RasGAP-Derived Fragment N Increases the Resistance of Beta Cells towards Apoptosis in NOD Mice and Delays the Progression from Mild to Overt Diabetes
Explore this paper's citation graph
Summary
Fragment N exerts therefore a protective effect on beta cells within the pro-diabetogenic NOD background and this prevents a fast progression from mild to overt diabetes.
- Type
- article
- Published
- 2011-07-25
- Cited by
- 16
- References
- 42
- Access
- Open access
- OpenAlex
- https://openalex.org/W1989448419
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:18402954
Keywords
Nod, NOD mice, Apoptosis, Endocrinology, Internal medicine
References
- Preparation of PCR-quality mouse genomic DNA with hot sodium hydroxide and tris (HotSHOT).
- Breeding of a non-obese, diabetic strain of mice.
- NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase
- The BCL-2 protein family: opposing activities that mediate cell death
- Role of the amino-terminal domains of MEKKs in the activation of NF kappa B and MAPK pathways and in the regulation of cell proliferation and apoptosis.
- Expression of an Uncleavable N-terminal RasGAP Fragment in Insulin-secreting Cells Increases Their Resistance toward Apoptotic Stimuli without Affecting Their Glucose-induced Insulin Secretion*
- Targeted expression of the anti-apoptotic gene CrmA to NOD pancreatic islets protects from autoimmune diabetes.
- Apoptotic signal transduction pathways in diabetes.
- Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation
- Cell Loss in Isolated Human Islets Occurs by Apoptosis
- The replication of beta cells in normal physiology, in disease and for therapy.
- β-Cell death during progression to diabetes
- Viral modulation of the host response via crmA/SPI‐2 expression
- Checkpoints in the progression of autoimmune disease: lessons from diabetes models.
- The NOD mouse: a model of immune dysregulation.
- The RasGAP N-terminal Fragment Generated by Caspase Cleavage Protects Cells in a Ras/PI3K/Akt-dependent Manner That Does Not Rely on NFκB Activation*
- Recovery from diabetes in mice by beta cell regeneration.
- Antiapoptotic Signaling Generated by Caspase-Induced Cleavage of RasGAP
- Mechanisms of β-Cell Death in Type 2 Diabetes
- Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes
Cited by
- HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality.
- RasGAP Shields Akt from Deactivating Phosphatases in Fibroblast Growth Factor Signaling but Loses This Ability Once Cleaved by Caspase-3*
- Role of mTOR, Bad, and Survivin in RasGAP Fragment N-Mediated Cell Protection
- The role of endogenous and exogenous RasGAP-derived fragment N in protecting cardiomyocytes from peroxynitrite-induced apoptosis.
- Caspase-3 and RasGAP: a stress-sensing survival/demise switch.
- HDLs Protect Pancreatic β-Cells Against ER Stress by Restoring Protein Folding and Trafficking
- Caspase-3 Protects Stressed Organs against Cell Death
- High-density lipoprotein, beta cells, and diabetes .
- The caspase-3–p120-RasGAP module generates a NF-κB repressor in response to cellular stress
- PAX4 preserves endoplasmic reticulum integrity preventing beta cell degeneration in a mouse model of type 1 diabetes mellitus
- Survival response in the skin
- The PI3K/Akt pathway is not a main driver in HDL-mediated cell protection.
- Crosstalk of the Caspase Family and Mammalian Target of Rapamycin Signaling
- Title : High-density lipoprotein , beta cells , and diabetes
- Cellular stress management by caspases.
Related papers
- Studies on the thymus of non-obese diabetic (NOD) mice: effect of transgene expression.
- Elevated glucagon-like peptide-1 plasma levels, as a possible adaptive response, in diabetic NOD mice.
- Direct evidence for the contribution of B cells to the progression of insulitis and the development of diabetes in non-obese diabetic mice.
- I-E+ nonobese diabetic mice develop insulitis and diabetes
- Altered autoimmune response in NOD-Alox15null mice
- Postnatal Hematopoiesis and Gut Microbiota in NOD Mice Deviate from C57BL/6 Mice
- Both central and peripheral tolerance mechanisms play roles in diabetes prevention in NOD-E transgenic mice
- Effect of the expression of DR alpha E beta NOD molecule on the development of insulitis and diabetes in the non-obese diabetic (NOD) mouse.
- Contribution of Different Mechanisms to Pancreatic Beta-cell Hyper-secretion in Non-obese Diabetic (NOD) Mice during Pre-diabetes*