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Publication : Optimal HSF1 activation in response to acute cold stress in BAT requires nuclear TXNIP.

First Author  Waldhart AN Year  2023
Journal  iScience Volume  26
Issue  5 Pages  106538
PubMed ID  37168572 Mgi Jnum  J:335573
Mgi Id  MGI:7481834 Doi  10.1016/j.isci.2023.106538
Citation  Waldhart AN, et al. (2023) Optimal HSF1 activation in response to acute cold stress in BAT requires nuclear TXNIP. iScience 26(5):106538
abstractText  While TXNIP (thioredoxin interacting protein) in the plasma membrane and vesicular location is known to negatively regulate cellular glucose uptake by facilitating glucose transporter endocytosis, the function of TXNIP in the nucleus is far less understood. Herein, we sought to determine the function of nuclear TXNIP in vivo, using a new HA-tagged TXNIP knock-in mouse model. We observed that TXNIP can be found in the nucleus of a variety of cells from different tissues including hepatocytes (liver), enterocytes (small intestine), exocrine cells (pancreas), and brown adipocytes (BAT). Further investigations into the role of nuclear TXNIP in BAT revealed that cold stress rapidly and transiently activated HSF1 (heat shock factor 1). HSF1 interaction with TXNIP during its activation is required for optimal HSF1 directed cold shock response in BAT.
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