IndraLab

Statements

Glucose inhibits RELA. 10 / 10
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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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"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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"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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"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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"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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"BE ameliorated serum and liver lipids, blood glucose, and insulin, liver LPO, prevented steatosis and fibrosis, suppressed NF-kB p65 and enhanced antioxidants in HFD-fed rats."
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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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"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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"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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