(Q53448525)

14 May 2018

title

R-Ras can activate the phosphoinositide 3-kinase but not the MAP kinase arm of the Ras effector pathways. (English)

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14 May 2018

author

Julian Downward

5

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14 May 2018

author name string

Marte BM

1

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14 May 2018

Rodriguez-Viciana P

2

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14 May 2018

Wennström S

3

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14 May 2018

Warne PH

4

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14 May 2018

language of work or name

English

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publication date

1 January 1997

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14 May 2018

number of pages

8

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inferred from page(s)

published in

Current Biology

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14 May 2018

volume

7

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14 May 2018

issue

1

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14 May 2018

page(s)

63-70

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14 May 2018

Structure of the human and murine R-ras genes, novel genes closely related to ras proto-oncogenes

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Platelet-derived growth factor-dependent activation of phosphatidylinositol 3-kinase is regulated by receptor binding of SH2-domain-containing proteins which influence Ras activity

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The phosphatidylinositol 3-kinase alpha is required for DNA synthesis induced by some, but not all, growth factors

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All ras proteins are polyisoprenylated but only some are palmitoylated

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Rapid induction of heparin-binding epidermal growth factor/diphtheria toxin receptor expression by Raf and Ras oncogenes.

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Requirement for Ras in Raf activation is overcome by targeting Raf to the plasma membrane

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7 January 2021

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Ionizing radiation stimulates a Grb2-mediated association of the stress-activated protein kinase with phosphatidylinositol 3-kinase

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R-Ras promotes apoptosis caused by growth factor deprivation via a Bcl-2 suppressible mechanism.

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A role for phosphatidylinositol 3-kinase in the regulation of beta 1 integrin activity by the CD2 antigen

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PI 3-kinase is a dual specificity enzyme: autoregulation by an intrinsic protein-serine kinase activity.

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7 January 2021

Direct interaction of Ras and the amino-terminal region of Raf-1 in vitro

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7 January 2021

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Identifiers

DOI

1 reference

14 May 2018

1 reference

14 May 2018