INT116950
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Finally, a p38 MAPK and a JNK1/2 inhibitor were also used but failed to inhibit SHP mRNA induction by TCA (data not shown). | |||||||||||||||
| |||||||||||||||
|
Selective inhibitors of ERK, p38 MAPK, and JNK suppressed the induction of GRP78, CHOP, and PPAR-beta, attenuated indomethacin-induced cytotoxicity and reduced increased caspase activity. | |||||||||||||||
| |||||||||||||||
|
In addition, significant upregulation of VEGF-C mRNA (Figure 7B) and a decreased level of phosphorylated JNK (Figure 7C) were also induced in H157 cells treated with siRNA-podoplanin. | |||||||||||||||
| |||||||||||||||
|
As a result, significant upregulation of VEGF-C mRNA (Figure 6C) and a decreased level of phosphorylated JNK (Figure 6D) were induced in EBC1-P4 cells treated with siRNA-podoplanin. | |||||||||||||||
| |||||||||||||||
|
This correlated with inhibition of the downstream target of MEKK1 activity, i.e. the SAPK/JNK kinase. | |||||||||||||||
| |||||||||||||||
|
Another set of experiments, developed to test the hypothesis that Akt kinase confers resistance to endocrine therapy through suppression of ASK1/JNK pathway, showed that combining RAD001 with letrozole restored activation of the ASK/JNK pathway and increased the sensitivity of MCF-7 cells with constitutively active Akt to endocrine therapy [48]. | |||||||||||||||
| |||||||||||||||
|
Consistently, pretreatment with JNK inhibitor SP600125 also decreased JNK activation (Fig. 5B, lane 4). | |||||||||||||||
| |||||||||||||||
|
Furthermore, silencing of JNK expression by siJNKs (24), which efficiently reduced the endogenous JNK protein level (Fig. 5E) but not the control siRNA, decreased H2O2-induced AICD level (Fig. 5E, compare lanes 4 and 6 to lane 2). | |||||||||||||||
| |||||||||||||||
|
Therefore, we hypothesized that leflunomide may protect from drugs that induce the mitochondrial permeability transition (mPT) by blocking the JNK signaling pathway. | |||||||||||||||
| |||||||||||||||
|
In the absence of JNK inhibition, the response of normal control fibroblasts after oxidative stress amounted to at most 30% apoptotic nuclei at both 250 µM (Figure 16A) and 500 µM (Figure 14) H2O2 by 10 hr after oxidative stress. | |||||||||||||||
| |||||||||||||||
|
Blockade of JNK did not significantly enhance apoptosis in normal control fibroblasts that were not subjected to oxidative stress, confirming the specificity of the JNK effect for the stress state. | |||||||||||||||
| |||||||||||||||
|
Overexpression of Galphat in COS-7 cells clearly suppressed kappa-opioid receptor-stimulated JNK activity, indicating that the pathway is primarily regulated by Gbetagamma. | |||||||||||||||
| |||||||||||||||
|
Only the dual inhibitor of p38 and JNK and the use of combined siRNA silencing of p38 and cJun abrogated the ability of NO-aspirin to block cell growth. | |||||||||||||||
| |||||||||||||||
|
Furthermore, Trolox attenuated indomethacin-induced increased phosphorylation in ERK, p38 MAPK, JNK, and AKT. | |||||||||||||||
| |||||||||||||||
|
Moreover, the podoplanin-mediated downregulation of the VEGF-C gene via JNK (the podoplanin-JNK-VEGF-C axis) was newly found as one of the possible underlying mechanisms. | |||||||||||||||
| |||||||||||||||
|
A decreased level of phosphorylated JNK but not of total JNK was induced by siRNA-mediated podoplanin knockdown (Figures 6D and 7C), suggesting that podoplanin could induce JNK phosphorylation. | |||||||||||||||
| |||||||||||||||
|
Real-time RT-PCR revealed that the VEGF-C gene expression level in EBC1-Ps treated with sp600125, a JNK inhibitor, was significantly improved, nearly to the level found in EBC1-Vs (Figure 6A), whereas no change in the VEGF-C expression was observed in EBC1-Ps treated with the ROCK inhibitor Y-27632 (data not shown). | |||||||||||||||
| |||||||||||||||
|
The body of our findings is that podoplanin in LSCCs can induce VEGF-C downregulation via the JNK signaling pathway(s), and can impair tumor-associated lymphangiogenesis and lymphogenous metastasis | |||||||||||||||
| |||||||||||||||
|
Using either parental NCTC2544 or vector expressing cells (not shown) we found no equivalent inhibition of JNK activity (Panel A) at any concentration of peptide tested. | |||||||||||||||
| |||||||||||||||
|
have not revealed a specific isoform to date responsible for JNK inhibition (not shown). | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.