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Publication : Temperature homeostasis in mice lacking the p43 mitochondrial T3 receptor.

First Author  Bertrand-Gaday C Year  2016
Journal  FEBS Lett Volume  590
Issue  7 Pages  982-91
PubMed ID  26970082 Mgi Jnum  J:232049
Mgi Id  MGI:5775849 Doi  10.1002/1873-3468.12129
Citation  Bertrand-Gaday C, et al. (2016) Temperature homeostasis in mice lacking the p43 mitochondrial T3 receptor. FEBS Lett 590(7):982-91
abstractText  Thyroid hormones and Thra gene play a key role in energy expenditure regulation, temperature homeostasis, and mitochondrial function. To decipher the function of the mitochondrial TRalpha receptor in these phenomena, we used mice lacking specifically the p43 mitochondrial T3 receptor. We found that these animals were hypermetabolic, hyperphagic, and displayed a down setting of the core body temperature. However, p43-/- animals do not present cold intolerance or defect of facultative thermogenesis. In addition, the mitochondrial function of BAT is slightly affected in the absence of p43. Our study, therefore, suggests a complementarity of action between the mitochondrial receptor and other proteins encoded by the Thra gene in the control of basal metabolism, facultative thermogenesis, and determination of the set point of temperature regulation.
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