ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Ablation of Sam68 in adult mice increases thermogenesis and energy expenditure.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation.Circulation · 2026Article
- Galactosylated LNP-mediated hepatic Sam68 silencing improves glucose homeostasis in diabetes by suppressing gluconeogenesis.Journal of nanobiotechnology · 2026Article
- RNA binding protein Sam68 promotes germinal center reaction and IgG response through regulation of miR29.Cellular and molecular life sciences : CMLS · 2026Article
- RNA-Binding Proteins in Adipose Biology: From Mechanistic Understanding to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- White-to-Beige and Back: Adipocyte Conversion and Transcriptional Reprogramming.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Hepatic Sam68 Regulates Systemic Glucose Homeostasis and Insulin Sensitivity.International journal of molecular sciences · 2022Article
- Sam68 contributes to intestinal inflammation in experimental and human colitis.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
Genetic deletion of Src associated in mitosis of 68kDa (Sam68), a pleiotropic adaptor protein prevents high-fat diet-induced weight gain and insulin resistance. To clarify the role of Sam68 in energy metabolism in the adult stage, we generated an inducible Sam68 knockout mice. Knockout of Sam68 was induced at the age of 7-10 weeks, and then we examined the metabolic profiles of the mice. Sam68 knockout mice gained less body weight over time and at 34 or 36 weeks old, had smaller fat mass without changes in food intake and absorption efficiency. Deletion of Sam68 in mice elevated thermogenesis, increased energy expenditure, and attenuated core-temperature drop during acute cold exposure. Furthermore, we examined younger Sam68 knockout mice at 11 weeks old before their body weights deviate, and confirmed increased energy expenditure and thermogenic gene program. Thus, Sam68 is essential for the control of adipose thermogenesis and energy homeostasis in the adult.
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Registered trials
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