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NGF activates JNK. 49 / 52
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"Withdrawal of NGF causes apoptosis in these cells and induces activation of both p38 and JNK pathways and inhibits activation of the MAPK pathway [3]."

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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)."

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"Similarly, sustained activation of JNK by NGF was observed."

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"Recent findings suggested that JNK can be stimulated by NGF via presynaptic p75 NTR receptor XREF_BIBR."

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"NGF activated NF-κB and JNK in WT Schwann cells, whereas their activation was significantly reduced in the absence of TRAF6."

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"We trained the PKN using gene expression of selected differentially regulated genes under NGF stimulus and inhibition of either MEK, JNK, or PI3K."

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"NGF enhances TrkA dependent cellular processes in a JNK dependent manner."

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"NGF enhances TrkA dependent cancer cell death in a JNK dependent manner."

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"NGF deprivation causes an increase in JNK activity in these neurones, and suppression of this activity rescues the neurones [34]."

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"It has been well established that NGF activates the ERK, JNK and p38 mitogen activated protein kinases pathways through the activation of RAS XREF_BIBR, XREF_BIBR."

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"Similarly, NGF activation of JNK was not apparent in Schwann cells from mice lacking traf6."

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"We observed that NGF withdrawal results in induction of not only JNK signaling, as previously described, but also the ISR, as shown by activation of PERK and ATF4 (XREF_FIG), and an elevation in the phosphorylated form of eIF2alpha."

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"By contrast, NGF activates JNK and NF-κB in the RN22 schwannoma cell line and induces apoptosis in cells with suppressed NF-κB activity ( xref )."

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"The results of our model of live GBS MAPKs activation and effects on macrophage apoptosis are in agreement with those of Xia et al. [30] in which NGF withdrawal in PC-12 cells causes apoptosis and act[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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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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"By contrast, NGF activates JNK and NF-kappaB in the RN22 schwannoma cell line and induces apoptosis in cells with suppressed NF-kappaB activity."

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"In cells, the signaling molecules PLC-gamma, PI3K, mTOR, p38 MAPK, JNK and Akt are activated by NGF."

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"Inhibitors of PKC-iota activity and PI3K had no effect on NGF-induced MAPK or p38 activation but reduced NGF-stimulated c-Jun N-terminal kinase activity."

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"NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events."

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"Although NGF can activate the protein kinase C, p38 MAPK and c-Jun N-terminal kinase (JNK) pathways, these pathways are not involved in its effect on the CGRP promoter."

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"These data suggest that the withdrawal of NGF induces JNK based stress response pathways in DRG neurons and that this activation is DLK dependent."

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"Overall the present study may unveil a new mechanism by which, in the absence of AbetaPP, NGF treatment may preferentially direct p75-neurotrophin-dependent JNK activation toward regeneration and plasticity in functionally relevant brain circuits."

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"Similarly, NGF did not activate JNK in TRAF6-KO Schwann cells."

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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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"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."

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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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"These observations suggested that NGF induced the activation of JNK/c-Jun, resulting in the expression of NF-L via promoter activity in the CRE/ATF site [87]."

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"Suppression of endogenous NGF level with neutralizing NGF antibody significantly blocked the increased activity of Akt, JNK, and ERK1/2 in the inflamed bladder during cystitis."

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"However, L5 had no effect on overall phosphotyrosine status after NGF stimulation or on NGF-induced ERK, JNK, and p38 activation."

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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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"Altogether, these findings suggest that caspase activation plays a role in 5-lipoxygenase inhibition induced apoptosis in prostate cancer cells, but not in JNK activation.In neuronal cells, withdrawal[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Inhibitors of PKC-iota activity and PI3K had no effect on NGF induced MAPK or p38 activation but reduced NGF stimulated c-Jun N-terminal kinase activity."

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"The overexpression of POSH promotes neuronal apoptosis and the silencing of POSH with antisense oligonucleotides and siRNA suppresses JNK activity and neuronal apoptosis induced by NGF withdrawal [44][MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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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)."

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"We therefore investigated whether JNK or p38 was activated by NGF withdrawal in sympathetic neurons."

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"Similarly, sustained activation of JNK by NGF was observed (Figure  xref c)."

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"Actions of NGF increasing MAPK family signaling (SAPK and ERK1/2) and preventing DRG apoptosis XREF_BIBR, are presumably impaired in the dorsal spinal nerves of Raldh2 -/- mutants."

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"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."

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"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."

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"We show that NGF treatment, which induces extensive neurite branching and cell soma enlargement in the N1 cells, stimulates a biphasic activation of JNK."

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"Similarly, both NGF and Sema6A stimulated a modest JNK MAPK activation, beginning within 5 min and lasting for at least 60 min."

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"Consistent with our finding with enhanced activation of Rac1 and Cdc42, AS transfectants exhibited a potentiation of JNK kinase activation induced by NGF stimulation in PC12 cells (XREF_FIG)."

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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."

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"Although NGF-induced JNK activation was obscure, a kinase-inactive form of MKK7 inhibited NGF-induced NF-L-luciferase activity."

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"Similarly, NGF activation of JNK was not apparent in Schwann cells from mice lacking traf6."

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"Related to this, the relationship between NGF expression and JNK activation should be further investigated: on one hand, several reports claim that NGF, whose levels are increased in inflamed tissues, induces the activation of JNK in DRGs [24]."

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"To better understand the mechanism of JNK activation induced by NGF withdrawal, we next examined p-JNK localization by immunostaining to determine the subcellular distribution of p-JNK protein."

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"Thus, a crucial role for NGF modulation of JNK (p54) activation may be in APP phosphorylation, metabolism and the related cognition in mammals."

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"The researchers looked for signaling pathways altered in DLK-null neurons and found that, in the absence of DLK, NGF withdrawal failed to stimulate JNK, a MAP kinase that promotes neuronal degeneration."
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