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Diabetes|July 26, 2023
Glucose Controls Glucagon Secretion by Regulating Fatty Acid Oxidation in Pancreatic α-CellsSarah L Armour, Alexander Frueh, Margarita V Chibalina, et al.Human Molecular Genetics|May 26, 2009
Uromodulin mutations causing familial juvenile hyperuricaemic nephropathy lead to protein maturation defects and retention in the endoplasmic reticulumSiân E Williams, Anita A C Reed, Juris Galvanovskis, et al.International Journal of Molecular Sciences|June 10, 2023
Chemerin as an Inducer of β Cell Proliferation Mediates Mitochondrial Homeostasis and Promotes β Cell Mass ExpansionMin Li, Ruifan Zhang, Qian Ge, et al.Nature Communications|November 25, 2016
Hyperglycaemia induces metabolic dysfunction and glycogen accumulation in pancreatic β-cellsMelissa F Brereton, Maria Rohm, Kenju Shimomura, et al.Nature Cell Biology|March 21, 2007
R-type Ca(2+)-channel-evoked CICR regulates glucose-induced somatostatin secretionQuan Zhang, Martin Bengtsson, Chris Partridge, et al.Diabetes|February 6, 2013
Tolbutamide controls glucagon release from mouse islets differently than glucose: involvement of K(ATP) channels from both α-cells and δ-cellsRui Cheng-Xue, Ana Gómez-Ruiz, Nancy Antoine, et al.The Journal of Biological Chemistry|October 2, 2014
Pancreatic and duodenal homeobox protein 1 (Pdx-1) maintains endoplasmic reticulum calcium levels through transcriptional regulation of sarco-endoplasmic reticulum calcium ATPase 2b (SERCA2b) in the islet β cellJustin S Johnson, Tatsuyoshi Kono, Xin Tong, et al.Biochemical and Biophysical Research Communications|July 4, 2021
LDHA is enriched in human islet alpha cells and upregulated in type 2 diabetesPaulina Karen Mendoza Sanchez, Mona Khazaei, Eva Gatineau, et al.Diabetes|August 23, 2018
Impaired Store-Operated Calcium Entry and STIM1 Loss Lead to Reduced Insulin Secretion and Increased Endoplasmic Reticulum Stress in the Diabetic β-CellTatsuyoshi Kono, Xin Tong, Solaema Taleb, et al.Diabetes|August 18, 2018
Somatostatin Is Only Partly Required for the Glucagonostatic Effect of Glucose but Is Necessary for the Glucagonostatic Effect of KATP Channel BlockersBao-Khanh Lai, Heeyoung Chae, Ana Gómez-Ruiz, et al.Pageof 23