ArticleMolecular metabolism2020
Genetic inactivation of the translin/trax microRNA-degrading enzyme phenocopies the robust adiposity induced by Translin (Tsn) deletion.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Genetic inactivation of Translin/Trax RNase disrupts miRNAs, hippocampal synaptic plasticity, and memory.iScience · 2026Article
- Translin deletion impairs cocaine-induced locomotor sensitization and RGS8 expression in the nucleus accumbens.Acta pharmacologica Sinica · 2025Article
- Conditional Deletion of Translin/Trax in Dopaminergic Neurons Reveals No Impact on Psychostimulant Behaviors or Adiposity.Biomolecules · 2025Article
- Adenosine AJournal of the American Heart Association · 2023Article
- Comparative Proteomic Analysis of tPVAT during Ang II Infusion.Biomedicines · 2021Article
- Degradation of Premature-miR-181b by the Translin/Trax RNase Increases Vascular Smooth Muscle Cell Stiffness.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Elevated body fat increases amphetamine accumulation in brain: evidence from genetic and diet-induced forms of adiposity.Translational psychiatry · 2021Article
- Deciphering the Role of microRNAs in Large-Artery Stiffness Associated With Aging: Focus on miR-181b.Frontiers in physiology · 2021Review
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Authors and funding
6 authors.
Funding
Abstract
objectiveDeletion of Translin (Tsn) from mice induces an unusual metabolic profile characterized by robust adiposity, normal body weight and glucose tolerance. Translin (TN) protein and its partner, trax (TX), form the TN/TX microRNA-degrading enzyme. Since the microRNA system plays a prominent role in regulating metabolism, we reasoned that the metabolic profile displayed by Tsn KO mice might reflect dysregulation of microRNA signaling.
methodsTo test this hypothesis, we inserted a mutation, E126A, in Tsnax, the gene encoding TX, that abolishes the microRNA-degrading enzymatic activity of the TN/TX complex. In addition, to help define the cell types that drive the adiposity phenotype, we have also generated mice with floxed alleles of Tsn or Tsnax.
resultsIntroduction of the E126A mutation in Tsnax does not impair expression of TN or TX proteins or their co-precipitation. Furthermore, these mice display selective increases in microRNAs that match those induced by Tsn deletion, confirming that this mutation in Tsnax inactivates the microRNA-degrading activity of the TN/TX complex. Mice homozygous for the Tsnax (E126A) mutation display a metabolic profile that closely mimics that of Tsn KO mice. Selective deletion of Tsn or Tsnax from either adipocytes or hepatocytes, two candidate cell types, does not phenocopy the elevated adiposity displayed by mice with constitutive Tsn deletion or the Tsnax (E126A) mutation. Furthermore, global, conditional deletion of Tsn in adulthood does not elicit increased adiposity.
conclusionTaken together, these findings indicate that inactivation of the TN/TX microRNA-degrading enzyme during development is necessary to drive the robust adiposity displayed by Tsn KO mice.
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