The selective and inducible activation of endogenous PI 3-kinase in PC12 cells results in efficient NGF-mediated survival but defective neurite outgrowth (Q57903651)

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English	The selective and inducible activation of endogenous PI 3-kinase in PC12 cells results in efficient NGF-mediated survival but defective neurite outgrowth	article

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The selective and inducible activation of endogenous PI 3-kinase in PC12 cells results in efficient NGF-mediated survival but defective neurite outgrowth (English)

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Julian Downward

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Julian Downward

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author name string

Margaret Ashcroft

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Robert M Stephens

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Bengt Hallberg

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David R Kaplan

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publication date

August 1999

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18

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32

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4586-4597

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Wortmannin inactivates phosphoinositide 3-kinase by covalent modification of Lys-802, a residue involved in the phosphate transfer reaction

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Microinjection of the ras oncogene protein into PC12 cells induces morphological differentiation

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Phosphotyrosine residues in the nerve-growth-factor receptor (Trk-A). Their role in the activation of inositolphospholipid metabolism and protein kinase cascades in phaeochromocytoma (PC12) cells

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Phosphatidylinositol 3-kinase and Akt protein kinase are necessary and sufficient for the survival of nerve growth factor-dependent sympathetic neurons.

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A target for Pl(3) kinase

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Regulation of neuronal survival by the serine-threonine protein kinase Akt

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A phosphatidylinositol-3 kinase binds to platelet-derived growth factor receptors through a specific receptor sequence containing phosphotyrosine

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Analysis of mutant platelet-derived growth factor receptors expressed in PC12 cells identifies signals governing sodium channel induction during neuronal differentiation

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Nerve growth factor prevents the death and stimulates the neuronal differentiation of clonal PC12 pheochromocytoma cells in serum-free medium

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Grb2-associated binder-1 mediates phosphatidylinositol 3-kinase activation and the promotion of cell survival by nerve growth factor

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TrkA Tyrosine Residues Involved in NGF‐induced Neurite Outgrowth of PC12 Cells

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Expression of a constitutively active phosphatidylinositol 3-kinase induces process formation in rat PC12 cells. Use of Cre/loxP recombination system

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Transfection with trk restores "slow" NGF binding, efficient NGF uptake, and multiple NGF responses to NGF-nonresponsive PC12 cell mutants

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10.1038/SJ.ONC.1202814

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