Endoplasmic reticulum stress-mediated apoptosis in pancreatic β-cells

Apoptosis

Volumn 7, Issue 4, 2002, Pages 335-345

  Oyadomari, S ^a   Araki, E ^a   Mori, M ^a  

^a KUMAMOTO UNIVERSITY   (Japan)

Author keywords

CHOP GADD153; Diabetes; Endoplasmic reticulum; Nitric oxide (NO); Pancreatic cells; PERK

Indexed keywords

ACTIVATING TRANSCRIPTION FACTOR 6; CASPASE 12; CHAPERONE; GROWTH ARREST AND DNA DAMAGE INDUCIBLE PROTEIN 153; INSULIN; NITRIC OXIDE; POTEIN GADD153; PROTEIN; PROTEIN IRE1; PROTEIN PERK; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG;

APOPTOSIS; CELL DEATH; CELL SURVIVAL; DIABETES MELLITUS; DNA DAMAGE; ENDOPLASMIC RETICULUM; INSULIN RELEASE; NON INSULIN DEPENDENT DIABETES MELLITUS; PANCREAS ISLET BETA CELL; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN DEGRADATION; PROTEIN FOLDING; REVIEW; SIGNAL TRANSDUCTION; STRESS; TRANSCRIPTION INITIATION; ANIMAL; BIOSYNTHESIS; GENETICS; METABOLISM; MOUSE; PANCREAS ISLET; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY;

ANIMAL; APOPTOSIS; DIABETES MELLITUS, NON-INSULIN-DEPENDENT; ENDOPLASMIC RETICULUM; ISLETS OF LANGERHANS; MICE; MOLECULAR CHAPERONES; NITRIC OXIDE; SUPPORT, NON-U.S. GOV'T; ANIMALS; DIABETES MELLITUS, TYPE 2;

MAMMALIA;

EID: 0036022403     PISSN: 13608185     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1016175429877     Document Type: Review

References (107)

1. Perspective: Postnatal pancreatic β cell growth
2. β-cell death during progression to diabetes
3. A choice of death - The signal - Transduction of immune-mediated β-cell apoptosis
4. Tripartite management of unfolded proteins in the endoplasmic reticulum
5. Stress signaling from the lumen of the endoplasmic reticulum: Coordination of gene transcriptional and translational controls
6. Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors
7. XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor
8. Complementary signaling pathways regulate the unfolded protein response and are required for C. elegans development
9. IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA
10. ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response
11. The lumenal domain of ATF6 senses ER stress and causes translocation of ATF6 from the ER to the Golgi
12. ER stress induces cleavage of membrane-bound ATF6 by the same proteases that process SREBPs
13. Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response
14. Identification and characterization of pancreatic eukaryotic initiation factor 2 α-subunit kinase, PEK, involved in translational control
15. Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase
16. Perk is essential for translational regulation and cell survival during the unfolded protein response
17. Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2α
18. Translational control by the ER transmembrane kinase/ribonuclease IRE1 under ER stress
19. Degradation of misfolded endoplasmic reticulum glycoproteins in Saccharomyces cerevisiae is determined by a specific oligosaccharide structure
20. Htm1 p, α mannosidase-like protein, is involved in glycoprotein degradation in yeast
21. Mnl1p, an α-mannosidase-like protein in yeast Saccharomyces cerevisiae, is required for endoplasmic reticulum-associated degradation of glycoproteins
22. A novel ER α-mannosidase-like protein accelerates ER-associated degradation
23. ER quality control: Towards an understanding at the molecular level
24. Molecular chaperones in the yeast endoplasmic reticulum maintain the solubility of proteins for retrotranslocation and degradation
25. Chaperone selection during glycoprotein translocation into the endoplasmic reticulum
26. Sec61p-independent degradation of the tail-anchored ER membrane protein Ubc6p
27. ER degradation of a misfolded luminal protein by the cytosolic ubiquitin-proteasome pathway
28. Degradation of subunits of the Sec61p complex, an integral component of the ER membrane, by the ubiquitin-proteasome pathway
29. Der1, a novel protein specifically required for endoplasmic reticulum degradation in yeast
30. Role of 26S proteasome and HRD genes in the degradation of 3-hydroxy-3-methylglutaryl-CoA reductase, an integral endoplasmic reticulum membrane protein
31. Der3p/Hrd1p is required for endoplasmic reticulum-associated degradation of misfolded lumenal and integral membrane proteins
32. Degradation of proteins from the ER of S. cerevisiae requires an intact unfolded protein response pathway
33. A regulatory link between ER-associated protein degradation and the unfolded-protein response
34. Functional and genomic analyses reveal an essential coordination between the unfolded protein response and ER-associated degradation
35. CHOP a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and functions as a dominant-negative inhibitor of gene transcription
36. Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153)
37. CHOP (GADD153) and its oncogenic variant, TLS-CHOP, have opposing effects on the induction of G1/S arrest
38. Ectopic expression of CHOP (GADD153) induces apoptosis in M1 myeloblastic leukemia cells
39. Nitric oxide-induced apoptosis in RAW 264.7 macrophages is mediated by endoplasmic reticulum stress pathway involving ATF6 and CHOP
40. CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum
41. Nitric oxide-induced apoprosis in pancreatic β cells is mediated by the endoplasmic reticulum stress pathway
42. Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes
43. Cloning of mammalian Irel reveals diversity in the ER stress responses
44. Regulated translation initiation controls stress-induced gene expression in mammalian cells
45. Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP kinase
46. Analysis of ATF3, a transcription factor induced by physiological stresses and modulated by gadd153/Chop10
47. CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins
48. Identification of novel stress-induced genes downstream of chop
49. CHOP-Dependent stress-inducible expression of a novel form of carbonic anhydrase VI
50. Inhibition of Bax channel-forming activity by Bcl-2
51. Proapoptotic BAX and BAK: A requisite gateway to mitochondrial dysfunction and death
52. Gadd153 sensitizes cells to endoplasmic reticulum stress by down-regulating Bcl2 and perturbing the cellular redox state
53. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1
54. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis
55. Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β
56. Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis
57. Activation of caspase-12, an endoplastic reticulum (ER) resident caspase, through tumor necrosis factor receptor-associated factor 2-dependent mechanism in response to the ER stress
58. Coupling endoplasmic reticulum stress to the cell death program. Mechanism of caspase activation
59. Different subcellular distribution of caspase-3 and caspase-7 following Fas-induced apoptosis in mouse liver
60. Apoptosis and the pathogenesis of IDDM: A question of life and death
61. Introduction and overview
62. p53 expression in nitric oxide-induced apoptosis
63. Poly (ADP-ribose) polymerase, nitric oxide and cell death
64. Cellular responses to DNA damage: Cell-cycle checkpoints, apoptosis and the roles of p53 and ATM
65. Nitric oxide-induced apoptosis: p53-dependent and p53-independent signalling pathways
66. Inactivation of the poly(ADP-ribose) polymerase gene affects oxygen radical and nitric oxide toxicity in islet cells
67. Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cells
68. Effect of nitric oxide on endoplasmic reticulum calcium homeostasis, protein synthesis and energy metabolism
69. Identification of novel cytokine-induced genes in pancreatic β-cells by high-density oligonucleotide arrays
70. Maintenance of calcium homeostasis in the endoplasmic reticulum by Bcl-2
71. 2+ stores and arachidonic acid metabolism
72. Calcium, a signaling molecule in the endoplasmic reticulum?
73. 2+-ATPase are differentially expressed in normal and diabetic islets of Langerhans
74. 2+-ATPase in skeletal muscle
75. Nitric oxide synthase in cardiac sarcoplasmic reticulum
76. The sarco/endoplasmic reticulum calcium-ATPase 2b is an endoplasmic reticulum stress-inducible protein
77. 3 R-3, expressed in pancreatic islets, kidney, gastrointestinal tract, and other tissues
78. 3 receptor and cGMP kinase Iβ
79. Activation of the cardiac calcium release channel (ryanodine receptor) by poly-S-nitrosylation
80. In situ activation of the type 2 ryanodine receptor in pancreatic cells requires cAMP-dependent phosphorylation
81. Insulin resistance. A multi-faceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease
82. Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans
83. Cellular composition of the human diabetic pancreas
84. A novel locus, Mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 (Akita) mutant mice
85. Mapping of murine diabetogenic gene mody on chromosome 7 at D7Mit258 and its involvement in pancreatic islet and β cell development during the perinatal period
86. A mutation in the insulin 2 gene induces diabetes with severe pancreatic β-cell dysfunction in the Mody mouse
87. Compensatory responses in mice carrying a null mutation for Ins1 or Ins2
88. -/- mice reveals a role for translational control in secretory cell survival
89. Translational control is required for the unfolded protein response and in vivo glucose homeostasis
90. EIF2AK3, encoding translation initiation factor 2-α kinase 3, is mutated in patients with Wolcott-Rallison syndrome
91. Autopsy findings in the Wolcott-Rallison syndrome
92. Beneficial effects of antioxidants in diabetes: Possible protection of pancreatic β-cells against glucose toxicity
93. Streptozotocin at low doses induces apoptosis and at high doses causes necrosis in a murine pancreatic β cell line, INS-1
94. Comparison of inhibition of glucose-stimulated insulin secretion in rat islets of Langerhans by streptozotocin and methyl and ethyl nitrosoureas and methanesulphonates. Lack of correlation with nitric oxide-releasing or O6-alkylating ability
95. Lipotoxic diseases
96. White ME Irs-2 coordinates Igf-1 receptor-mediated βcell development and peripheral insulin signalling
97. Disruption of IRS-2 causes type 2 diabetes in mice
98. Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors
99. Attenuation of FGF signalling in mouse β-cells leads to diabetes
100. Glucose stimulates protein modification by O-linked GIcNAc in pancreatic β cells: Linkage of O-linked GIcNAc to β cell death
101. β-cell death and mass in syngeneically transplanted islets exposed to short-and long-term hyperglycemia
102. Induction of apoptosis by human amylin in RINm5F islet β-cells is associated with enhanced expression of p53 and p21WAF1/CIP1
103. Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia
104. Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine differentiation in BETA2/neuroD-deficient mice
105. Dominant-negative suppression of HNF-1α results in mitochondrial dysfunction, INS-1 cell apoptosis, and increased sensitivity to ceramide-, but not to high glucose-induced cell death
106. Impaired insulin secretion and β-cell loss in tissue-specific knockout mice with mitochondrial diabetes
107. ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats