Disease relevance of 3-(2-PYRIDIN-4-YLETHYL)-1H-INDOLE

• Pretreatment of hepatoma cells with a selective JNK inhibitor, anthra[1,9-cd]pyrazol-6(2H)-one (SP600125), significantly reduced the rate of TRO-induced cell death, whereas 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580), an inhibitor of p38 kinase, had little effect on apoptosis [1].
• Moreover, pretreatment with an inhibitor of p38 kinase acted synergistically with hyperthermia to further sensitize EW36 cells [2].

High impact information on 3-(2-PYRIDIN-4-YLETHYL)-1H-INDOLE

• For all stimuli, 5-LO kinase activation was counteracted by SB203580 (3 microM or less), an inhibitor of p38 kinase [3].
• Treatment of infected cells with SB 239063, a potent pyridinyl imidazole inhibitor of p38 kinase, resulted in up to 100% inhibition of mediator production and partially reduced levels of IL-8 mRNA as determined by quantitative RT-PCR [4].
• LPS-induced IL-8 and TNF-alpha production was inhibited in a similar pattern by pretreatment with either EtOH or SB202190 (1 microM), a specific inhibitor of p38 kinase [5].
• Both meningococcus-induced translocation of nuclear factor-kB (NF-kB) and endothelial cell death were blocked by a known inhibitor of p38 kinase [6].
• CRP-induced p38 kinase activity in HPBMC was blocked by treatment with an inhibitor of p38 kinase, SD-282 [7].

Anatomical context of 3-(2-PYRIDIN-4-YLETHYL)-1H-INDOLE

• In HCT116 cells, pretreatment with PD98059, an inhibitor of ERK1/2, or SB203580, an inhibitor of p38 kinase, had no marked effect on GSNO-induced apoptosis [8].

Gene context of 3-(2-PYRIDIN-4-YLETHYL)-1H-INDOLE

• In conclusion we could remark that SB203580, an inhibitor of p38 kinase pathway, reversed the MDR resistance of L1210/VCR cells [9].
• LY83583 decreased the production of both metalloproteases below basal levels, whereas the inhibitor of p38 kinase, SB202190, suppressed ET-1-stimulated production only [10].
• Moreover, in cells overexpressing HCV core protein, PMA also stimulated p38 kinase more potently than that of the control cells, and an inhibitor of p38 kinase abolished PMA-induced PLD activation in cells overexpressing HCV core protein [11].
• Moreover, cells pretreated with an inhibitor of p38 kinase (SB 208530) inhibited Gal-lectin induced TLR-2 mRNA expression by 40% [12].
• SB203580, an inhibitor of p38 kinase, did not attenuate the effects of hyper-osmotic conditions on APOBEC-1 editing [13].

References