ArticleMolecular and cellular biology2015
Sam68 Regulates S6K1 Alternative Splicing during Adipogenesis.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 32 citations in OpenAlex.
- SAM68 is a multifunctional post-transcriptional regulator of cardiomyocyte differentiation.Nucleic acids research · 2026Article
- The splicing factor SRRM2 modulates two S6K kinases to promote colorectal cancer growth.Oncogene · 2025Article
- Khdrbs1 drives re-differentiation of bipotential progenitor cells by inhibiting p53 in zebrafish biliary-mediated liver regeneration.Development (Cambridge, England) · 2025Article
- SRSF1 Is Required for Mitochondrial Homeostasis and Thermogenic Function in Brown Adipocytes Through its Control of Ndufs3 Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- The Role of Splicing Factors in Adipogenesis and Thermogenesis.Molecules and cells · 2023Review
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Review
- Beyond controlling cell size: functional analyses of S6K in tumorigenesis.Cell death & disease · 2022Review
- Arginine methylation of SARS-Cov-2 nucleocapsid protein regulates RNA binding, its ability to suppress stress granule formation, and viral replication.The Journal of biological chemistry · 2021Article
- Regulatory roles and mechanisms of alternative RNA splicing in adipogenesis and human metabolic health.Cell & bioscience · 2021Review
- Bovine Pre-adipocyte Adipogenesis Is Regulated by bta-miR-150 Through mTOR Signaling.Frontiers in genetics · 2021Article
- Alternative splicing in mesenchymal stem cell differentiation.Stem cells (Dayton, Ohio) · 2020Review
- DDX5 resolves R-loops at DNA double-strand breaks to promote DNA repair and avoid chromosomal deletions.NAR cancer · 2020Article
- Alternative splicing in aging and longevity.Human genetics · 2020Review
- SAM68 interaction with U1A modulates U1 snRNP recruitment and regulates mTor pre-mRNA splicing.Nucleic acids research · 2019Article
- Accumulation of poly(A) RNA in nuclear granules enriched in Sam68 in motor neurons from the SMNΔ7 mouse model of SMA.Scientific reports · 2018Article
- Signaling Pathways Involved in the Regulation of mRNA Translation.Molecular and cellular biology · 2018Review
- Clinical significance and effect of Sam68 expression in gastric cancer.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The requirement for alternative splicing during adipogenesis is poorly understood. The Sam68 RNA binding protein is a known regulator of alternative splicing, and mice deficient for Sam68 exhibit adipogenesis defects due to defective mTOR signaling. Sam68 null preadipocytes were monitored for alternative splicing imbalances in components of the mTOR signaling pathway. Herein, we report that Sam68 regulates isoform expression of the ribosomal S6 kinase gene (Rps6kb1). Sam68-deficient adipocytes express Rps6kb1-002 and its encoded p31S6K1 protein, in contrast to wild-type adipocytes that do not express this isoform. Sam68 binds an RNA sequence encoded by Rps6kb1 intron 6 and prevents serine/arginine-rich splicing factor 1 (SRSF1)-mediated alternative splicing of Rps6kb1-002, as assessed by cross-linking and immunoprecipitation (CLIP) and minigene assays. Depletion of p31S6K1 with small interfering RNAs (siRNAs) partially restored adipogenesis of Sam68-deficient preadipocytes. The ectopic expression of p31S6K1 in wild-type 3T3-L1 cells resulted in adipogenesis differentiation defects, showing that p31S6K1 is an inhibitor of adipogenesis. Our findings indicate that Sam68 is required to prevent the expression of p31S6K1 in adipocytes for adipogenesis to occur.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.