 catalytic domain defines the regulatory phosphopeptide docking site.Essential role of PDK1 in regulating endothelial cell migration Protein kinase Czeta and glycogen synthase kinase-3beta control neuronal polarity in developing rodent enteric neurons, whereas SMAD specific E3 ubiquitin protein ligase 1 promotes neurite growth but does not influence polarity Akt-PDK1 complex mediates epidermal growth factor-induced membrane protrusion through Ral activation.PDK1-mediated activation of MRCKα regulates directional cell migration and lamellipodia retraction.RalA activation at nascent lamellipodia of epidermal growth factor-stimulated Cos7 cells and migrating Madin-Darby canine kidney cells.Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras Host-pathogen systems biology: logical modelling of hepatocyte growth factor and Helicobacter pylori induced c-Met signal transduction Elevated RalA activity in the hippocampus of PI3Kγ knock-out mice lacking NMDAR-dependent long-term depression The adaptor protein Grb14 regulates the localization of 3-phosphoinositide-dependent kinase-1.Ral small GTPase signaling and oncogenesis: More than just 15minutes of fame A Ral guanine exchange factor-Ral pathway is conserved in Drosophila melanogaster and sheds new light on the connectivity of the Ral, Ras, and Rap pathways Inhibiting the cyclin-dependent kinase CDK5 blocks pancreatic cancer formation and progression through the suppression of Ras-Ral signaling Activated α2-macroglobulin binding to cell surface GRP78 induces T-loop phosphorylation of Akt1 by PDK1 in association with Raptor.The anti-inflammatory TIPE2 is an inhibitor of the oncogenic Ras.An activating mutation in sos-1 identifies its Dbl domain as a critical inhibitor of the epidermal growth factor receptor pathway during Caenorhabditis elegans vulval development.3-phosphoinositide-dependent kinase 1 controls breast tumor growth in a kinase-dependent but Akt-independent manner.RILP suppresses invasion of breast cancer cells by modulating the activity of RalA through interaction with RalGDS Ral GTPases regulate neurite branching through GAP-43 and the exocyst complex.Negative regulation of the RalGAP complex by 14-3-3.Inhibition of ERK promotes collagen gel compaction and fibrillogenesis to amplify the osteogenesis of human mesenchymal stem cells in three-dimensional collagen I culture Principles of K-Ras effector organization and the role of oncogenic K-Ras in cancer initiation through G1 cell cycle deregulation.The secret life of kinases: functions beyond catalysis RalGDS couples growth factor signaling to Akt activation.Single-molecule fluorescence imaging of RalGDS on cell surfaces during signal transduction from Ras to Ral.Integrin signaling switches the cytoskeletal and exocytic machinery that drives neuritogenesis.Pathway- and expression level-dependent effects of oncogenic N-Ras: p27(Kip1) mislocalization by the Ral-GEF pathway and Erk-mediated interference with Smad signaling Ral signaling pathway in health and cancer.

P2860

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P2860

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

http://www.wikidata.org/entity/Q24536252

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2002 nî lūn-bûn

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2002 թուականի Մարտին հրատարակուած գիտական յօդուած

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2002 թվականի մարտին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

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PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@en

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

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PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@ast

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@en

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@nl

prefLabel

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@ast

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@en

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@nl

P1433

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P1433

The EMBO Journal

P1476

PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism

@en

P2093

Brian Schaffhausen

http://www.w3.org/2001/XMLSchema#string

Gabriel Rusanescu

http://www.w3.org/2001/XMLSchema#string

Larry A Feig

http://www.w3.org/2001/XMLSchema#string

Weimin Hou

http://www.w3.org/2001/XMLSchema#string

Xuejun Tian

http://www.w3.org/2001/XMLSchema#string

P2860

The small GTPase RalA targets filamin to induce filopodia

Direct control of the Forkhead transcription factor AFX by protein kinase B

Identification and characterization of a new family of guanine nucleotide exchange factors for the ras-related GTPase Ral

Identification and characterization of a novel protein interacting with Ral-binding protein 1, a putative effector protein of Ral

The structural basis of the activation of Ras by Sos

Bridging Ral GTPase to Rho pathways. RLIP76, a Ral effector with CDC42/Rac GTPase-activating protein activity

Small G protein Ral and its downstream molecules regulate endocytosis of EGF and insulin receptors

Ral-GTPase influences the regulation of the readily releasable pool of synaptic vesicles.

Ral-GTPases mediate a distinct downstream signaling pathway from Ras that facilitates cellular transformation

Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation

P304

1327-1338

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scholarly article

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10.1093/EMBOJ/21.6.1327

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P433

6

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P478

21

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2002-03-01T00:00:00Z

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11474330

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P698

11889038

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P932

125928

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