INT103282
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Experiments using siRNA and an intracellular Ca(2+) chelator revealed that Ca(2+)-dependent up-regulation of ATF4 and CHOP is involved in this up-regulation of PUMA. | |||||||||||||||
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Both the ATF4 and ATF6 pathways were activated by celecoxib, and suppression of ATF4 and ATF6 mRNA expression by small interfering RNA (siRNA) inhibited the celecoxib-dependent up-regulation of ORP150. | |||||||||||||||
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The celecoxib-mediated up-regulation of S100P was suppressed by the transfection of cells with small interfering RNA for activating transcription factor 4 (ATF4), a transcription factor involved in the endoplasmic reticulum stress response. | |||||||||||||||
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Celecoxib increased the intracellular Ca2+ concentration, while 1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid, an intracellular Ca2+ chelator, inhibited the upregulation of GRP78 and ATF4. | |||||||||||||||
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Celecoxib administration led to an increase in the intracellular concentration of Ca2+, whereas 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester, an intracellular Ca2+ chelator, inhibited the up-regulation of ORP150 and the activation of the ATF4 and ATF6 pathways. | |||||||||||||||
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-phosphorylation the translation of most mRNAs is inhibited, but paradoxically the translation of activating transcription factor 4 (ATF4) is increased. | |||||||||||||||
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These results suggest that the Ca2+-dependent activation of the PERK-eIF2alpha-ATF4 pathway is involved in the upregulation of ER chaperones by celecoxib. | |||||||||||||||
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phosphorylation promotes the induction of activating transcription factor 4 (ATF4) through a mechanism that relies upon unique features in its 5' untranslated region [54]. | |||||||||||||||
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phosphorylation promotes the induction of activating transcription factor 4 (ATF4) through a mechanism that relies upon unique features in its 5' untranslated region [54]. | |||||||||||||||
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Figure 3 (Panel A) shows an increase in the level of nuclear ATF4 in NHBE cells in response to CS treatment at 4 hrs post-exposure which diminishes by 7 hrs. | |||||||||||||||
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Several other redox-sensitive genes were upregulated after short-term exposure to the high concentration of curcumin, like AREG, ATF4, EGR1, FGFR1 (Table 2) [44]. | |||||||||||||||
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Calcium/calmodulin-dependent protein kinase IV, the cAMP-responsive-element binding protein activating enzyme, was also activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin in an activity-dependent manner. | |||||||||||||||
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Furthermore, TTX and MK801 differentially affected the association of AhR and its transcriptional co-activator cAMP-responsive-element binding protein with the cytochrome P450 1A1 (cyp1A1) gene enhancer. | |||||||||||||||
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In addition, its action via progesterone response element cis-elements, PR appeared to inhibit trans-activation of a nuclear factor-kappaB-responsive element, further suppressing RANTES expression. | |||||||||||||||
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