2018
DOI: 10.1016/j.ygcen.2017.08.023
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Egr2 enhances insulin resistance via JAK2/STAT3/SOCS-1 pathway in HepG2 cells treated with palmitate

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Cited by 25 publications
(19 citation statements)
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“…SOCS1 is a speci c negative regulator that regulates the JAK/STAT pathway [32]. The expression of SOCS1 increases under insulin resistance and overexpression of SOCS1 decreases the phosphorylation of IRS-1; overexpression of SOCS-1 can inhibit insulin-induced glycogen synthesis in L6 myotubes [33].…”
Section: Discussionmentioning
confidence: 99%
“…SOCS1 is a speci c negative regulator that regulates the JAK/STAT pathway [32]. The expression of SOCS1 increases under insulin resistance and overexpression of SOCS1 decreases the phosphorylation of IRS-1; overexpression of SOCS-1 can inhibit insulin-induced glycogen synthesis in L6 myotubes [33].…”
Section: Discussionmentioning
confidence: 99%
“…Chen et al found that the regulation of EGR2 expression by the competitive combination of LINC01939 with mir-17-5p may inhibit the metastasis and EMT of gastric cancer (Chen et al, 2019). EGR2 can reduce the phosphorylation of JAK2 and STAT3 by regulating the expression of SOCS-1 (Lu et al, 2017). In addition, a lack of EGR2 results in defective cloning amplification of T-cells as a response to viral infection, with overactivation and overdifferentiation (Miao et al, 2017).…”
Section: Discussionmentioning
confidence: 99%
“…EGR plays a crucial role in the expression of FasL mediated by HBx, thus affecting the occurrence of HBV-related HCC[36]. Inhibition of EGR2 in HCC cell lines reduces the expression of SOCS-1 and the phosphorylation of JAK2 and STAT3, thus affecting cell proliferation[37]. FOS signal transduction is associated with TLR9-mediated IFN production in plasma-like dendritic cells, and the gene expression level of it is also significantly changed in HCC[38,39].…”
Section: Discussionmentioning
confidence: 99%