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Deletion of translin (Tsn) induces robust adiposity and hepatic steatosis without impairing glucose tolerance.

Aparna P Shah | Miranda D Johnson | Xiuping Fu | Gretha J Boersma | Madhura Shah | Michael J Wolfgang | Kellie L Tamashiro | Jay M Baraban
International journal of obesity (2005) | 2020

Translin knockout (KO) mice display robust adiposity. Recent studies indicate that translin and its partner protein, trax, regulate the microRNA and ATM kinase signaling pathways, both of which have been implicated in regulating metabolism. In the course of characterizing the metabolic profile of these mice, we found that they display normal glucose tolerance despite their elevated adiposity. Accordingly, we investigated why translin KO mice display this paradoxical phenotype.

Pubmed ID: 30647452

Research resources used in this publication

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Associated grants

  • Agency: NINDS NIH HHS, United States
    Id: P30 NS050274
  • Agency: NIDA NIH HHS, United States
    Id: P50 DA000266
  • Agency: NIDA NIH HHS, United States
    Id: P50 DA044123

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