IndraLab
Statements
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"Moreover, NGF induced c-Jun N-terminal kinase (JNK) activation to promote cell death and neurite outgrowth in PC12 cells, and NGF-induced JNK phosphorylation was significantly suppressed by specific inhibitors of the ERK1/2, p38 MAPK, JAK3, Src and G i proteins, but not by the PI3K inhibitor wortmannin, xref suggesting that various signaling pathways, except for PI3K-Akt signaling, are involved in NGF-induced cell death and neuronal differentiation."
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"However, the upregulation of TrkA tyrosine 490 phosphorylatin by NGF was significantly downregulated during the long-term inactivation of JNK caused by SP600125 treatment for 12h, but not by wortmannin, suggesting a role of JNK in the maintenance of TrkA tyrosine 490 phosphorylation enhanced by NGF (XREF_FIG)."
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"Moreover, NGF induced c-Jun N-terminal kinase (JNK) activation to promote cell death and neurite outgrowth in PC12 cells, and NGF induced JNK phosphorylation was significantly suppressed by specific inhibitors of the ERK1/2, p38 MAPK, JAK3, Src and G i proteins, but not by the PI3K inhibitor wortmannin, 4 suggesting that various signaling pathways, except for PI3K-Akt signaling, are involved in NGF induced cell death and neuronal differentiation."
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"We did not determine whether the low affinity p75 neurotrophin receptor for NGF might also be a target of NK-4, but this appears unlikely because selective activation of p75 NTR by NGF stimulates JNK activity and apoptotic cell death XREF_BIBR, in contrast to the inability of NK-4 to activate JNK and apoptosis."
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"For example, survival of differentiated rat PC-12 pheochromocytoma cells in culture is dependent upon the presence of nerve growth factor (NGF) and removal of NGF from the medium causes an increase in the activities of p38 MAPK and JNK which is necessary and sufficient to induce apoptosis XREF_BIBR."