2021
DOI: 10.1101/2021.07.23.453596
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FTO suppresses STAT3 activation and modulates proinflammatory interferon-stimulated gene expression

Abstract: Signaling initiated by type I interferon (IFN) results in the induction of hundreds of IFN-stimulated genes (ISGs). The type I IFN response is important for antiviral restriction, but aberrant activation of this response can lead to inflammation and autoimmunity. Regulation of this response is incompletely understood. We previously reported that the mRNA modification m6A and its deposition enzymes, METTL3 and METTL14 (METTL3/14), promote the type I IFN response by directly modifying the mRNA of a subset of ISG… Show more

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Cited by 2 publications
(3 citation statements)
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“…It has been reported that inactivation of FTO inhibits STAT3-mediated signaling pathways in cancer cells and adipocytes [42,43], and the STAT3 signaling pathways play important roles in hypothalamic POMC neurons [44][45][46]. Furthermore, a previous work has shown that activation of ERK1/2 in cultured hypothalamic cells promoted STAT3 phosphorylation at the residue S727 but not at Y705 [47].…”
Section: Inhibition Of Fto Leads To Phosphorylation Of Stat3-s727 And...mentioning
confidence: 99%
See 1 more Smart Citation
“…It has been reported that inactivation of FTO inhibits STAT3-mediated signaling pathways in cancer cells and adipocytes [42,43], and the STAT3 signaling pathways play important roles in hypothalamic POMC neurons [44][45][46]. Furthermore, a previous work has shown that activation of ERK1/2 in cultured hypothalamic cells promoted STAT3 phosphorylation at the residue S727 but not at Y705 [47].…”
Section: Inhibition Of Fto Leads To Phosphorylation Of Stat3-s727 And...mentioning
confidence: 99%
“…A previous study has shown that the altered hypothalamic FTO level could increase or decrease the sensitivity of neurons in response to leptin [34], and leptin-related synthetic peptides were identified to lead to STAT3 phosphorylation via activation of ERK1/2 [35]. Furthermore, depletion of FTO could induce expression of a subset of genes by activation of STAT3 [36], and another work has suggested that FTO inactivation can prevent tumor formation by inhibiting ERK1/2 [37]. Therefore, we propose that inactivation of hypothalamic FTO might lead to an anorexia effect by activating STAT3 and/or ERK1/2.…”
Section: Introductionmentioning
confidence: 99%
“…Through the differential analysis of the expression levels of 23 m6A methylation regulators in the gene expression data of normal control group and COPD patients, it was found that METTL3、RBM15、RNM15B、CBLL1、YTHDC2、YTHDF1、YTHDF2、 HNNRPC、LPPPRC、RBMX、FTO、ALKBH5 and other methylation regulators were significantly overexpressed in COPD patients.Some studies have found that METTL3、 YTHDC2 、 FTO and other methylation regulators can significantly promote the biological process in the development of COPD [29].Several studies have shown that overexpression of METTL3 can promote the level of TRAF6 to induce NF KB and MAPK signaling pathways to enhance inflammatory response, while inhibition of METTL3 can inhibit IL-1 β Induced inflammatory response [30].FTO is an important mRNA demethylation regulator, which can inhibit the inflammatory response induced by type I interferon by inhibiting the chemotaxis of interferon stimulating factor (ISG) and proinflammatory factors TNF, IL6, IL9, IL10 and IL11 [31].…”
Section: Discussmentioning
confidence: 99%