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Article ; Online: Retraction: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion.

Fonseca, Sonya G / Urano, Fumihiko / Weir, Gordon C / Gromada, Jesper / Burcin, Mark

2014 Volume 17, Issue 1, Page(s) 105

Language	English
Publishing date	2014-12-23
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb3088
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Article ; Online: Endoplasmic reticulum stress and pancreatic β-cell death.

Fonseca, Sonya G / Gromada, Jesper / Urano, Fumihiko

Trends in endocrinology and metabolism: TEM

2011 Volume 22, Issue 7, Page(s) 266–274

Abstract: In pancreatic β-cells, the endoplasmic reticulum (ER) is an important cellular compartment for insulin biosynthesis, which accounts for half of the total protein production in these cells. Protein flux through the ER must be carefully monitored to ... ...

Abstract	In pancreatic β-cells, the endoplasmic reticulum (ER) is an important cellular compartment for insulin biosynthesis, which accounts for half of the total protein production in these cells. Protein flux through the ER must be carefully monitored to prevent dysregulation of ER homeostasis and stress. ER stress elicits a signaling cascade known as the unfolded protein response (UPR), which influences both life and death decisions in cells. β-cell loss is a pathological component of both type 1 and type 2 diabetes, and recent findings suggest that ER stress is involved. In this review, we address the transition from the physiological ER stress response to the pathological response, and explore the mechanisms of ER stress-mediated β-cell loss during the progression of diabetes.
MeSH term(s)	Animals ; Cell Death ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/prevention & control ; Disease Progression ; Endoplasmic Reticulum/metabolism ; Humans ; Insulin-Secreting Cells/metabolism ; Molecular Targeted Therapy ; Oxidative Stress ; Protein Biosynthesis ; Stress, Physiological ; Unfolded Protein Response
Language	English
Publishing date	2011-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2011.02.008
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Article: Endoplasmic reticulum stress and pancreatic β-cell death

Fonseca, Sonya G / Gromada, Jesper / Urano, Fumihiko

Trends in endocrinology & metabolism. 2011 July, v. 22, no. 7

2011

Abstract	In pancreatic β-cells, the endoplasmic reticulum (ER) is an important cellular compartment for insulin biosynthesis, which accounts for half of the total protein production in these cells. Protein flux through the ER must be carefully monitored to prevent dysregulation of ER homeostasis and stress. ER stress elicits a signaling cascade known as the unfolded protein response (UPR), which influences both life and death decisions in cells. β-cell loss is a pathological component of both type 1 and type 2 diabetes, and recent findings suggest that ER stress is involved. In this review, we address the transition from the physiological ER stress response to the pathological response, and explore the mechanisms of ER stress-mediated β-cell loss during the progression of diabetes.
Keywords	biosynthesis ; endoplasmic reticulum ; homeostasis ; insulin ; islets of Langerhans ; noninsulin-dependent diabetes mellitus ; stress response ; unfolded protein response
Language	English
Dates of publication	2011-07
Size	p. 266-274.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2011.02.008
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Stress hypERactivation in the β-cell.

Fonseca, Sonya G / Urano, Fumihiko / Burcin, Mark / Gromada, Jesper

Islets

2010 Volume 2, Issue 1, Page(s) 1–9

Abstract: In pancreatic β-cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the β-cell, such as a high demand for ... ...

Abstract	In pancreatic β-cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the β-cell, such as a high demand for insulin secretion, can lead to an imbalance in protein homeostasis and lead to ER stress. This stress can be mitigated by an adaptive, cellular response, the unfolded protein response (UPR). UPR activation is vital to the survival of β-cells, as these cells represent one of the most susceptible tissues for ER stress, due to their highly secretory function. However, in some cases, this response is not sufficient to relieve stress, leading to apoptosis and contributing to the pathogenesis of diabetes. Recent evidence shows that ER stress plays a significant role in both type 1 and type 2 diabetes. In this review, we outline the mechanisms of ER stress-mediated β-cell death and focus on the role of ER stress in various forms of diabetes, particularly a genetic form of diabetes called Wolfram syndrome.
MeSH term(s)	Animals ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/physiology ; Homeostasis/physiology ; Humans ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/physiology ; Models, Biological ; Stress, Physiological/physiology ; Unfolded Protein Response/physiology ; Wolfram Syndrome/etiology ; Wolfram Syndrome/metabolism
Language	English
Publishing date	2010-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1938-2022
ISSN (online)	1938-2022
DOI	10.4161/isl.2.1.10456
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Article: Endoplasmic reticulum stress signaling in pancreatic beta-cells.

Fonseca, Sonya G / Lipson, Kathryn L / Urano, Fumihiko

Antioxidants & redox signaling

2007 Volume 9, Issue 12, Page(s) 2335–2344

Abstract: Pancreatic beta-cells are specialized for the production and regulated secretion of insulin to control blood-glucose levels. Increasing evidence indicates that stress-signaling pathways emanating from the endoplasmic reticulum (ER) are important in the ... ...

Abstract	Pancreatic beta-cells are specialized for the production and regulated secretion of insulin to control blood-glucose levels. Increasing evidence indicates that stress-signaling pathways emanating from the endoplasmic reticulum (ER) are important in the maintenance of beta-cell homeostasis. Under physiological conditions, ER stress signaling has beneficial effects on beta-cells. Timely and proper activation of ER stress signaling is crucial for generating the proper amount of insulin in proportion to the need for it. In contrast, chronic and strong activation of ER stress signaling has harmful effects, leading to beta-cell dysfunction and death. Therefore, to dissect the molecular mechanisms of beta-cell failure and death in diabetes, it is necessary to understand the complex network of ER stress-signaling pathways. This review focuses on the function of the ER stress-signaling network in pancreatic beta-cells.
MeSH term(s)	Animals ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/physiology ; Humans ; Insulin-Secreting Cells/physiology ; Models, Biological ; Pancreas/cytology ; Pancreas/physiology ; Signal Transduction ; Stress, Physiological
Language	English
Publishing date	2007-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2007.1790
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5488: Show issues

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Article ; Online: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion.

Fonseca, Sonya G / Urano, Fumihiko / Weir, Gordon C / Gromada, Jesper / Burcin, Mark

publication RETRACTED

Nature cell biology

2012 Volume 14, Issue 10, Page(s) 1105–1112

Abstract: Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes. Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; ... ...

Abstract	Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes. Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear. Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion. Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling. ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion. These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion. The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes.
MeSH term(s)	Adenylyl Cyclases/chemistry ; Adenylyl Cyclases/metabolism ; Animals ; Cell Membrane/chemistry ; Cell Membrane/metabolism ; Cells, Cultured ; Cyclic AMP/biosynthesis ; Endoplasmic Reticulum Stress ; Glucagon-Like Peptide 1/pharmacology ; Glucose/pharmacology ; Humans ; Insulin/biosynthesis ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Male ; Membrane Proteins/chemistry ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mutation ; Rats ; Rats, Sprague-Dawley ; Signal Transduction
Chemical Substances	Insulin ; Membrane Proteins ; wolframin protein ; Glucagon-Like Peptide 1 (89750-14-1) ; Cyclic AMP (E0399OZS9N) ; Adenylyl Cyclases (EC 4.6.1.1) ; adenylyl cyclase 8 (EC 4.6.1.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2012-09-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Retracted Publication
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb2578
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes.

Lipson, Kathryn L / Fonseca, Sonya G / Urano, Fumihiko

Current molecular medicine

2006 Volume 6, Issue 1, Page(s) 71–77

Abstract: Increasing evidence suggests that stress signaling pathways emanating from the endoplasmic reticulum (ER) are important to the pathogenesis of both type 1 and type 2 diabetes. Recent observations indicate that ER stress signaling participates in ... ...

Abstract	Increasing evidence suggests that stress signaling pathways emanating from the endoplasmic reticulum (ER) are important to the pathogenesis of both type 1 and type 2 diabetes. Recent observations indicate that ER stress signaling participates in maintaining the ER homeostasis of pancreatic beta-cells. Either a high level of ER stress or defective ER stress signaling in beta-cells may cause an imbalance in ER homeostasis and lead to beta-cell apoptosis and autoimmune response. In addition, it has been suggested that ER stress attributes to insulin resistance in patients with type 2 diabetes. It is necessary to study the relationship between ER stress and diabetes in order to develop new therapeutic approaches to diabetes based on drugs that block the ER stress-mediated cell-death pathway and insulin resistance.
MeSH term(s)	Apoptosis ; Autoimmunity/immunology ; Diabetes Mellitus/immunology ; Diabetes Mellitus/pathology ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/pathology ; Humans ; Insulin-Secreting Cells/immunology ; Insulin-Secreting Cells/pathology
Language	English
Publishing date	2006-01-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064873-X
ISSN	1566-5240
ISSN	1566-5240
DOI	10.2174/156652406775574613
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5580: Show issues

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Article ; Online: Endoplasmic reticulum stress in beta-cells and development of diabetes.

Fonseca, Sonya G / Burcin, Mark / Gromada, Jesper / Urano, Fumihiko

Current opinion in pharmacology

2009 Volume 9, Issue 6, Page(s) 763–770

Abstract: The endoplasmic reticulum (ER) is a cellular compartment responsible for multiple important cellular functions including the biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. A myriad of pathological and ... ...

Abstract	The endoplasmic reticulum (ER) is a cellular compartment responsible for multiple important cellular functions including the biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. A myriad of pathological and physiological factors perturb ER function and cause dysregulation of ER homeostasis, leading to ER stress. ER stress elicits a signaling cascade to mitigate stress, the unfolded protein response (UPR). As long as the UPR can relieve stress, cells can produce the proper amount of proteins and maintain ER homeostasis. If the UPR, however, fails to maintain ER homeostasis, cells will undergo apoptosis. Activation of the UPR is critical to the survival of insulin-producing pancreatic beta-cells with high secretory protein production. Any disruption of ER homeostasis in beta-cells can lead to cell death and contribute to the pathogenesis of diabetes. There are several models of ER-stress-mediated diabetes. In this review, we outline the underlying molecular mechanisms of ER-stress-mediated beta-cell dysfunction and death during the progression of diabetes.
MeSH term(s)	Cell Death/genetics ; Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Models, Biological ; Signal Transduction ; Stress, Physiological ; Unfolded Protein Response ; Wolfram Syndrome/metabolism
Chemical Substances	Membrane Proteins ; wolframin protein
Language	English
Publishing date	2009-08-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2009.07.003
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Zs.A 5608: Show issues

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Article ; Online: Valproate, a mood stabilizer, induces WFS1 expression and modulates its interaction with ER stress protein GRP94.

Chihiro Kakiuchi / Shinsuke Ishigaki / Christine M Oslowski / Sonya G Fonseca / Tadafumi Kato / Fumihiko Urano

PLoS ONE, Vol 4, Iss 1, p e

2009 Volume 4134

Abstract: Valproate is a standard treatment for bipolar disorder and a first-line mood stabilizer. The molecular mechanisms underlying its actions in bipolar disorder are unclear. It has been suggested that the action of valproate is linked to changes in gene ... ...

Abstract	Valproate is a standard treatment for bipolar disorder and a first-line mood stabilizer. The molecular mechanisms underlying its actions in bipolar disorder are unclear. It has been suggested that the action of valproate is linked to changes in gene expression and induction of endoplasmic reticulum (ER) stress-response proteins.Here we show that valproate modulates the ER stress response through the regulation of WFS1, an important component for mitigating ER stress. Therapeutic concentrations of valproate induce expression of WFS1 mRNA and activate the WFS1 promoter. In addition, WFS1 forms a complex with GRP94, an ER stress-response protein, in which valproate dose-dependently enhances its dissociation from GRP94.These results suggest that the therapeutic effects of valproate in bipolar disorder may be mediated by WFS1 expression and its dissociation from GRP94.
Keywords	Medicine ; R ; Science ; Q
Subject code	612
Language	English
Publishing date	2009-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Valproate, a mood stabilizer, induces WFS1 expression and modulates its interaction with ER stress protein GRP94.

Kakiuchi, Chihiro / Ishigaki, Shinsuke / Oslowski, Christine M / Fonseca, Sonya G / Kato, Tadafumi / Urano, Fumihiko

PloS one

2009 Volume 4, Issue 1, Page(s) e4134

Abstract: Background: Valproate is a standard treatment for bipolar disorder and a first-line mood stabilizer. The molecular mechanisms underlying its actions in bipolar disorder are unclear. It has been suggested that the action of valproate is linked to changes ...

Abstract	Background: Valproate is a standard treatment for bipolar disorder and a first-line mood stabilizer. The molecular mechanisms underlying its actions in bipolar disorder are unclear. It has been suggested that the action of valproate is linked to changes in gene expression and induction of endoplasmic reticulum (ER) stress-response proteins. Principal findings: Here we show that valproate modulates the ER stress response through the regulation of WFS1, an important component for mitigating ER stress. Therapeutic concentrations of valproate induce expression of WFS1 mRNA and activate the WFS1 promoter. In addition, WFS1 forms a complex with GRP94, an ER stress-response protein, in which valproate dose-dependently enhances its dissociation from GRP94. Conclusions: These results suggest that the therapeutic effects of valproate in bipolar disorder may be mediated by WFS1 expression and its dissociation from GRP94.
MeSH term(s)	Animals ; Antimanic Agents/pharmacology ; Antimanic Agents/therapeutic use ; Biomarkers/metabolism ; Bipolar Disorder/drug therapy ; Cell Line ; Endoplasmic Reticulum/metabolism ; Gene Expression Regulation/drug effects ; Humans ; Lithium/pharmacology ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Promoter Regions, Genetic ; Stress, Physiological ; Valproic Acid/pharmacology ; Valproic Acid/therapeutic use
Chemical Substances	Antimanic Agents ; Biomarkers ; Membrane Glycoproteins ; Membrane Proteins ; endoplasmin ; wolframin protein ; Valproic Acid (614OI1Z5WI) ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2009-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0004134
Database	MEDical Literature Analysis and Retrieval System OnLINE

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