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• W3201320786 abstract "Fasting induces profound changes in the hypothalamic-pituitary-thyroid (HPT) axis. After binding thyroid hormone (TH), the TH receptor beta 2 isoform (THRB2) represses Trh and Tsh subunit genes and is the principle negative regulator of the HPT axis. Using mass spectrometry, we identified a major phosphorylation site in the AF-1 domain of THRB2 (serine 101, S101), which is conserved among many members of the nuclear hormone receptor superfamily. More than 50% of THRB2 is phosphorylated at S101 in cultured thyrotrophs (TαT1.1) and in the mouse pituitary. All other THR isoforms lack this site and exhibit limited overall levels of phosphorylation. To determine the importance of THRB2 S101 phosphorylation, we used the TαT1.1 cell line and S101A mutant knock-in mice (Thrb2S101A ). We found that TH promoted S101 THRB2 phosphorylation and was essential for repression of the axis at physiologic TH concentrations. In mice, THRB2 phosphorylation was also increased by fasting and mimicked Trh and Tshb repression by TH. In vitro studies demonstrated that a master metabolic sensor, AMP-activated kinase (AMPK) induced phosphorylation at the same site and caused Tshb repression independent of TH. Furthermore, we identified cyclin-dependent kinase 2 (CDK2) as a direct kinase phosphorylating THRB2 S101 and propose that AMPK or TH increase S101 phosphorylation through the activity of CDK2. This study provides a physiologically relevant function for THR phosphorylation, which permits nutritional deprivation and TH to use a common mechanism for acute suppression of the HPT axis." @default.
• W3201320786 created "2021-09-27" @default.
• W3201320786 creator A5018387665 @default.
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• W3201320786 creator A5077652405 @default.
• W3201320786 date "2021-09-20" @default.
• W3201320786 modified "2023-10-16" @default.
• W3201320786 title "Thyroid hormone receptor phosphorylation regulates acute fasting-induced suppression of the hypothalamic–pituitary–thyroid axis" @default.
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• W3201320786 doi "https://doi.org/10.1073/pnas.2107943118" @default.
• W3201320786 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8488655" @default.
• W3201320786 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34544870" @default.
• W3201320786 hasPublicationYear "2021" @default.
• W3201320786 type Work @default.
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• W3201320786 hasAuthorship W3201320786A5049313563 @default.

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