The v-Crk oncogene enhances cell survival and induces activation of protein kinase B/Akt. (Q30168223)

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6 November 2019

title

The v-Crk oncogene enhances cell survival and induces activation of protein kinase B/Akt (English)

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6 November 2019

2

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6 November 2019

Henri H Versteeg

3

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6 November 2019

author name string

Stam JC

1

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6 November 2019

Verkleij AJ

4

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6 November 2019

van Bergen en Henegouwen PM

5

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6 November 2019

language of work or name

English

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publication date

25 April 2001

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Journal of Biological Chemistry

6 November 2019

number of pages

8

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based on heuristic

inferred from page(s)

published in

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6 November 2019

volume

276

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6 November 2019

issue

27

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6 November 2019

page(s)

25176-25183

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A novel viral oncogene with structural similarity to phospholipase C

6 November 2019

cites work

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Physiological signals and oncogenesis mediated through Crk family adapter proteins

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Possible v-Crk-induced transformation through activation of Src kinases.

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Identification and characterization of a high-affinity interaction between v-Crk and tyrosine-phosphorylated paxillin in CT10-transformed fibroblasts

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Casting light on focal adhesions.

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Integrin signaling and cell growth control

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Integrins, adhesion and apoptosis.

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The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene

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Role of the adapter protein CRKL in signal transduction of normal hematopoietic and BCR/ABL-transformed cells

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BCAR1, a human homologue of the adapter protein p130Cas, and antiestrogen resistance in breast cancer cells

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Bcar1/p130Cas protein and primary breast cancer: prognosis and response to tamoxifen treatment.

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Activation of Rac1 by a Crk SH3-binding protein, DOCK180

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Activation of Rho-dependent cell spreading and focal adhesion biogenesis by the v-Crk adaptor protein

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v-Crk, an effector of the nerve growth factor signaling pathway, delays apoptotic cell death in neurotrophin-deprived PC12 cells

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Crk is required for apoptosis in Xenopus egg extracts

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Integrin-mediated activation of focal adhesion kinase is required for signaling to Jun NH2-terminal kinase and progression through the G1 phase of the cell cycle

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Expression of the v-crk oncogene product in PC12 cells results in rapid differentiation by both nerve growth factor- and epidermal growth factor-dependent pathways

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Insulin-like growth factor-I stimulates tyrosine phosphorylation of endogenous c-Crk

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Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays

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The PI 3-kinase/Akt signaling pathway delivers an anti-apoptotic signal.

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Rap1 mediates sustained MAP kinase activation induced by nerve growth factor

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Activation of the Drosophila C3G leads to cell fate changes and overproliferation during development, mediated by the RAS-MAPK pathway and RAP1.

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Oncogenic K-Ras and basic fibroblast growth factor prevent Fas-mediated apoptosis in fibroblasts through activation of mitogen-activated protein kinase

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The activation of p38 and apoptosis by the inhibition of Erk is antagonized by the phosphoinositide 3-kinase/Akt pathway

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The regulation and activities of the multifunctional serine/threonine kinase Akt/PKB.

21 January 2018

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The Ras/phosphatidylinositol 3-kinase and Ras/ERK pathways function as independent survival modules each of which inhibits a distinct apoptotic signaling pathway in sympathetic neurons.

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v-Crk activates the phosphoinositide 3-kinase/AKT pathway in transformation

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Extracellular-regulated kinase activation and CAS/Crk coupling regulate cell migration and suppress apoptosis during invasion of the extracellular matrix

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