RIPK1 is dispensable for cell death regulation in β-cells during hyperglycemia.

Saved in:
Bibliographic Details
Title: RIPK1 is dispensable for cell death regulation in β-cells during hyperglycemia.
Authors: Veli Ö; Department of Translational Genomics, Faculty of Medicine, University of Cologne, Cologne, Germany; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany., Kaya Ö; Department of Translational Genomics, Faculty of Medicine, University of Cologne, Cologne, Germany; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany., Varanda AB; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany; Institute of Biochemistry I, Medical Faculty, University of Cologne, 50931 Cologne, Germany., Hildebrandt X; Department of Translational Genomics, Faculty of Medicine, University of Cologne, Cologne, Germany; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany., Xiao P; Inflammation and Cell Death Signalling group, Signal Transduction and Metabolism Laboratory, Université libre de Bruxelles, Brussels, Belgium., Estornes Y; VIB Center for Inflammation Research, 9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium., Poggenberg M; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany., Wang Y; Department of Translational Genomics, Faculty of Medicine, University of Cologne, Cologne, Germany; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany., Pasparakis M; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany; Institute for Genetics, University of Cologne, Cologne, Germany., Bertrand MJM; VIB Center for Inflammation Research, 9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium., Walczak H; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany; Institute of Biochemistry I, Medical Faculty, University of Cologne, 50931 Cologne, Germany., Annibaldi A; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany., Cardozo AK; Inflammation and Cell Death Signalling group, Signal Transduction and Metabolism Laboratory, Université libre de Bruxelles, Brussels, Belgium., Peltzer N; Department of Translational Genomics, Faculty of Medicine, University of Cologne, Cologne, Germany; Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne, Germany. Electronic address: m.peltzer@uni-koeln.de.
Source: Molecular metabolism [Mol Metab] 2024 Sep; Vol. 87, pp. 101988. Date of Electronic Publication: 2024 Jul 14.
Publication Type: Journal Article
Journal Info: Publisher: Elsevier GmbH Country of Publication: Germany NLM ID: 101605730 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2212-8778 (Electronic) Linking ISSN: 22128778 NLM ISO Abbreviation: Mol Metab Subsets: MEDLINE
Database: MEDLINE Ultimate
Description
ISSN:2212-8778
DOI:10.1016/j.molmet.2024.101988