Endoplasmic reticulum stress in health and disease

Zhao, Lihong; Ackerman, Susan L.

doi:10.1016/j.ceb.2006.06.005

Cited by 396 publications

(336 citation statements)

References 75 publications

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“…Targeted disruption of the CHOP gene in Akita mice, a mouse line that spontaneously develops hyperglycemia with reduced β-cell mass, delayed the onset of diabetes [72]. Thus, it has been proposed that chronic disruption of ER homeostasis may contribute to the attrition of β-cell function and to impaired regulation of glucose homeostasis in diabetes [73][74][75].…”

Section: The Endoplasmic Reticulum Is a Target For Saturated Fatty Acidsmentioning

confidence: 99%

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

Gentile

Pagliassotti

2008

The Journal of Nutritional Biochemistry

206

156

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Section: The Endoplasmic Reticulum Is a Target For Saturated Fatty Acidsmentioning

confidence: 99%

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

Gentile

Pagliassotti

2008

The Journal of Nutritional Biochemistry

206

156

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“…For instance, halting of the global protein synthesis, through general translation arrest, elevates the expression of ER chaperons which enhances protein folding so as to maintain the quality control of proteins while the misfolded proteins get degraded through the ER-associated degradation (ERAD) and autophagy. However, if the ER stress is prolonged, then UPR activates apoptotic signaling which may progress through mitochondrial dependent or independent pathways [Reviews; [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

2015

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Endoplasmic reticulum (ER) is the site of protein synthesis, protein folding, maintainance of calcium homeostasis, synthesis of lipids and sterols. Genetic or environmental insults can alter its function generating ER stress. ER senses stress mainly by three stress sensor pathways, namely protein kinase R-like endoplasmic reticulum kinase-eukaryotic translation-initiation factor 2a, inositol-requiring enzyme 1a-X-box-binding protein 1 and activating transcription factor 6-CREBH, which induce unfolded protein responses (UPR) after the recognition of stress. Recent studies have demonstrated that ER stress and UPR signaling are involved in cancer, metabolic disorders, inflammatory diseases, osteoporosis and neurodegenerative diseases. However, the precise knowledge regarding involvement of ER stress in different disease processes is still debatable. Here we discuss the possible role of ER stress in various disorders on the basis of existing literature. An attempt has also been made to highlight the present knowledge of this field which may help to elucidate and conjure basic mechanisms and novel insights into disease processes which could assist in devising better future diagnostic and therapeutic strategies.

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“…ER stress can be a primary cause and a modifier of many important human diseases (6). For example, diabetes is a common metabolic disease, caused by misregulation of blood glucose levels.…”

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confidence: 99%

Using natural variation in Drosophila to discover previously unknown endoplasmic reticulum stress genes

Chow

Wolfner

Clark

2013

Proc. Natl. Acad. Sci. U.S.A.

111

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Natural genetic variation is a rich resource for identifying novel elements of cellular pathways such as endoplasmic reticulum (ER) stress. ER stress occurs when misfolded proteins accumulate in the ER and cells respond with the conserved unfolded protein response (UPR), which includes large-scale gene expression changes. Although ER stress can be a cause or a modifying factor of human disease, little is known of the amount of variation in the response to ER stress and the genes contributing to such variation. To study natural variation in ER stress response in a model system, we measured the survival time in response to tunicamycin-induced ER stress in flies from 114 lines from the sequenced Drosophila Genetic Reference Panel of wildderived inbred strains. These lines showed high heterogeneity in survival time under ER stress conditions. To identify the genes that may be driving this phenotypic variation, we profiled ER stressinduced gene expression and performed an association study. Microarray analysis identified variation in transcript levels of numerous known and previously unknown ER stress-responsive genes. Survival time was significantly associated with polymorphisms in candidate genes with known (i.e., Xbp1) and unknown roles in ER stress. Functional testing found that 17 of 25 tested candidate genes from the association study have putative roles in ER stress. In both approaches, one-third of ER stress genes had human orthologs that contribute to human disease. This study establishes Drosophila as a useful model for studying variation in ER stress and identifying ER stress genes that may contribute to human disease.

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Endoplasmic reticulum stress in health and disease

Cited by 396 publications

References 75 publications

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

Using natural variation in Drosophila to discover previously unknown endoplasmic reticulum stress genes

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