ArticleInternational journal of molecular sciences2022
Phospholipid Scramblase 4 (PLSCR4) Regulates Adipocyte Differentiation via PIP3-Mediated AKT Activation.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- In vitro study of TSC1 deficiency in preadipocytes: insights into development and treatment options for tuberous sclerosis related lipomatosis.Orphanet journal of rare diseases · 2026Article
- Multi-omics characterization identifies conserved candidate gene and reveals breed-specific regulatory mechanisms underlying growth-related traits in pigs.BMC genomics · 2026Article
- Modulation of renal fibrosis-related signaling pathways by traditional Chinese medicine: molecular mechanisms and experimental evidence.International urology and nephrology · 2025Review
- Identification of PI3K-AKT Pathway-Related Genes and Construction of Prognostic Prediction Model for ccRCC.Cancer reports (Hoboken, N.J.) · 2024Article
- Genomic structural variation contributes to evolved changes in gene expression in high-altitude Tibetan sheep.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Z-Ligustilide Combined with Cisplatin Reduces PLPP1-Mediated Phospholipid Synthesis to Impair Cisplatin Resistance in Lung Cancer.International journal of molecular sciences · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Phospholipid scramblase 4 (PLSCR4) is a member of a conserved enzyme family with high relevance for the remodeling of phospholipid distribution in the plasma membrane and the regulation of cellular signaling. While PLSCR1 and -3 are involved in the regulation of adipose-tissue expansion, the role of PLSCR4 is so far unknown. PLSCR4 is significantly downregulated in an adipose-progenitor-cell model of deficiency for phosphatase and tensin homolog (PTEN). PTEN acts as a tumor suppressor and antagonist of the growth and survival signaling phosphoinositide 3-kinase (PI3K)/AKT cascade by dephosphorylating phosphatidylinositol-3,4,5-trisphosphate (PIP3). Patients with PTEN germline deletion frequently develop lipomas. The underlying mechanism for this aberrant adipose-tissue growth is incompletely understood. PLSCR4 is most highly expressed in human adipose tissue, compared with other phospholipid scramblases, suggesting a specific role of PLSCR4 in adipose-tissue biology. In cell and mouse models of lipid accumulation, we found PLSCR4 to be downregulated. We observed increased adipogenesis in PLSCR4-knockdown adipose progenitor cells, while PLSCR4 overexpression attenuated lipid accumulation. PLSCR4 knockdown was associated with increased PIP3 levels and the activation of AKT. Our results indicated that PLSCR4 is a regulator of PI3K/AKT signaling and adipogenesis and may play a role in PTEN-associated adipose-tissue overgrowth and lipoma formation.
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