In rice, the ideal plant architecture for high yield includes effective Lei Wang, For negative feedback, LIC bound to the core element CTCGC in the Proc Natl Acad Sci U S A – Li J, Nam KH, Vafeados D, Chory J ( ) BIN2, a new brassinosteroid-insensitive locus in Arabidopsis. A controversy exists as to whether de novo-generated neuronal tetraploid cells (Mosch et al., ; Yang et al., ) that undergo delayed. was added onto the cells in well culture plates for 3 hours, followed by addition of the original .. Acknowledgments. We thank Dr Jeffrey Vieira for providing rKSHV-GFP; Dr Lei Yao ; 9. Rubartelli A, Poggi A, Sitia R, Zocchi MR. HIV-I. Tat: a polypeptide for ; Masuzawa M.
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Endoplasmic reticulum ER stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. The PLA 2 family of enzymes catalyse the hydrolysis of the sn -2 substituent i. Apoptosis can be mediated via an extrinsic death receptor or intrinsic mitochondrial pathway [ 18 lel, 19 ]. Recently, apoptosis as a result of prolonged endoplasmic reticulum ER stress has gained recognition [ 1820 — 22 ] and this process has been implicated as a causative factor in Alzheimer’s and Parkinson’s diseases and cancer [ 23 ].
Interruption of any of these functions can lead to production of malfolded proteins and their accumulation in the ER.
When an imbalance between the load of client proteins on the ER and the ER’s ability to process the load occurs, it results in ER stress [ 3536 ].
Prolonged ER stress promotes induction of stress factors and activation of caspase, localizedintheER [ 192137 ], andcansubsequently lead to downstream activation of caspase-3, a protease that is central to the execution of apoptosis [ 38 ]. The PLA 2 s are a diverse group of enzymes that catalyse the hydrolysis of the sn -2 substituent from glycerophospholipid substrates to yield a free fatty acid and a 2-lysophospholipid [ 40 ].
Arachidonic acid and its oxygenated metabolites are potent bioactive mediators that can regulate physiological and pathophysiological processes. These include ankyrin repeats, acyl-CoA esterase activity, caspase-3 cleavage consensus sequence, bipartite nuclear localization sequence and calmodulin-binding domain.
Ceramides are lipid messengers that can suppress cell growth and induce apoptosis [ 60 ] and they can be generated via multiple mechanisms de novo synthesis, sphingomyelin hydrolysis, inhibition of ceramide degradation or salvage pathway. While examining lipid profiles that might be associated with ER stress, we unexpectedly found a temporal increase in ceramides in the INS-1 cells [ 61 ].
Ceramide accumulation has been linked to apoptosis through the intrinsic mitochondrial pathway. Although the ER- and mitochondria-associated apoptotic pathways can be activated independently, it has been suggested that induction of ER stress may lead to the triggering of intrinsic apoptotic processes [ 6263 ]. The authors would like to thank the expert technical assistance of Dr Mary Wohltmann and Mr Alan Bohrer for contributing to the work reviewed here. The authors do not declare any conflict of interest relevant to this manuscript.
National Center for Biotechnology InformationU. Author manuscript; available in PMC Jul Zhang1 B. Emani2 S. Barbour2 and S. Author information Copyright and License information Disclaimer. The publisher’s final edited version of this article is available at Diabetes Obes Metab. See other articles in PMC that cite the published article. Abstract Endoplasmic reticulum ER stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus.
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Acknowledgements The authors would like to lwi the expert technical assistance of Dr Mary Wohltmann and Mr Alan Bohrer for contributing to the work reviewed here. Footnotes Conflict leii Interests The authors do not declare any conflict of interest relevant to lie manuscript.
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Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes. The role of endoplasmic reticulum stress in nonimmune diabetes: Ann N Y Acad Sci. EIF2AK3, encoding translation initiation factor 2-alpha kinase 3, se mutated in patients with Wolcott-Rallison syndrome.
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Endoplasmic reticulum stress and the development of diabetes: Semin Cell Dev Biol. Quantitative distribution of phospholipids in neurons and glial cells isolated from rat cerebral cortex. Mass spectrometric characterization of arachidonate-containing plasmalogens in human pancreatic islets and in rat islet beta-cells and subcellular membranes. Mass spectrometric identification and quantitation of arachidonate-containing phospholipids in pancreatic islets: The phospholipase A 2 superfamily and its group numbering system.
Turk J, Ramanadham S. Can J Physiol Pharmacol. Regulation of group VIA phospholipase A 2 expression by sterol availability. Rat and human pancreatic islet cells contain a calcium ion independent phospholipase A 2 activity selective for hydrolysis of arachidonate which is stimulated by adenosine triphosphate and is specifically localized to islet beta-cells. Inhibition of arachidonate release by secretagogue-stimulated pancreatic islets suppresses both insulin secretion and the rise in beta-cell cytosolic calcium ion concentration.
Studies of the role of group vi phospholipase A 2 in fatty acid incorporation, phospholipid remodeling, lysophosphatidylcholine generation, and secretagogue-induced arachidonic acid release in pancreatic islets and insulinoma cells. Apoptosis in insulin-secreting cells. Distinct roles of two intracellular phospholipase A 2 s in fatty acid release in the cell death pathway. The Group VIA calcium-independent phospholipase A 2 participates in ER stress-induced INS-1 insulinoma cell apoptosis by promoting ceramide generation via hydrolysis of sphingomyelins by neutral sphingomyelinase.