IndraLab

Statements



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"The results showed that SP600125 significantly inhibited JNK/c-Jun signaling ( Fig. 4 B) and improved RGC death induced by ITON ( Fig. 4 C and D)."

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"Notably, to investigate whether the JNK and c-jun pathway participated in mediating the protective functions of 14,15-EET in OGD induced injury of CSMC, SP600125 was used to block the JNK and c-jun pathway."

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"SP600125 has been shown to inhibit Jun N-terminal kinases (JNKs) and other kinases."

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"SP600125, a specific inhibitor of JNK signaling, inhibits the MPTP activated JNK and c-Jun pathway in DA neurons and suppresses cox-2, thereby protecting DA neurons."

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"Administration of SP600125 60 min before renal ischemia significantly inhibited p-c-Jun immunoreactivity at 3 h of reperfusion after ischemia (d)."

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"Further, the inhibitors SB202190 (Sigma-Aldrich) and SP600125 (Sigma-Aldrich) were used to block p38 mitogen activated protein kinase (p38-MAPK) and Jun N-terminal kinase (JNK) respectively in control and siPrdx2 transfected HTR8 cells."

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"To clarify the signaling pathways underlying the BDNF expression changes due to Kir4.1 knockdown, astrocytes were pretreated with U0126 [a non competitive inhibitor of mitogen activated protein kinase (MEK) 1/2, 10 muM], SB202190 (an inhibitor of p38 MAPK, 10 muM), or SP600125 [an inhibitor of Jun amino-terminal kinase (JNK), 10 muM] for 30 min before the transfection with Kir4.1 siRNA or a negative control."

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"This rescue depended on PDGF mediated JNK signaling because SP600125 treatment abolished the induction of c-Jun expression (XREF_FIG B)."

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"Furthermore, MEKK2 immunoprecipitates activated c-Jun in an IL-1 dependent manner and this activity was inhibited by the selective JNK inhibitor SP600125."

sparser
"As expected, the phosphorylation of p65 and c-jun was inhibited in M0 and M1 macrophages by Bay11-7082 and SP600125, respectively."

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"Our results demonstrate that ischemia/reperfusion induced c-Jun activation and SP600125 significantly diminished the increased of p-c-Jun at 3 h after renal ischemia."

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"Addition of SP600125 (20 μM) inhibited the PTX-induced increase of p-c-Jun."

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"In this study, we also showed that SP600125 dramatically inhibited Cd activated c-Jun, a substrate of JNK in the cells (XREF_FIG)."

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"Immunoprecipitation assay showed that hyperosmolarity increased the association of nuclear Sp1 with c-Jun, which was inhibited by U0126 and SP600125."

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"In some experiments, SP600125 (10 μmol/L; Sigma-Aldrich) and SB203580 (10 μmol/L; Sigma-Aldrich) were used to block c-jun NH 2 -terminal kinase (JNK) and mitogen-activated protein kinase (MAPK) p38, r[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In previously published experiments, 10 muM SP600125 effectively inhibits 90 to 100% of Jun N-terminal kinase activity (Bennett et al., 2001)."

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"We have determined that SP600125 blocked c-Jun activation in B leukemia cell lines."

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"As shown in Fig. 8 A, SP600125 efficiently attenuated the alkannin-induced increases in p-JNK and p-c-Jun in the MDA-MB-231, HCT116 and Huh7 cells."

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"Thrombin (0.3-3.0 U/mL) increased activator protein-1 (AP-1)-luciferase activity, which was inhibited by the JNK inhibitor SP600125."

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"In the present study, we demonstrate that an anthrapyrazole SP600125, a reversible ATP-competitive inhibitor of JNK inhibits proliferation of human HMC-1 showed constitutive activation of JNK and c-Jun, and the inhibitory effect of SP600125 on cell proliferation was associated with cell cycle arrest at the G1 phase and apoptosis accompanied by the cleavage of caspase-3 and PARP."

sparser
"TGFβ also induced phosphorylation of (S351) NR4A1, JNK1, c-jun and c-fos which was also inhibited by SP600125, demonstrating that TGFβ induces JNK and genes downstream from JNK."

sparser
"In contrast, inhibition of c-Jun NH(2)-terminal kinase (JNK) by SP600125 significantly enhanced apoptosis."

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"Further, 17β-estradiol increased the c-Jun expression, a member of AP-1, and the increased c-Jun induced by 17β-estradiol was abrogated by SP600125 at mRNA and protein levels."

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"SP600125 inhibited interleukin-1beta-induced JNK activity and activator protein-1 activation, but it did not affect the activation of extracellular regulated kinase, p38 mitogen activated protein kinase, and nuclear factor-kappaB."

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"As shown in Fig. 5 A, the TNF-α-induced c-jun activation was inhibited by the treatment with wortmannin (PI3K inhibitor), PD98059 (ERK inhibitor) and SP600125 (JNK inhibitor), but not with SB203589 (p[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"We observed that 20 μM PD98059, SP600125, and GF109203X blocked the activity of c-Jun/AP-1 (∼50%) ( Fig. 5 B)."

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"Our Western blot results showed that repeated intrathecal injections of SP600125 significantly reduced the up-regulation of p-JNK and p-c-Jun in the spinal cord (Figure 6(b) and (c)), and immunofluorescence results further showed that p-JNK and p-c-Jun co-localization in both the microglia and astrocytes also decreased (Figure 7(a) and (b), Supplementary Figure 3(a) and (b))."

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"SP600125 and TAM67 specifically inhibited JNK and c-Jun signaling as neither agent altered ERK1/2 phosphorylation (XREF_FIG)."

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"SP600125 inhibited AP-1 and c-Jun."

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"Also, SP600125 almost abolishes the increased mRNA of c-Jun, a major component of AP-1, induced by estrogen, which suggests that 17β-estradiol suppresses the expression of Ces1d and Ces1e via AP-1 pat[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

sparser
"Furthermore, inhibition of c-Jun N -terminal kinase (JNK) by SP600125 led to a dramatic decrease of the GLP-induced apoptosis."

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"While these effects were reversed after JNK/c-Jun pathway was blocked by SP600125 (JNK pathway inhibitor), indicating the pathway was involved in NiONPs-induced excessive collagen formation."

sparser
"Moreover, we also found that pretreatment with U0126 and SP600125 inhibited IL-1β-induced c-Jun bound to VCAM-1 promoter region."

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"To investigate whether the JNK and c-jun and mTOR pathways were involved in mediating the protective functions of 14,15-EET during OGD induced injury, RAPA and SP600125 were used to block the mTOR and JNK and c-jun pathways, respectively."

sparser
"Moreover, siG6PD increased the reporter activity of MGAT3 promoters, while inhibition of c-Jun by SP600125 decreased the reporter activity (Fig.  xref , Supplementary Fig.  xref )."

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"Incubation of the cells with DEM caused a significant increase in phosphorylated JNK 1 and 2, cJun and MKK4 and the JNK inhibitor, SP600125 inhibited the stimulation in cystathionine-γ-lyase expressio[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The application of JNK inhibitor, SP600125, blocked this increase in phospho-c-Jun, as well as c-Jun activity produced by mustard oil stimulation."

eidos
"Moreover , siG6PD increased the reporter activity of MGAT3 promoters , while inhibition of c-Jun by SP600125 decreased the reporter activity ( Fig. 5g , Supplementary Fig. 6F ) ."

sparser
"In this study, we also showed that SP600125 dramatically inhibited Cd-activated c-Jun, a substrate of JNK in the cells ( xref )."

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"Administration of the JNK inhibitor SP600125 or MLK3 (an upstream kinase of MKK7 or MKK4) inhibitor CEP11004 greatly abrogated c-Jun and proliferation, suggesting that the MLK3-MKK4 or 7-JNK cascade contributes to c-Jun activation and cell viability and proliferation."

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"Although the SP600125 inhibitor efficiently suppresses activation of c-Jun and the upregulation of ATF-3 in sensory neurons [XREF_BIBR], it did not inhibit neither c-Jun activation nor ATF-3 upregulation in SCs."

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"The JNK activity specific inhibitor, SP600125, and siRNA directed against JNK were used to block JNK and c-Jun pathway."

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"Interestingly, the addition of LY294002, SP600125 and PD98059 prevented the fibroin stimulation of c-Jun (XREF_FIG)."

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"To test this possibility, the CXCL14 overexpressing cells (clone H) were incubated with the c-Jun-NH 2 -kinase (JNK) inhibitor SP600125 to block c-Jun (a component of AP-1) activation and then tested if this would cause a decrease of CXCL14 transcription."

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"To further study the functions of transcription factors under hypoxic conditions, JSH-23 and SP600125 were used to block the NF-kappaB and AP-1 and c-Jun pathways."

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"As shown in XREF_FIG, SP600125 prevented the cerebral ischemia activation of JNK and c-Jun, an effect that was correlated with a significant attenuation of the induction of Dkk1."

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"Moreover, the present study showed that IL-17A induced the nuclear translocation of c-Jun and c-Fos, which could be effectively inhibited by the JNK inhibitor SP600125 or the p38 inhibitor SB203580 (Fig. 6a)."