ArticleMolecular metabolism2019
Dysregulation of PP2A-Akt interaction contributes to Sucrose non-fermenting related kinase (SNRK) deficiency induced insulin resistance in adipose tissue.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring the Phosphoregulatory Network of Human Sucrose Non-Fermenting 1-Related Kinase.Biology · 2026Article
- Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.Biochemistry and biophysics reports · 2025Article
- PP2A-B56α is a key determinant of cardiac protein phosphorylation and functional responses to β-adrenergic signalling.Journal of molecular and cellular cardiology plus · 2025Article
- SNRK tames mTOR against metabolic dysfunction-associated steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- SNRK modulates mTOR-autophagy pathway for liver lipid homeostasis in MAFLD.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Navigating the Maze of Kinases: CaMK-like Family Protein Kinases and Their Role in Atherosclerosis.International journal of molecular sciences · 2024Review
- Sphingosine-1-phosphate suppresses GLUT activity through PP2A and counteracts hyperglycemia in diabetic red blood cells.Nature communications · 2023Article
- DNA Damage and Nuclear Morphological Changes in Cardiac Hypertrophy Are Mediated by SNRK Through Actin Depolymerization.Circulation · 2023Article
- DNA damage and nuclear morphological changes in cardiac hypertrophy are mediated by SNRK through actin depolymerization.bioRxiv : the preprint server for biology · 2023Article
- Ser/Thr phosphatases: One of the key regulators of insulin signaling.Reviews in endocrine & metabolic disorders · 2022Review
- Inflammatory Signaling and Brown Fat Activity.Frontiers in endocrinology · 2020Review
- Article
- A disorder-related variant (E420K) of a PP2A-regulatory subunit (PPP2R5D) causes constitutively active AKT-mTOR signaling and uncoordinated cell growth.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveWe previously identified Sucrose non-fermenting related kinase (SNRK) as a regulator of adipose inflammation and energy homeostasis. In this study, we aimed to investigate the role of SNRK in insulin signaling in white (WAT) and brown adipose tissue (BAT).
methodsAdipose tissue specific (SNRK deficiency in both WAT and BAT) and BAT specific knockout mouse models were employed. Phosphoproteomic studies were conducted to identify the novel SNRK pathway regulating insulin signaling in adipose tissue.
resultsSNRK ablation is sufficient to inhibit insulin-stimulated AKT phosphorylation and glucose uptake in both WAT and BAT. Phosphoproteomic study using SNRK deficient versus wild type BAT samples revealed 99% reduction of phosphorylation on Serine 80 of PPP2R5D, the regulatory subunit of Protein phosphatase 2A (PP2A). Drastic (142.5-fold) induction of phosphorylation on Serine 80 of PPP2R5D was observed in SNRK-deficient primary brown adipocytes overexpressing SNRK compared to control protein. In vitro phosphorylation reaction followed by targeted phosphoproteomic detection further confirms that human recombinant SNRK is able to phosphorylate human recombinant PPP2R5D. Dephosphorylated PPP2R5D promotes constitutive assembly of PP2A-AKT complex, therefore inhibits insulin-induced AKT phosphorylation and subsequent glucose uptake in both BAT and WAT. Knockdown of PPP2R5D in adipocytes can improve insulin sensitivity in adipocytes without SNRK expression.
conclusionsOur findings demonstrate that SNRK regulates insulin signaling through controlling PPP2R5D phosphorylation, which subsequently impacts PP2A activity and then AKT phosphorylation in both WAT and BAT. SNRK may represent a promising potential target for treating insulin resistance-related metabolic disorders.
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