Готові списки джерел за темами / Reticular stress

Добірка наукової літератури з теми "Reticular stress"

Автор: Grafiati

Опубліковано: 15 червня 2024

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Статті в журналах з теми "Reticular stress":

Anyanwu, GE, and CA Agbor. "Correlation Between Oxidative Stress Generation, Reticular Fiber Density and Testicular Histomorphometric Parameters Of Streptozotocin-Induced Diabetic Wistar Rat." Journal of Bio-Science 29, no. 2 (August 4, 2021): 1–8. http://dx.doi.org/10.3329/jbs.v29i2.54949.

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The actual underlying mechanism of alterations in testicular histomorphometric parameters resulting from diabetes-induced oxidative stress is still not well understood because of the absence of supporting evidence from scientific experiments. This study was conducted to investigate the correlation between serum oxidative stress markers with testicular histomorphometric parameters and reticular fiber density of Streptozotocin-induced diabetic Wistar rat. The experiment included twenty eight adult male rats sorted into four groups, Group A (Control), other animals were sorted into treatment groups based on their blood glucose levels after inducing diabetes with 65 mg/kg/bw of streptozotocin, Groups B (100 - 200 mmol/l), Group C (210 - 250 mmol/l), Group D (260 - 300 mmol/l). At termination, Serum superoxide dimutase (SOD), catalase and melondialdehyde where evaluated using reagent based antioxidant enzyme assay while reticulum stain kits was used to demonstrate for reticular fiber density. Histomorphometric measurements were carried out using ocular micrometer after calibration on a light microscope. Statistical analysis was done using analysis of variance with p<0.05 considered significant. Results reveal that the higher the blood glucose levels in diabetic animals, the higher the serum concentration of oxidative stress markers. Density of reticular fiber increased with increase in blood glucose levels, while tubular diameter and epithelial height decreased with increase in increase in hyperglycaemic levels. In conclusion, there was a progressive increase in reticular fiber density and decrease in tubular diameter and epithelial height as a consequence of increase oxidative stress generation in diabetic model. J. Bio-Sci. 29(2): 01-08, 2021 (December)

Groenendyk, Jody, Xiao Fan, Zhenling Peng, Lukasz Kurgan, and Marek Michalak. "Endoplasmic reticulum and the microRNA environment in the cardiovascular system." Canadian Journal of Physiology and Pharmacology 97, no. 6 (June 2019): 515–27. http://dx.doi.org/10.1139/cjpp-2018-0720.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in the biology of the cardiac myocyte, and are involved in pathological cardiac function and remodeling. In this paper, we review a link between endoplasmic reticulum homeostasis and microRNA with an emphasis on the impact on stress responses in the cardiovascular system.

Carew, Nolan, Ashley Nelson, Zhitao Liang, Sage Smith, and Christine Milcarek. "Linking Endoplasmic Reticular Stress and Alternative Splicing." International Journal of Molecular Sciences 19, no. 12 (December 7, 2018): 3919. http://dx.doi.org/10.3390/ijms19123919.

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RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 (eleven-nineteen lysine-rich leukemia gene 2) induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response comprising a highly conserved set of genes crucial for cell survival; among these is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 mRNA and yet degrades other cellular mRNAs with related motifs. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2, a transcription elongation factor. ELL2 is necessary for immunoglobulin secretion and does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes.

Kim, Min Hwan, Yeon Hee Kim, Woobong Choi та Jong-Hwan Lee. "Alteration of Stress Fiber in Fibroblastic Reticular Cells via Lymphotoxin β Receptor Stimulation is Associated with Myosin". Journal of Life Science 25, № 5 (30 травня 2015): 585–93. http://dx.doi.org/10.5352/jls.2015.25.5.585.

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Milcarek, Christine. "Linking Endoplasmic Reticular Stress, ELL2, and Alternative Splicing." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 123.9. http://dx.doi.org/10.4049/jimmunol.202.supp.123.9.

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Abstract RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 transcription elongation factor induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response; among these stress proteins is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 and yet degrades other cellular mRNAs with related motifs, in a cell-specific manner. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2 which is necessary for immunoglobulin secretion; it does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes. unexpectedly, ubiquitination of c-myc by the ELL family members also plays a role in plasma-blast survival.

Griendling, Kathy K., Livia L. Camargo, Francisco J. Rios, Rhéure Alves-Lopes, Augusto C. Montezano, and Rhian M. Touyz. "Oxidative Stress and Hypertension." Circulation Research 128, no. 7 (April 2, 2021): 993–1020. http://dx.doi.org/10.1161/circresaha.121.318063.

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A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.

Aghili-Mehrizi, Sina, Eric Williams, Sandra Yan, Matthew Willman, Jonathan Willman, and Brandon Lucke-Wold. "Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence." Diseases 10, no. 2 (May 23, 2022): 30. http://dx.doi.org/10.3390/diseases10020030.

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Traumatic central nervous system injury is a leading cause of neurological injury worldwide. While initial neuroresuscitative efforts are focused on ameliorating the effects of primary injury through patient stabilization, secondary injury in neurotrauma is a potential cause of cell death, oxidative stress, and neuroinflammation. These secondary injuries lack defined therapy. The major causes of secondary injury in neurotrauma include endoplasmic reticular stress, mitochondrial dysfunction, and the buildup of reactive oxygen or nitrogenous species. Stress to the endoplasmic reticulum in neurotrauma results in the overactivation of the unfolded protein response with subsequent cell apoptosis. Mitochondrial dysfunction can lead to the release of caspases and the buildup of reactive oxygen species; several characteristics make the central nervous system particularly susceptible to oxidative damage. Together, endoplasmic reticulum, mitochondrial, and oxidative stress can have detrimental consequences, beginning moments and lasting days to months after the primary injury. Understanding these causative pathways has led to the proposal of various potential treatment options.

Pecoraro, Michela, Adele Serra, Maria Pascale, and Silvia Franceschelli. "Vx-809, a CFTR Corrector, Acts through a General Mechanism of Protein Folding and on the Inflammatory Process." International Journal of Molecular Sciences 24, no. 4 (February 20, 2023): 4252. http://dx.doi.org/10.3390/ijms24044252.

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Correct protein folding is the basis of cellular well-being; thus, accumulation of misfolded proteins within the endoplasmic reticulum (ER) leads to an imbalance of homeostasis that causes stress to the ER. Various studies have shown that protein misfolding is a significant factor in the etiology of many human diseases, including cancer, diabetes, and cystic fibrosis. Misfolded protein accumulation in the ER triggers a sophisticated signal transduction pathway, the unfolded protein response (UPR), which is controlled by three proteins, resident in ER: IRE1α, PERK, and ATF6. Briefly, when ER stress is irreversible, IRE1α induces the activation of pro-inflammatory proteins; PERK phosphorylates eIF2α which induces ATF4 transcription, while ATF6 activates genes encoding ER chaperones. Reticular stress causes an alteration of the calcium homeostasis, which is released from the ER and taken up by the mitochondria, leading to an increase in the oxygen radical species production, and consequently, to oxidative stress. Accumulation of intracellular calcium, in combination with lethal ROS levels, has been associated with an increase of pro-inflammatory protein expression and the initiation of the inflammatory process. Lumacaftor (Vx-809) is a common corrector used in cystic fibrosis treatment which enhances the folding of mutated F508del-CFTR, one of the most prevalent impaired proteins underlying the disease, promoting a higher localization of the mutant protein on the cell membrane. Here, we demonstrate that this drug reduces the ER stress and, consequently, the inflammation that is caused by such events. Thus, this molecule is a promising drug to treat several pathologies that present an etiopathogenesis due to the accumulation of protein aggregates that lead to chronic reticular stress.

Pogrebnyak, Tatyana, Elena Khorolskaya, Anzhelika Gorbacheva, and Irina Sagalaeva. "The dynamics of EEG correlates of activity of subcortical structures of the bird brain in conditions of chronic stress." BIO Web of Conferences 40 (2021): 01012. http://dx.doi.org/10.1051/bioconf/20214001012.

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In birds, acute stress (a three-day 12-hour inversion of the photomode) is associated with the dominant activity of the sympathetic hypothalamus and hippocampus, which suppress the tone of the parasympathetic section and the reticular formation of the midbrain. The effect of hyperglycemia on the background of a negative chronotropic effect indicates a mismatch of the functions of the autonomic sections of the hypothalamus on the 30th day. Chronic stress in birds (30-days crowding) causes persistent pathological stress of the functions of the anterior hypothalamus and reticular formation of the middle brain with the suppression of parasympathetic tone of the posterior hypothalamus and high functional activity of the hippocampus, determining the switching of the ventricles of the heart to a more economical mode of functioning by the 30th day. Using central cholinoblockers or tranquilizers, having a cholinoblocking component in the mechanism of its influence during neurogenic stress and in the post-stress period is excluded, but it is possible to use stressprotektors.

Jafarova, A. M., A. M. Mammadov, A. G. Gaziyev, and Sh R. Eyvazova. "Functional relationships of the cerebral cortex with subcortical structures in emotionally stressful conditions." Azerbaijan Journal of Physiology 38, no. 2 (December 31, 2023): 26–31. http://dx.doi.org/10.59883/ajp.7.

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Multidirectional and stable changes in phase shifts and cross-correlation coefficients of the cortical and subcortical stress rhythms occur under conditions of repeated irregular photostimulation, especially in the initial periods. Thus, cross-correlation functional connections, characterized by changes in the spatio-temporal relationships of the brain structures (posterior nuclei of the hypothalamus, reticular formation, and visual projection zones of the cerebral cortex), can be one of the indicators of the formation of stress. By using the parameters mentioned above, we can solve many issues related to the central mechanisms of stress. Our results show that functional connections between the cortical projection area and subcortical structures decrease under stress conditions, while connections between subcortical structures increase. We furthermore found that these EEG changes correlated with autonomic reactions in animals. Thus, these changes may lie based on central mechanisms of stress, and the results of changes in the EEG activity of the cerebral cortex and the cross-correlation parameters in the posterior nuclei of the hypothalamus and the reticular formation may allow preventive measures to be taken to affect these structures to reduce emotional stress.

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Дисертації з теми "Reticular stress":

Kraupner, Nicolas. "Conception d'outils pharmacologiques pour comprendre le rôle de l'Insulin Degrading Enzyme (IDE) dans la gestion du stress protéotoxique." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS039.

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L'Insulin Degrading Enzyme (IDE) est une métalloprotéase à zinc ubiquitaire retrouvée dans les compartiments extracellulaires et intracellulaires. IDE est impliquée dans la dégradation de peptides physiologiquement importants tels que l'insuline et d'autres peptides amyloïdogènes. Cependant, elle est remarquablement conservée dans les espèces et les tissus ne produisant pas ces peptides substrats. Cette observation suggère un rôle important d'IDE, non complétement identifié, et pas seulement corrélé à son activité catalytique. IDE est une enzyme pour laquelle on continue de découvrir de nouvelles implications biologiques et sa caractérisation est nécessaire pour mieux comprendre ces nouveaux rôles physiologiques ou pathologiques. En particulier, ces dernières années des études ont mis en évidence le lien entre IDE et le stress du réticulum endoplasmique (ER) notamment dans la voie ubiquitine-protéasome et la voie de l'Unfolded Protein Response (UPR). L'unité a récemment breveté l'utilisation d'une première série d'inhibiteurs d'IDE dont le chef de file est le BDM 44768 pour booster des cytotoxiques, notamment les inhibiteurs du protéasome tels que le carfilzomib, un des traitements de référence du myélome multiple.Basé sur cette série chimique du BDM 44768 et guidé par la structure cristallographique de nos composés dans IDE, plusieurs modulations ont été réalisées sur quatre différentes parties du pharmacophore ainsi que l'élaboration d'une série macrocyclique. Ces pharmacomodulations ont permis l'obtention de plusieurs molécules puissantes avec une activité de l'ordre du nanomolaire et possédant des propriétés pharmacocinétiques qui pourraient permettre leurs utilisations dans des modèles in vivo.Dans le but d'explorer les fonctions et l'implication d'IDE dans différents processus cellulaires cette thèse a également permis la conception et la synthèse de différents outils chimiques d'exploration. Premièrement, suite aux différents modes de liaison de nos molécules dans IDE, deux séries de sondes PROTAC ont été synthétisées. Leurs évaluations biologiques ont révélé qu'elles n'induisent pas la dégradation d'IDE mais de deux autres protéines, une protéine homologue à IDE, la pitrilysine, ainsi que la DPP3, une dipeptidyl peptidase. Pour terminer, deux sondes fluorescentes, qui restent à être optimisées, ont été conçues et synthétisées afin de pouvoir suivre la localisation d'IDE au sein de la cellule et plus particulièrement dans le réticulum endoplasmique dans le but de corréler cette localisation au cours du temps avec les effets sur les protéines de l'UPR et le stress réticulaire.Ainsi, lors de cette thèse de précieux résultats pour concevoir de futurs outils chimiques permettant l'étude d'IDE et l'élucidation des différents rôles de cette protéine ont été obtenus. De plus, plusieurs petites molécules puissantes, modulant l'activité d'IDE, ont été synthétisées dans le but de répondre aux différents besoins thérapeutiques associés à cette cible
Insulin Degrading Enzyme (IDE) is a ubiquitous zinc metalloprotease found in extracellular and intracellular compartments. IDE is involved in the degradation of physiologically important peptides such as insulin and other amyloidogenic peptides. However, it is remarkably conserved in species and tissues that do not produce these substrate peptides. This observation suggests an important role for IDE, not fully identified, and not only correlated with its catalytic activity. IDE is an enzyme for which new biological implications continue to be discovered and its characterization is necessary to better understand these new physiological or pathological roles. In particular, in the last few years studies have highlighted the link between IDE and endoplasmic reticulum (ER) stress, notably in the ubiquitin-proteasome pathway and the Unfolded Protein Response (UPR) pathway.The unit has recently patented the use of a first series of IDE inhibitors, with the BDM 44768 as lead compound, to boost cytotoxics, including proteasome inhibitors such as carfilzomib, one of the gold standard treatments for multiple myeloma.Based on this chemical series of BDM 44768 and guided by the crystallographic structure of our compounds in IDE, several modulations were performed on four different parts of the pharmacophore as well as the development of a macrocyclic series. These pharmacomodulations resulted in several potent molecules with nanomolar activity and pharmacokinetic properties that could allow their use in in vivo models.In order to explore the functions and involvement of IDEs in different cellular processes, this thesis also allowed the design and synthesis of different chemical exploration tools. First, following the different binding modes of our molecules in IDE, two series of PROTAC probes were synthesized. Their biological evaluations revealed that they do not induce the degradation of IDE but of two other proteins, a protein homologous to IDE, pitrilysin, and DPP3, a dipeptidyl peptidase. Finally, two fluorescent probes, that still need to be optimized, were designed and synthesized in order to be able to follow the localization of IDE within the cell and more particularly in the endoplasmic reticulum with the aim of correlating this localization over time with the effects on the UPR proteins and reticular stress.Thus, during this thesis, valuable results to design future chemical tools to study IDE and to elucidate the different roles of this protein were obtained. In addition, several potent small molecules modulating the activity of IDE were synthesized in order to address the different therapeutic needs associated with this target

Johnson, Charlotte. "Targeting endoplasmic reticulum stress and autophagy in cancer." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/84379/.

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Mammalian/mechanistic target of mTOR complex 1 (mTORC1) regulates multiple cellular processes, including de novo protein synthesis, autophagy and apoptosis. mTORC1 overactivation occurs in a range of cancers and benign tumour dispositions as a result of mutations which increase mitogenic stimulus or cause malfunction of the tuberous sclerosis complex, the prime regulator of mTORC1 activity. mTORC1 overactivation results in elevated endoplasmic reticulum (ER) stress which, at low levels, elicits a pro-survival response. However, prolonged or excessive ER stress causes cell death. The present study utilised clinically relevant drug combinations to simultaneously enhance levels of ER stress and inhibit compensatory survival pathways in in vitro models of mTORC1 overactivity in order to cause non-genotoxic cell death. The main drugs used in this study were nelfinavir, an ER stress-inducer, chloroquine, an autophagy inhibitor, and bortezomib, a proteasome inhibitor. The key findings of this study include identification of drug combinations nelfinavir and chloroquine, nelfinavir and mefloquine, or nelfinavir and bortezomib to induce significant and selective cell death in mTORC1-driven cells, as measured by flow cytometry with DRAQ7 staining and western blot analysis for cleavage of apoptotic markers. Cell death is likely mediated through ER stress signalling, as shown by increased ER stress markers at both the level of mRNA and protein. Of interest, this study found cell death as a result of combined treatment with nelfinavir was not dependent on proteasome inhibition by nelfinavir, or autophagy inhibition by chloroquine. Additionally, nelfinavir-chloroquine-mediated cell death was completely rescued by inhibition of the vacuolar ATPase by bafilomycin-A1. In conclusion, mTORC1 overactive cells have higher basal levels of ER stress which can be manipulated with drug treatment beyond a survivable threshold, whereas cells capable of reducing mTORC1 signalling are able to survive. This study ascertained a combination of nelfinavir and chloroquine, nelfinavir and mefloquine, or nelfinavir and bortezomib, to cause effective cytotoxicity in mTORC1-driven cells.

Chan, Cheuk-wing Wilson. "ER stress in the pathogenesis of osteochondrodysplasia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085192.

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Zachariah, Matshediso. "High selenium induces endothelial dysfunction via endoplasmic reticulum stress." Thesis, University of Surrey, 2017. http://epubs.surrey.ac.uk/845246/.

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Selenium (Se) is associated with insulin resistance and may affect endothelial function thereby increasing the risk of type 2 diabetes and associated cardiovascular disease (CVD). However, the molecular mechanisms involved are not clear. The endoplasmic-reticulum (ER) stress response is a mechanism involved in apoptosis induced by high Se in some cancer cells and, also in the pathogenesis of insulin resistance and endothelial dysfunction (ED). Thus, we hypothesised that high Se status causes ED through ER stress response. Endothelial cells (HUVECs) and EA.hy926 cell lines were treated with selenite (0.5-10 µM) for 24 hours in the presence or absence of the ER chemical chaperone, 4-phenylbutryic acid (PBA). ER stress markers were investigated using qPCR and western-blot technique. Endothelial function was assessed by the Griess assay, flow cytometry, Matrigel® and colourimetric assays. Data were expressed as S.E.M (p < 0.05) vs. control. High Se concentration (5-10 µM) compared to physiological concentration (0.5–2.0 µM) enhanced mRNA expression of ER-stress markers:- activating transcription factor-4 (ATF4), CAAA/enhanced-binding homologous protein (CHOP) and X-binding box-1 (XBP-1). In addition, high selenite concentration reduced nitric oxide production and angiogenic capacity in endothelial cells. Moreover, high selenite treatment significantly (p < 0.05) increased production of reactive oxygen species (ROS) and induced apoptosis through caspase-3/7 activity. Interestingly, PBA completely reversed all the effects of high selenite on endothelial function, indicating the involvement of the ER-stress response. High Se treatment caused endothelial dysfunction through the activation of the ER-stress response. This thesis additionally warns the public to be aware of the risks of the use of Se supplements as a prophylactic agent against oxidative-stress disease.

Voyias, Philip D. "Regulation of endoplasmic reticulum stress in adipose tissue metabolism." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/74256/.

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Obesity is the most significant risk factor for developing type II diabetes mellitus (T2DM). Obesity induces adipocyte endoplasmic reticulum (ER) stress, prior to onset of insulin resistance. A pathological inability of white adipose tissue (WAT) to expand to accommodate excess energy is predominantly due to impaired adipogenesis. The research hypothesis was that ER stress in human WAT is important in inducing WAT dysfunction and subsequent insulin resistance and T2DM. The aims of this study were to elucidate interactions of ER stress in human WAT and to characterise the role of ER stress in human adipogenesis. Abdominal SAT biopsies and anthropometry were collected from T2DM subjects before and after bariatric surgery and non-diabetic subjects. Preadipocytes were extracted from human WAT and differentiated into adipocytes. Lipogenesis, lipolysis, glucose uptake, insulin sensitivity, and ER stress and adipogenesis gene and protein expression were assessed in control cells and with ER stress inducers, inhibitors or siRNA. The results of this study found both restrictive and malabsorptive bariatric interventions are effective weight loss interventions for obese T2DM patients and result in significantly improved glucose and insulin levels six months after surgery. WAT health is better following restrictive procedures as shown by lower and better regulation of ER stress markers. Adipogenesis in primary human preadipocytes is influenced by adiposity and WAT depot and the IRE1-XBP1s UPR is essential in human adipogenesis. XBP1s plays a vital role upstream of CEBP and PPAR in human adipogenesis and it is necessary for mediating the action of insulin. Wnt10b plays an inhibitory role in human adipogenesis and acts independently of XBP1s. Collectively these findings suggest that WAT function is key for metabolic health and can be impaired by ER stress; however regulated adipogenesis may serve to improve WAT function and therefore improve metabolic health.

Furmanik, Malgorzata. "The role of endoplasmic reticulum stress in vascular calcification." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-endoplasmic-reticulum-stress-in-vascular-calcification(a0138614-e3d8-42ef-9cbf-02a01f6e6eaf).html.

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Vascular calcification (VC) is a health problem common in ageing populations, diabetes and chronic kidney disease. It leads to vascular stiffening and heart failure. VC is a regulated process mediated by vascular smooth muscle cells (VSMCs), with similarities to developmental osteogenesis. The exact molecular events responsible for triggering it are unknown. The endoplasmic reticulum (ER) is involved in folding of proteins. ER stress occurs as a result of unfolded protein accumulation and has been implicated in osteoblast differentiation and bone mineralization. Therefore, I hypothesized that ER stress signalling regulates osteogenic differentiation and calcification of VSMCs. I showed that calcification of human aortas was associated with changes in ER stress marker expression. Warfarin and TNFα, which are both established inducers of vascular calcification, increased expression of ER stress markers in VSMCs. ER stress modelled in human primary VSMCs in vitro increased their calcification and was shown to modulate expression of a number of bone related genes, such as BMP-2, Runx2, Osterix, ALP, BSP and OPG in VSMCs in vitro. I also demonstrated that ER stress activated features characteristic of a secretory phenotype in VSMCs, such as downregulation of SMC markers and components of TGFβ signalling related to contractile differentiation, as well as BMP-2. Taken together these results suggested that ER stress can induce changes that lead to osteogenic differentiation. To further explore the relationship between ER stress and osteogenic differentiation of VSMCs Osterix and ALP were studied in more detail. ALP activity was upregulated by ER stress, but did not change when VSMCs calcified. Promoter analysis showed that ALP might be regulated by ER stress via indirect mechanisms and potential regulators of ALP transcription were identified using proteomic analysis.

Darling, Nicola Jane. "Regulation of ER stress-induced cell death by the ERK1/2 signalling pathway." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708709.

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Preston, Amanda Miriam Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "The role of endoplasmic reticulum stress in beta-cell lipoapoptosis." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41231.

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Beta-cell failure is a key step in the progression from metabolic disorder to overt type 2 diabetes (T2D). This failure is characterised by both secretory defects and loss of beta-cell mass, the latter most likely through increases in the rate of apoptosis. Although the mechanisms underlying these beta-cell defects are unclear, evidence suggests that chronic exposure of beta-cells to elevated fatty acid (FA) plays a role in disease development in genetically susceptible individuals. Furthermore, it has been postulated that endoplasmic reticulum (ER) stress signalling pathways (the unfolded protein response; UPR) play a role in FA-induced beta-cell dysfunction. The broad aim of this thesis was to explore the nature of these relationships. Experiments detailed in this thesis demonstrate that MIN6 beta-cells mount a comprehensive ER stress response with exposure to elevated saturated fatty acid palmitate, but not the unsaturated fatty acid, oleate, within the low elevated physiological range. This response was time-dependent and involved both transcriptional and translational changes in UPR transducers and targets. The differential activation of ER stress in MIN6 beta-cells by saturated, but not unsaturated FA species may represent a mechanism of differential beta-cell death described in many studies with these FA. Furthermore, these experiments describe defects in ER to Golgi trafficking with chronic palmitate treatment, but not oleate or thapsigagin treatment, identifying this as a potential mechanism by which palmitate treatment induces ER stress. Moreover, these studies have shown the relevance to ER stress to a whole body model of T2D by demonstrating UPR activation in the islets of the db/db mouse. In conclusion, studies detailed in this thesis have demonstrated that ER stress occurs in in vitro and in vivo models of beta-cell lipotoxicity and apoptosis. In addition, these studies have identified defects in ER to Golgi trafficking as a mechanism by which palmitate treatment induces ER stress. These studies highlight the importance of ER stress in the development of T2D.

Katsoulieris, Elias. "Oxidatives and Endoplasmic Reticulum Stress in Kidney Priximal Tubule Cells." Thesis, University of Brighton, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506517.

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Niederreiter, Lukas. "Endoplasmic reticulum (ER) stress transcription factor Xbp1 in intestinal tumourigenesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708846.

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Книги з теми "Reticular stress":

Agostinis, Patrizia, and Samali Afshin, eds. Endoplasmic Reticulum Stress in Health and Disease. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9.

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Cornell, Paul. Saucer Country: The Reticulan Candidate. New York: DC Comics, 2013.

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Conn, P. Michael. The unfolded protein response und cellular stress. Amsterdam [etc.]: Elsevier, 2011.

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Robbins, Trevor. The Neuropsycho–Pharmacology of Attention. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.028.

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Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.

Endoplasmic Reticulum Stress In Health And Disease. Springer, 2012.

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Zhang, Kezhong, ed. Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-436-0.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2014.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer London, Limited, 2012.

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Wagner, Cameron. Endoplasmic Reticulum Stress: Regulation, Function and Role in Health and Disease. Nova Science Publishers, Incorporated, 2016.

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Schäfer, Patrick, Lorenzo Frigerio, Federica Brandizzi, and Stephen H. Howell, eds. Endoplasmic reticulum - shape and function in stress translation. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-344-8.

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Частини книг з теми "Reticular stress":

van Vliet, Alex, and Patrizia Agostinis. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1888-2.

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van Vliet, Alex, and Patrizia Agostinis. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer, 1519–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_1888.

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Agostinis, Patrizia. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer, 1240–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1888.

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Parmar, Vipul M., and Martin Schröder. "Sensing Endoplasmic Reticulum Stress." In Advances in Experimental Medicine and Biology, 153–68. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1680-7_10.

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Garg, Abhishek D., Agnieszka Kaczmarek, Dmitri V. Krysko, and Peter Vandenabeele. "ER Stress and Inflammation." In Endoplasmic Reticulum Stress in Health and Disease, 257–79. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_11.

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Qi, Zhihao, and Linxi Chen. "Endoplasmic Reticulum Stress and Autophagy." In Autophagy: Biology and Diseases, 167–77. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0602-4_8.

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Kaser, Arthur. "Autophagy and Endoplasmic Reticulum Stress." In Crohn's Disease and Ulcerative Colitis, 131–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33703-6_12.

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Yilmaz, Erkan. "Endoplasmic Reticulum Stress and Obesity." In Obesity and Lipotoxicity, 261–76. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48382-5_11.

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Xu, Hui, Feng-Yang Guo, and Zhong-Yuan Zhang. "Alteration of Endoplasmic Reticulum Stress." In Coal-burning Type of Endemic Fluorosis, 269–82. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1498-9_16.

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Madkour, Loutfy H. "Consequences of Oxidative Stress and ROS-Mediated Pathways Cellular Signaling Stress Response." In Nanoparticles Induce Oxidative and Endoplasmic Reticulum Stresses, 193–260. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-37297-2_5.

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Тези доповідей конференцій з теми "Reticular stress":

Carew, Jennifer S., Claudia M. Espitia, Kevin R. Kelly, Matt Coffey, James W. Freeman, and Steffan T. Nawrocki. "Abstract 2717: Reolysin: A novel reovirus-based agent that induces endoplasmic reticular stress in RAS-activated pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2717.

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Wark, Peter, Prabuddha Pathinyake, Alan Hsu, Kristy Parsons, and Lisa Wood. "Effect of oxidative stress and rhinovirus infection on mitochondrial/endoplasmic reticular function in human primary bronchial epithelial cells." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3989.

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Ponomareva, A. A., S. A. Dmitrieva, and F. V. Minibaeva. "Endoplasmic reticulum: stress from stress." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-361.

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Barbieri, Bruna. "ASPECTOS BIOQUÍMICOS DO PROCESSO INFLAMATÓRIO GERADO NO LÍQUEN PLANO ORAL E RELAÇÃO COM O POTENCIAL DE MALIGNIZAÇÃO DESTA PATOLOGIA: REVISÃO BIBLIOGRÁFICA." In I Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/661.

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Introdução: O líquen plano oral é uma doença mucocutânea inflamatória crônica mediada por células T, que por induzirem apoptose de células epiteliais, levam a uma inflamação crônica. Pode se apresentar de diversas formas, como reticular, atrófica, bolhosa, eritematosa ou erosiva. Tratando-se desta doença, existem muitas controvérsias principalmente acerca do seu potencial de malignização, para o qual os fatores de risco descritos são multifatoriais, e, dentre eles, a associação com o quadro inflamatório gerado. Objetivo: Identificar na literatura os eventos bioquímicos envolvidos no quadro inflamatório crônico gerado pelo líquen plano oral e sua relação com o potencial de malignização. Material e métodos: Revisão bibliográfica, sendo a busca feita em bancos e base de dados, além de livros consagrados na área. Das leituras encontradas, foram selecionadas 10 , os quais abordavam aspectos relacionados com a etiopatogenia, patogênese, bioquímica do processo inflamatório crônico causado e potencial de malignização da doença, Resultados: Diversos trabalhos mostram que a presença de um processo inflamatório crônico nos tecidos favorece a malignização do líquen oral. Em tais circunstâncias, ocorre liberação crônica de células inflamatórias e citocinas, e esse passa a ser o microambiente local, o que pode acarretar em stress oxidativo. Consequentemente, há ativação de oncogenes e inativação de genes supressores tumorais, ou seja o conjunto de substâncias gerada pode atuar como mutagênicos e diversos mecanismos essenciais da células serão prejudicadas como a proliferação celular e apoptose. Tem-se assim, a progressão de células tumorais, e ativação de fatores de transcrição que induzem a proliferação celular, angiogênese e metástase. Conclusão: Para aqueles autores que defendem o potencial de malignização, tem-se atualmente os eventos bioquímicos associados ao curso crônico da inflamação, como principais associações a transformação maligna do líquen plano oral, pois a situação criada gera danos ao DNA celular, assim tornando ciclo celular desregulado.

Song, Yue, Yueqi Wang, and Yikai Jiang. "Endoplasmic reticulum stress and related diseases." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3021655.

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O’reilly, S. "P105 Endoplasmic reticulum stress mediates dermal fibrosis." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.121.

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O’reilly, S. "AB0196 Endoplasmic reticulum stress in systemic sclerosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6443.

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Hassan, Ihab, Michael S. Zhang, Linda S. Powers, Kevin L. Legge, and Martha M. Monick. "Influenza A Infection Modulates Endoplasmic Reticulum Stress." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1805.

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Ma, X., E. Dobrinskikh, J. S. Kurche, I. T. Stancil, E. Kim, I. V. Yang, and D. A. Schwartz. "Endoplasmic Reticulum Stress in MUC5B-Driven Lung Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4216.

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Delbrel, E., P. S. Fenwick, C. Wrench, J. R. Baker, L. E. Donnelly, and P. J. Barnes. "Endoplasmic reticulum stress implication in fibroblast senescence in COPD." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.97.

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Звіти організацій з теми "Reticular stress":

Murphy-Ullrich, Joanne E. The Endoplasmic Reticulum Stress Protein Calreticulin in Diabetic Chronic Kidney Disease. Fort Belvoir, VA: Defense Technical Information Center, July 2015. http://dx.doi.org/10.21236/ada624022.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada430729.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada462341.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada476094.

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Christopher, David A., and Avihai Danon. Plant Adaptation to Light Stress: Genetic Regulatory Mechanisms. United States Department of Agriculture, May 2004. http://dx.doi.org/10.32747/2004.7586534.bard.

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Original Objectives: 1. Purify and biochemically characterize RB60 orthologs in higher plant chloroplasts; 2. Clone the gene(s) encoding plant RB60 orthologs and determine their structure and expression; 3. Manipulate the expression of RB60; 4. Assay the effects of altered RB60 expression on thylakoid biogenesis and photosynthetic function in plants exposed to different light conditions. In addition, we also examined the gene structure and expression of RB60 orthologs in the non-vascular plant, Physcomitrella patens and cloned the poly(A)-binding protein orthologue (43 kDa RB47-like protein). This protein is believed to a partner that interacts with RB60 to bind to the psbA5' UTR. Thus, to obtain a comprehensive view of RB60 function requires analysis of its biochemical partners such as RB43. Background & Achievements: High levels of sunlight reduce photosynthesis in plants by damaging the photo system II reaction center (PSII) subunits, such as D1 (encoded by the chloroplast tpsbAgene). When the rate of D1 synthesis is less than the rate of photo damage, photo inhibition occurs and plant growth is decreased. Plants use light-activated translation and enhanced psbAmRNA stability to maintain D1 synthesis and replace the photo damaged 01. Despite the importance to photosynthetic capacity, these mechanisms are poorly understood in plants. One intriguing model derived from the algal chloroplast system, Chlamydomonas, implicates the role of three proteins (RB60, RB47, RB38) that bind to the psbAmRNA 5' untranslated leader (5' UTR) in the light to activate translation or enhance mRNA stability. RB60 is the key enzyme, protein D1sulfide isomerase (Pill), that regulates the psbA-RN :Binding proteins (RB's) by way of light-mediated redox potentials generated by the photosystems. However, proteins with these functions have not been described from higher plants. We provided compelling evidence for the existence of RB60, RB47 and RB38 orthologs in the vascular plant, Arabidopsis. Using gel mobility shift, Rnase protection and UV-crosslinking assays, we have shown that a dithiol redox mechanism which resembles a Pill (RB60) activity regulates the interaction of 43- and 30-kDa proteins with a thermolabile stem-loop in the 5' UTR of the psbAmRNA from Arabidopsis. We discovered, in Arabidopsis, the PD1 gene family consists of II members that differ in polypeptide length from 361 to 566 amino acids, presence of signal peptides, KDEL motifs, and the number and positions of thioredoxin domains. PD1's catalyze the reversible formation an disomerization of disulfide bonds necessary for the proper folding, assembly, activity, and secretion of numerous enzymes and structural proteins. PD1's have also evolved novel cellular redox functions, as single enzymes and as subunits of protein complexes in organelles. We provide evidence that at least one Pill is localized to the chloroplast. We have used PDI-specific polyclonal and monoclonal antisera to characterize the PD1 (55 kDa) in the chloroplast that is unevenly distributed between the stroma and pellet (containing membranes, DNA, polysomes, starch), being three-fold more abundant in the pellet phase. PD1-55 levels increase with light intensity and it assembles into a high molecular weight complex of ~230 kDa as determined on native blue gels. In vitro translation of all 11 different Pill's followed by microsomal membrane processing reactions were used to differentiate among PD1's localized in the endoplasmic reticulum or other organelles. These results will provide.1e insights into redox regulatory mechanisms involved in adaptation of the photosynthetic apparatus to light stress. Elucidating the genetic mechanisms and factors regulating chloroplast photosynthetic genes is important for developing strategies to improve photosynthetic efficiency, crop productivity and adaptation to high light environments.