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Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies

International journal of molecular sciences, 2021-05, Vol.22 (10), p.5303

2021

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GLP-1 and GIP receptors signal through distinct β-arrestin 2-dependent pathways to regulate pancreatic β cell function

Cell reports (Cambridge), 2023-11, Vol.42 (11), p.113326-113326, Article 113326

2023

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Insulin-Degrading Enzyme Inhibition, a Novel Therapy for Type 2 Diabetes?

Cell metabolism, 2014-08, Vol.20 (2), p.201-203

2014

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The nuclear receptor REV-ERBα is implicated in the alteration of β-cell autophagy and survival under diabetogenic conditions

Cell death & disease, 2022-04, Vol.13 (4), p.353-353, Article 353

2022

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Targeting protein misfolding to protect pancreatic beta-cells in type 2 diabetes

Current opinion in pharmacology, 2018-12, Vol.43, p.104-110

Costes, Safia

2018

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The CDK4-pRB-E2F1 pathway controls insulin secretion

Nature cell biology, 2009-08, Vol.11 (8), p.1017-1023

2009

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Calcium-activated Calpain-2 Is a Mediator of Beta Cell Dysfunction and Apoptosis in Type 2 Diabetes

The Journal of biological chemistry, 2010-01, Vol.285 (1), p.339-348

2010

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Degradation of cAMP-Responsive Element–Binding Protein by the Ubiquitin-Proteasome Pathway Contributes to Glucotoxicity in β-Cells and Human Pancreatic Islets

Diabetes (New York, N.Y.), 2009-05, Vol.58 (5), p.1105-1115

2009

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Autophagy defends pancreatic β cells from human islet amyloid polypeptide-induced toxicity

The Journal of clinical investigation, 2014-08, Vol.124 (8), p.3489-3500

2014

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Glucagon Promotes cAMP-response Element-binding Protein Phosphorylation via Activation of ERK1/2 in MIN6 Cell Line and Isolated Islets of Langerhans

The Journal of biological chemistry, 2004-05, Vol.279 (19), p.20345-20355

2004

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Activation of Melatonin Signaling Promotes β-Cell Survival and Function

Molecular endocrinology (Baltimore, Md.), 2015-05, Vol.29 (5), p.682-692

2015

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β-Cell Failure in Type 2 Diabetes: A Case of Asking Too Much of Too Few?

Diabetes (New York, N.Y.), 2013-02, Vol.62 (2), p.327-335

2013

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UCHL1 deficiency exacerbates human islet amyloid polypeptide toxicity in β-cells: Evidence of interplay between the ubiquitin/proteasome system and autophagy

Autophagy, 2014-06, Vol.10 (6), p.1004-1014

2014

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Erratum. β-Cell Dysfunctional ERAD/Ubiquitin/Proteasome System in Type 2 Diabetes Mediated by Islet Amyloid Polypeptide–Induced UCH-L1 Deficiency. Diabetes 2011;60:227–238

Diabetes (New York, N.Y.), 2023-12, Vol.72 (12), p.1881-1881

2023

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GLP-1 Mediates Antiapoptotic Effect by Phosphorylating Bad through a β-Arrestin 1-mediated ERK1/2 Activation in Pancreatic β-Cells

The Journal of biological chemistry, 2010-01, Vol.285 (3), p.1989-2002

2010

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325-LB: Circadian Clock Nuclear Receptor REV-ERBa Is a Novel Regulator of Beta-Cell Function, Survival, and Autophagy under Diabetogenic Conditions

Diabetes (New York, N.Y.), 2019-06, Vol.68 (Supplement_1)

2019

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β-Cell Dysfunctional ERAD/Ubiquitin/Proteasome System in Type 2 Diabetes Mediated by Islet Amyloid Polypeptide-Induced UCH-L1 Deficiency

Diabetes (New York, N.Y.), 2011-01, Vol.60 (1), p.227-238

2011

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ERK1/2 Control Phosphorylation and Protein Level of cAMP-Responsive Element–Binding Protein

Diabetes (New York, N.Y.), 2006-08, Vol.55 (8), p.2220-2230

2006

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Roles and Regulation of the Transcription Factor CREB in Pancreatic β -Cells

Current molecular pharmacology, 2011-11, Vol.4 (3), p.187-195

2011

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Cyclin-Dependent Kinase 5 Promotes Pancreatic β-Cell Survival via Fak-Akt Signaling Pathways

Diabetes (New York, N.Y.), 2011-04, Vol.60 (4), p.1186-1197

2011

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ERK1 is dispensable for mouse pancreatic beta cell function but is necessary for glucose-induced full activation of MSK1 and CREB

Diabetologia, 2017-10, Vol.60 (10), p.1999-2010

2017

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CA-100 - Rôle clé de la β-arrestine 1 dans la préservation de la fonction et de la masse des cellules β pancréatiques in vivo

Diabetes & metabolism, 2017-03, Vol.43 (2), p.A84-A85

2017

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CA-103 - L’altération fonctionnelle de l’histone acétyl-transférase p300 contribue à un déficit des cellules bêta pancréatiques dans des situations diabétogènes

Diabetes & metabolism, 2017-03, Vol.43 (2), p.A85-A85

2017

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CO-65 - La β-arrestine 2 joue un rôle clé dans la signalisation du récepteur GLP-1 dans les cellules β pancréatiques

Diabetes & metabolism, 2017-03, Vol.43 (2), p.A25-A26

2017

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L’altération fonctionnelle de l’histone acétyl-transférase p300 contribue à un déficit des cellules bêta pancréatiques dans des situations diabétogènes

Diabetes & metabolism, 2017-03, Vol.43 (2), p.A85

2017

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Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies

GLP-1 and GIP receptors signal through distinct β-arrestin 2-dependent pathways to regulate pancreatic β cell function

Insulin-Degrading Enzyme Inhibition, a Novel Therapy for Type 2 Diabetes?

The nuclear receptor REV-ERBα is implicated in the alteration of β-cell autophagy and survival under diabetogenic conditions

Targeting protein misfolding to protect pancreatic beta-cells in type 2 diabetes

The CDK4-pRB-E2F1 pathway controls insulin secretion

Calcium-activated Calpain-2 Is a Mediator of Beta Cell Dysfunction and Apoptosis in Type 2 Diabetes

Degradation of cAMP-Responsive Element–Binding Protein by the Ubiquitin-Proteasome Pathway Contributes to Glucotoxicity in β-Cells and Human Pancreatic Islets

Autophagy defends pancreatic β cells from human islet amyloid polypeptide-induced toxicity

Glucagon Promotes cAMP-response Element-binding Protein Phosphorylation via Activation of ERK1/2 in MIN6 Cell Line and Isolated Islets of Langerhans

Activation of Melatonin Signaling Promotes β-Cell Survival and Function

β-Cell Failure in Type 2 Diabetes: A Case of Asking Too Much of Too Few?

UCHL1 deficiency exacerbates human islet amyloid polypeptide toxicity in β-cells: Evidence of interplay between the ubiquitin/proteasome system and autophagy

Erratum. β-Cell Dysfunctional ERAD/Ubiquitin/Proteasome System in Type 2 Diabetes Mediated by Islet Amyloid Polypeptide–Induced UCH-L1 Deficiency. Diabetes 2011;60:227–238

GLP-1 Mediates Antiapoptotic Effect by Phosphorylating Bad through a β-Arrestin 1-mediated ERK1/2 Activation in Pancreatic β-Cells

325-LB: Circadian Clock Nuclear Receptor REV-ERBa Is a Novel Regulator of Beta-Cell Function, Survival, and Autophagy under Diabetogenic Conditions

β-Cell Dysfunctional ERAD/Ubiquitin/Proteasome System in Type 2 Diabetes Mediated by Islet Amyloid Polypeptide-Induced UCH-L1 Deficiency

ERK1/2 Control Phosphorylation and Protein Level of cAMP-Responsive Element–Binding Protein

Roles and Regulation of the Transcription Factor CREB in Pancreatic β -Cells

Cyclin-Dependent Kinase 5 Promotes Pancreatic β-Cell Survival via Fak-Akt Signaling Pathways

ERK1 is dispensable for mouse pancreatic beta cell function but is necessary for glucose-induced full activation of MSK1 and CREB

CA-100 - Rôle clé de la β-arrestine 1 dans la préservation de la fonction et de la masse des cellules β pancréatiques in vivo

CA-103 - L’altération fonctionnelle de l’histone acétyl-transférase p300 contribue à un déficit des cellules bêta pancréatiques dans des situations diabétogènes

CO-65 - La β-arrestine 2 joue un rôle clé dans la signalisation du récepteur GLP-1 dans les cellules β pancréatiques

L’altération fonctionnelle de l’histone acétyl-transférase p300 contribue à un déficit des cellules bêta pancréatiques dans des situations diabétogènes

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