IndraLab

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TNF dephosphorylates INSR. 16 / 16
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"TNF-alpha has been shown to induce the expression of SOCS-3 (Suppressor of cytokine signalling-3), which specifically inhibits insulin receptor phosphorylation [XREF_BIBR]."

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"In adipocytes, TNF-α suppresses the transcription of the adiponectin gene [27] and impairs insulin receptor phosphorylation and kinase pathways by activating NF-κB and c-Jun NH2-terminal kinase (JNK) signaling, thereby promoting IR [85]."

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"Data indicates that the inhibition of TNFα significantly increased insulin receptor and Akt phosphorylation (Figures 6(b) and 6(d))."

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"In addition, TNF-alpha mediates insulin resistance by reducing insulin receptor kinase activity, down-regulating insulin receptor substrate (IRS) -1 and GLUT-4 phosphorylation and activity, and inducing lipolysis 2."

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"Insulin resistance is one of the first consequences of sustained inflammation, since pro inflammatory cytokines such as interleukins, and TNF-alpha abrogate insulin receptor phosphorylation and post-r[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, LG100754 blocks TNF α-mediated inhibition of the insulin receptor (IR) phosphorylation in mature adipocytes."

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"TNF-α, IL-6, IL-1β, and resistin induce IRS1,2 degradation, and in the liver, dephosphorylate insulin receptor and IRS through STAT3."

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"TNFalpha appears to inhibit insulin receptor phosphorylation and has been ascribed a role in the pathogenesis of insulin resistance."

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"Sequential studies showed that TNFalpha not only decreased the amount of (tyrosine) phosphorylation of the insulin receptor substrate (IRS) [13] but also initiated serine phosphorylation of IRS, which[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The upregulated TNF-α levels increase insulin resistivity and inhibit the insulin receptor phosphorylation and atheromatous plaque deposition with aging (Nilsson et al., 1998; Skoog et al., 2002)."

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"TNF-alpha activates c-Jun N-terminal kinase (JNK) to phosphorylate and suppress the activity of insulin receptor (IR) substrate 1."

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"The overproduction of TNF could decrease the phosphorylation of insulin receptor substrates 1 and 2, inhibit phosphoinositol 3-kinase and protein kinase B, block the phosphorylation of glucose transporter 4, prevent the cell uptake of glucose [29], and increase plasma glucose levels."

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"Increased TNFalpha causes an adipocyte specific decrease in insulin receptor phosphorylation; decreased insulin receptor function; resistance to the antilipolytic effects of insulin; de-repression of adipocyte hormone sensitive lipase; increased, continuous lipolysis of the enlarged adipocyte TG mass; and a further increase in plasma LCFA."

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"URGCP overexpression correlates with upregulation of TNFα, which reduces insulin sensitivity by facilitating phosphorylation of the insulin receptor."

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"Additionally, ADP can prevent the proliferation of monocyte precursor cells and have a negative regulatory effect on the expression of TNF-α, thereby reducing the degree of inflammatory response.19Imanparst F et al.20 have shown that TNF-α can inhibit insulin receptor self-phosphorylation, block insulin-stimulated glucose uptake, and downregulate the number of insulin receptors, thereby inducing hyperinsulinemia and exacerbating insulin resistance."

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"Mechanistically, TNFalpha contributes to insulin resistance by inhibiting the activating phosphorylation of the insulin receptor and insulin receptor substrate 1 (IRS1) in muscle and adipose tissues [XREF_BIBR]."