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NGF activates JNK. 10 / 39
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"NGF induces SAPK and JNK activation within 1 day of treatment XREF_BIBR, whereas NK-4 (~ 6.3 microM) did not induce SAPK and JNK activation for up to 3 days (data not shown)."
"Similarly, sustained activation of JNK by NGF was observed."
"Similarly, sustained activation of JNK by NGF was observed (Figure  xref c)."
"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)."
"Consistent with a pro apoptotic function of p75 NTR and JNK in SCs, pro and mature isoforms of NGF activate JNK and induce apoptosis in SCs."
"Since NGF deprivation alone results in SCG neuron death and JNK activation, the additive effect of proNT-3 on JNK activation, if any, might be masked in such an experimental paradigm."
"Recent findings suggested that JNK can be stimulated by NGF via presynaptic p75 NTR receptor XREF_BIBR."
"This discrepancy can be explained by the fact that, in addition to ERK5, NGF deprivation inhibits ERK1/2 and PKB activity, and stimulates the JNK signaling pathway."
"We show that NGF treatment, which induces extensive neurite branching and cell soma enlargement in the N1 cells, stimulates a biphasic activation of JNK."
"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."
NGF activates JNK. 1 / 1
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"Fibroblast growth factor (Yoshida et al., 1997), insulin-like growth factor-1 (Rhoads et al., 1997), epidermal growth factor (Heinrich and Kraiem, 1997), endothelin-1 (Salamonsen et al., 1997), oncostatin M (Isozaki et al., 1997), nerve growth factor (Courtney et al., 1997), tumor necrosis factor alpha (Yoshida et al., 1997), and interleukin-1alpha and beta (Lu et al., 1997) activate Jun kinase and increase c-jun gene expression."