Nerve growth factor-induced PKB/Akt activity is sustained by phosphoinositide 3-kinase dependent and independent signals in sympathetic neurons. (Q48144694)

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English	Nerve growth factor-induced PKB/Akt activity is sustained by phosphoinositide 3-kinase dependent and independent signals in sympathetic neurons.	scientific article

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scholarly article

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

Nerve growth factor-induced PKB/Akt activity is sustained by phosphoinositide 3-kinase dependent and independent signals in sympathetic neurons. (English)

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

3

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B A Hemmings

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

author name string

K Virdee

1

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

L Xue

2

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

C Goemans

4

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

R Heumann

5

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

A M Tolkovsky

6

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

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1 August 1999

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

837

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

1-2

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

127-142

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Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

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Mechanism of activation of protein kinase B by insulin and IGF-1

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Role of translocation in the activation and function of protein kinase B

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Activation and phosphorylation of a pleckstrin homology domain containing protein kinase (RAC-PK/PKB) promoted by serum and protein phosphatase inhibitors

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Wortmannin is a potent phosphatidylinositol 3-kinase inhibitor: the role of phosphatidylinositol 3,4,5-trisphosphate in neutrophil responses.

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In sympathetic but not sensory neurones, phosphoinositide-3 kinase is important for NGF-dependent survival and the retrograde transport of 125I-betaNGF.

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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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Direct inhibition of the signaling functions of the mammalian target of rapamycin by the phosphoinositide 3-kinase inhibitors, wortmannin and LY294002.

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Nerve Growth Factor is Required for Induction of c-Fos Immunoreactivity by Serum, Depolarization, Cyclic AMP or Trauma in Cultured Rat Sympathetic Neurons

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Mitogen-activated protein kinase-independent pathways mediate the effects of nerve growth factor and cAMP on neuronal survival

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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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Insulin-like growth factor and potassium depolarization maintain neuronal survival by distinct pathways: possible involvement of PI 3-kinase in IGF-1 signaling.

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

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Characterization of apoptosis in cultured rat sympathetic neurons after nerve growth factor withdrawal

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The trkA receptor mediates growth cone turning toward a localized source of nerve growth factor

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4E-BP1, a repressor of mRNA translation, is phosphorylated and inactivated by the Akt(PKB) signaling pathway

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Identification of four novel human phosphoinositide 3-kinases defines a multi-isoform subfamily

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Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB.

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

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Antiapoptotic signalling by the insulin-like growth factor I receptor, phosphatidylinositol 3-kinase, and Akt.

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Wortmannin blocks goldfish retinal phosphatidylinositol 3-kinase and neurite outgrowth.

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PKB/Akt: connecting phosphoinositide 3-kinase to cell survival and beyond

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Inhibition of phosphatidylinositol 3-kinase activity blocks depolarization- and insulin-like growth factor I-mediated survival of cerebellar granule cells.

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Rho, rac, and cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodia

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Neutralizing anti-p21ras Fabs suppress rat sympathetic neuron survival induced by NGF, LIF, CNTF and cAMP

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Insulin-like Growth Factor 1 Inhibits Apoptosis Using the Phosphatidylinositol 3′-Kinase and Mitogen-activated Protein Kinase Pathways

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Evidence that a kinase distinct from protein kinase C and phosphatidylinositol 3-kinase mediates ligation-dependent serine/threonine phosphorylation of the T-lymphocyte co-stimulatory molecule CD28.

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Activated phosphatidylinositol 3-kinase and Akt kinase promote survival of superior cervical neurons

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A single gene encodes two isoforms of the p70 S6 kinase: activation upon mitogenic stimulation

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Signalling events regulating the retrograde axonal transport of 125I-beta nerve growth factor in vivo.

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Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras

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cAMP stimulates protein kinase B in a Wortmannin-insensitive manner

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Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling

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Activation of p44 and p42 MAP kinases is not essential for the survival of rat sympathetic neurons

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Inhibition of p42 and p44 mitogen-activated protein kinase activity by PD98059 does not suppress nerve growth factor-induced survival of sympathetic neurones

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Calcium promotes cell survival through CaM-K kinase activation of the protein-kinase-B pathway

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Identifiers

10.1016/S0006-8993(99)01643-1

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

1 reference

Europe PubMed Central

9 February 2018

http://europepmc.org/abstract/MED/10433995

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