ArticleJournal of lipid research2025
MUSTN1 and FABP3 interact to regulate adipogenesis and lipid deposition.
Article in Journal of lipid research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Single-cell transcriptional mapping ofJBMR plus · 2026Article
- Genome-Wide Association Study of Abdominal and Intramuscular Fat Deposition Traits in Huainan Yellow-Feathered Chickens.Animals : an open access journal from MDPI · 2025Article
- Thermal challenge significantly alters gene expression in breast muscle of commercial turkey poults.Frontiers in physiology · 2025Article
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Authors and funding
7 authors.
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Abstract
Lipid deposition is related to agricultural animal production and human health, and elucidating its molecular regulatory mechanisms is a topic of interest and a challenge in current scientific research. Musculoskeletal embryonic nuclear protein 1 (MUSTN1) regulates growth and development, including muscle tissue; however, its role in fat deposition remains unknown. Thus, our objective was to determine this role. Our new findings were as follows: MUSTN1 was highly expressed in the fat tissue of pigs with strong adipose deposition capacity; functionally, MUSTN1 promoted the proliferation and adipogenic differentiation of porcine and mouse preadipocytes. MUSTN1 knockout mice were protected against HFD-induced obesity, hepatic steatosis, and insulin resistance; and fatty acid binding protein 3 was identified as an interacting protein of MUSTN1, which facilitated preadipocyte proliferation and differentiation by activating the phosphatidylinositol 3 kinase/AKT signaling pathways. This study reveals a positive regulator for fat development, which suggests a novel approach for studying obesity and animal genetic improvement through the modulation of MUSTN1 expression.
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