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Glucose inhibits RELA. 13 / 13
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"Like GFP-Cx43, transfection with Flag-Cx43CT also significantly inhibited high glucose induced NF-kappaB p65 nuclear translocation (P < 0.05; Figures XREF_FIG B)."
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"Another example of existing regulatory intricacies comes from the finding that starvation for either glucose or lipids can deplete amino acid precursors and activate RelA in addition of SpoT ( Fern a ndez-Coll and Cashel , 2018 ; Sinha et al ., 2019 ) ."
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"As mentioned before, RelA synthetase activation can be stimulated by glucose starvation only during amino acid limitation (Gentry and Cashel, 1996)."
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"alpha-T and alpha-TP attenuated high glucose and hypoxia induced cell apoptosis by promoting Bcl-2 and Akt and inhibiting nuclear factor kappaB p65, JNK, Notch-1, and p38MAPK genes."
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"Further, CSF ameliorated dysfunction in HUVECs caused by HG, which decreased ICAM-1, VCAM-1, TLR4, and p65, as well as down-regulated IL-6 and TNF-α."
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"The results demonstrated that high glucose stimulation for 30 min induced a notable increase in the NF-κB p65 contents in the nucleus and decrease in the NF-κB p65 contents in the cytoplasm in GMCs co[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"This resulted in a marked decrease of ATP levels in glucose starved RelA deficient cells, but not in starved wild-type cells (XREF_FIG and XREF_SUPPLEMENTARY)."
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"As shown in XREF_FIG, HG enhanced the nuclear and decreased the cytoplasmic localization of NFkappaB p65 (P < 0.05)."
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"HG also significantly inhibited signaling via the activated B cell subunit p65."
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"Additionally, we found that TAK-242 treatment significantly suppressed the TLR4 and NF-kappaB pathway in HG induced podocytes by reducing the protein level of TLR4, p-IkappaBalpha and IkappaBalpha ratio and p-p65 and p65 ratio."
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"Hence, defective macroautophagy is not responsible for the demise of glucose starved RelA deficient cells."
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"Compared with the control, HG treatment for 30 min resulted in significantly increased p65 contents in the nucleus and decreased p65 contents in the cytoplasm in GMCs (P < 0.05, XREF_FIG B and 5 C)."
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"However, FGF-21 treatment can completely restore mitochondrial damage and morphological changes in endothelial cells caused by glucose (Fig. 2).3.3 FGF-21 inhibited NF-kappaB p65 and NLRP3 inflammasome activation in vitro."
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