دورية أكاديمية
أعرض في EDS

Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis.

التفاصيل البيبلوغرافية
العنوان: Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis.
المؤلفون: Nagao H; Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA., Jayavelu AK; Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152, Martinsried, Germany.; Proteomics and Cancer Cell Signaling Group, Clinical Cooperation Unit Pediatric Leukemia, German Cancer Research Center (DKFZ), Heidelberg, Germany., Cai W; Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA.; Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, 11568, USA., Pan H; Bioinformatics and Biostatistics Core, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA., Dreyfuss JM; Bioinformatics and Biostatistics Core, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA., Batista TM; Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA., Brandão BB; Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA., Mann M; Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152, Martinsried, Germany., Kahn CR; Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA. c.ronald.kahn@joslin.harvard.edu.
المصدر: Nature communications [Nat Commun] 2023 Jan 04; Vol. 14 (1), pp. 57. Date of Electronic Publication: 2023 Jan 04.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Apoptosis*/genetics , Cell Division*/genetics , Protein-Tyrosine Kinases*/metabolism , Receptor, Insulin*/genetics , Receptor, Insulin*/metabolism , Cellular Senescence*/genetics, Insulin/metabolism ; Ligands ; Phosphorylation ; Humans ; Animals ; Mice
مستخلص: Insulin acts through the insulin receptor (IR) tyrosine kinase to exert its classical metabolic and mitogenic actions. Here, using receptors with either short or long deletion of the β-subunit or mutation of the kinase active site (K1030R), we have uncovered a second, previously unrecognized IR signaling pathway that is intracellular domain-dependent, but ligand and tyrosine kinase-independent (LYK-I). These LYK-I actions of the IR are linked to changes in phosphorylation of a network of proteins involved in the regulation of extracellular matrix organization, cell cycle, ATM signaling and cellular senescence; and result in upregulation of expression of multiple extracellular matrix-related genes and proteins, down-regulation of immune/interferon-related genes and proteins, and increased sensitivity to apoptosis. Thus, in addition to classical ligand and tyrosine kinase-dependent (LYK-D) signaling, the IR regulates a second, ligand and tyrosine kinase-independent (LYK-I) pathway, which regulates the cellular machinery involved in senescence, matrix interaction and response to extrinsic challenges.
(© 2023. The Author(s).)
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معلومات مُعتمدة: K01 DK120740 United States DK NIDDK NIH HHS; P30 DK036836 United States DK NIDDK NIH HHS; R01 DK128429 United States DK NIDDK NIH HHS; P30 DK057521 United States DK NIDDK NIH HHS; R01 DK031036 United States DK NIDDK NIH HHS
المشرفين على المادة: 0 (Insulin)
0 (Ligands)
EC 2.7.10.1 (Protein-Tyrosine Kinases)
EC 2.7.10.1 (Receptor, Insulin)
تواريخ الأحداث: Date Created: 20230104 Date Completed: 20230123 Latest Revision: 20230306
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9812992
DOI: 10.1038/s41467-022-35693-5
PMID: 36599833
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-022-35693-5