Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release (original) (raw)

Nerve Growth Factor-dependent Survival of CESS B Cell Line Is Mediated by Increased Expression and Decreased Degradation of MAPK Phosphatase 1

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Nerve Growth Factor Is an Autocrine Survival Factor for Memory B Lymphocytes

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Nerve growth factor pretreatment attenuates oxygen and glucose deprivation-induced c-Jun amino-terminal kinase 1 and stress-activated kinases p38α and p38β activation and confers neuroprotection in the pheochromocytoma PC12 model

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The Cyclic Adenosine Monophosphate-dependent Protein Kinase (PKA) Is Required for the Sustained Activation of Mitogen-activated Kinases and Gene Expression by Nerve Growth Factor

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NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation

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Pro-apoptotic Bim Induction in Response to Nerve Growth Factor Deprivation Requires Simultaneous Activation of Three Different Death Signaling Pathways

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Bcl-2 Phosphorylation by p38 MAPK IDENTIFICATION OF TARGET SITES AND BIOLOGIC CONSEQUENCES

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Nerve growth factor-mediated inhibition of apoptosis post-caspase activation is due to removal of active caspase-3 in a lysosome-dependent manner

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