IndraLab

Statements


NAC inhibits JUN. 11 / 11
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"NAC can inhibit activity of several signal transduction components such as nuclear factor kappa B, activator protein 1, and c- jun N-terminal kinase (JNK) by redox modulation [42, 43]."

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"showed that the administration of N-acetylocysteine (NAC), a ROS scavenger, reduced colonic cancer cell apoptosis via inhibition of JNK, p38 MAPK and activation of c-jun."

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"As we might expected, NAC could inhibit JNK and cJun activation caused by DCZ0358 in DLBCL cells ( Fig. 5 D)."

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"At the molecular level, NAC has been shown to inhibit the activation of C Jun N-terminal kinase, p38 MAP kinase, redox sensitive activating protein-1 (AP-1) and the NF-kappaB transcriptional factor, thereby resulting in the suppression of numerous genes regulating the expression of many cytokines, such as TNF-alpha and IL-1 XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"As displayed in Fig. 3 F, we found similar results in UVB-stimulated HFDs combined with Iso, NAC or MitoQ that JNK and c-Jun activation induced by UVB were dramatically inhibited by Iso, NAC and MitoQ[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"As shown in xref , both 15(S)-HETE and 15(S)-HPETE upregulated the mRNA levels of c-FOS and c-JUN, which was inhibited by NAC."

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"NAC in combination with vanadate appeared to increase the efficacy of c-fos and c-jun inhibition, while decreasing toxicity."

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"Thus, NAC can inhibit activation of the JNK and c-Jun signaling pathway by reducing excessive ROS production, thereby reversing the cytotoxic effects of Dex."

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"Furthermore, NAC inhibited the salvicine-mediated DNA damage, the subsequent trigger of apoptosis, and the activation of c-Jun and its aforementioned downstream effects."

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"NAC was shown to inhibit the activation of c-Jun-N-terminal kinase (JNK) and transcription factor c-Jun ( Cai et al., 2007 )."

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"Induction of the pro-inflammatory transcription factors activator protein1 (AP-1) and NF-κB is inhibited by NAC."