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"We found that in HaCaT cells induced with TNF-I +/-, Rapamycin inhibited key steps in activation of central pro inflammatory factor NF-I (o) B : II (o) BI +/- phosphorylation and degradation; and nucl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"We found that in HaCaT cells induced with TNF-I +/-, Rapamycin inhibited key steps in activation of central pro inflammatory factor NF-I (o) B : II (o) BI +/- phosphorylation and degradation; and nucl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, immunofluorescent staining showed that rapamycin reduced the accumulation of p65 in the nucleus after ox-LDL treatment for 30 h. mTOR knockdown decreased LOX-1 protein production and IkappaBalpha phosphorylation induced by ox-LDL."

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"The rapamycin treatment significantly decreased the level of phospho-NF-kappaB p65 protein in the IL-23-treated cells, suggesting that mTOR functioned as an upstream regulator to mediate NF-kappaB p65 activation in IL-23-stimulated TFCs."

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"Moreover, a combination of rapamycin (80 nM) and MPA (20 nM) inhibited the TNF-alpha-induced nuclear localization of NF-kappaB p65 in HaCaT cells when compared with individual drug treatments and other combinations of the two drugs."

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"PCA, Bay 11-7085, Akt inhibitor, rapamycin and N -acetylcysteine inhibited lipopolysaccharide caused increase in the NF-kappaB p65 to DNA binding activity."