Relevant bibliographies by topics / ATF6α

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'ATF6α'

Author: Grafiati
Published: 7 December 2024
Last updated: 31 July 2025

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Journal articles on the topic "ATF6α"

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Davis, Emery, Mohammad-Reza Shokri, Mary B. Rowland та ін. "ATF6β is not essential for the development of physiological cardiac hypertrophy". PLOS ONE 20, № 4 (2025): e0320178. https://doi.org/10.1371/journal.pone.0320178.

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Physiological cardiac hypertrophy is a compensatory remodeling of the heart in response to stimuli such as exercise training or pregnancy that is reversible and well-tolerated. We previously described how the activating transcription factor 6 (ATF6) proteins, ATF6α and ATF6β, were required for pathological hypertrophy in response to hemodynamic stress. Here, we examine the functional roles of both ATF6 proteins in the context of exercise-induced physiological hypertrophy. After 20 days of swim training, we found differential roles: whole body gene-deleted mice lacking ATF6α had an attenuated h
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Amyot, Julie, Isma Benterki, Ghislaine Fontés, et al. "Binding of activating transcription factor 6 to the A5/Core of the rat insulin II gene promoter does not mediate its transcriptional repression." Journal of Molecular Endocrinology 47, no. 3 (2011): 273–83. http://dx.doi.org/10.1530/jme-11-0016.

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Pancreatic β-cells have a well-developed endoplasmic reticulum due to their highly specialized secretory function to produce insulin in response to glucose and nutrients. It has been previously reported that overexpression of activating transcription factor 6 (ATF6) reduces insulin gene expression in part via upregulation of small heterodimer partner. In this study, we investigated whether ATF6 directly binds to the insulin gene promoter, and whether its direct binding represses insulin gene promoter activity. A bioinformatics analysis identified a putative ATF6 binding site in the A5/Core reg
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Yoshida, Hiderou, Tetsuya Okada, Kyosuke Haze та ін. "Endoplasmic Reticulum Stress-Induced Formation of Transcription Factor Complex ERSF Including NF-Y (CBF) and Activating Transcription Factors 6α and 6β That Activates the Mammalian Unfolded Protein Response". Molecular and Cellular Biology 21, № 4 (2001): 1239–48. http://dx.doi.org/10.1128/mcb.21.4.1239-1248.2001.

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ABSTRACT The levels of molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) are controlled by a transcriptional induction process termed the unfolded protein response (UPR). The mammalian UPR is mediated by the cis-acting ER stress response element (ERSE), the consensus sequence of which is CCAAT-N9-CCACG. We recently proposed that ER stress response factor (ERSF) binding to ERSE is a heterologous protein complex consisting of the constitutive component NF-Y (CBF) binding to CCAAT and an inducible component binding to CCACG and identified the basic leucine zipper-type tra
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Lee, Ann-Hwee, Neal N. Iwakoshi, and Laurie H. Glimcher. "XBP-1 Regulates a Subset of Endoplasmic Reticulum Resident Chaperone Genes in the Unfolded Protein Response." Molecular and Cellular Biology 23, no. 21 (2003): 7448–59. http://dx.doi.org/10.1128/mcb.23.21.7448-7459.2003.

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ABSTRACT The mammalian unfolded protein response (UPR) protects the cell against the stress of misfolded proteins in the endoplasmic reticulum (ER). We have investigated here the contribution of the UPR transcription factors XBP-1, ATF6α, and ATF6β to UPR target gene expression. Gene profiling of cell lines lacking these factors yielded several XBP-1-dependent UPR target genes, all of which appear to act in the ER. These included the DnaJ/Hsp40-like genes, p58IPK, ERdj4, and HEDJ, as well as EDEM, protein disulfide isomerase-P5, and ribosome-associated membrane protein 4 (RAMP4), whereas expre
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Ishikawa, Tokiro, Tetsuya Okada, Tomoko Ishikawa-Fujiwara та ін. "ATF6α/β-mediated adjustment of ER chaperone levels is essential for development of the notochord in medaka fish". Molecular Biology of the Cell 24, № 9 (2013): 1387–95. http://dx.doi.org/10.1091/mbc.e12-11-0830.

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ATF6α and ATF6β are membrane-bound transcription factors activated by regulated intramembrane proteolysis in response to endoplasmic reticulum (ER) stress to induce various ER quality control proteins. ATF6α- and ATF6β single-knockout mice develop normally, but ATF6α/β double knockout causes embryonic lethality, the reason for which is unknown. Here we show in medaka fish that ATF6α is primarily responsible for transcriptional induction of the major ER chaperone BiP and that ATF6α/β double knockout, but not ATF6α- or ATF6β single knockout, causes embryonic lethality, as in mice. Analyses of ER
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Sharma, Rohit B., Christine Darko, and Laura C. Alonso. "Intersection of the ATF6 and XBP1 ER stress pathways in mouse islet cells." Journal of Biological Chemistry 295, no. 41 (2020): 14164–77. http://dx.doi.org/10.1074/jbc.ra120.014173.

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Success or failure of pancreatic beta cell adaptation to ER stress is a determinant of diabetes susceptibility. The ATF6 and IRE1/XBP1 pathways are separate ER stress-response effectors important to beta cell health and function. ATF6α. and XBP1 direct overlapping transcriptional responses in some cell types. However, the signaling dynamics and interdependence of ATF6α and XBP1 in pancreatic beta cells have not been explored. To assess pathway-specific signal onset, we performed timed exposures of primary mouse islet cells to ER stressors and measured the early transcriptional response. Compar
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Teodoro, Tracy, Tanya Odisho, Elena Sidorova та Allen Volchuk. "Pancreatic β-cells depend on basal expression of active ATF6α-p50 for cell survival even under nonstress conditions". American Journal of Physiology-Cell Physiology 302, № 7 (2012): C992—C1003. http://dx.doi.org/10.1152/ajpcell.00160.2011.

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Activating transcription factor 6 (ATF6) is one of three principle endoplasmic reticulum (ER) stress response proteins and becomes activated when ER homeostasis is perturbed. ATF6 functions to increase ER capacity by stimulating transcription of ER-resident chaperone genes such as GRP78. Using an antibody that recognizes active ATF6α-p50, we found that active ATF6α was detected in insulinoma cells and rodent islets even under basal conditions and the levels were further increased by ER stress. To examine the function of ATF6α-p50, we depleted endogenous ATF6α-p50 levels using small interfering
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Xue, Fei, Jianwen Lu, Samuel C. Buchl та ін. "Coordinated signaling of activating transcription factor 6α and inositol-requiring enzyme 1α regulates hepatic stellate cell-mediated fibrogenesis in mice". American Journal of Physiology-Gastrointestinal and Liver Physiology 320, № 5 (2021): G864—G879. http://dx.doi.org/10.1152/ajpgi.00453.2020.

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ATF6α is a critical driver of hepatic stellate cell (HSC) activation in vitro. HSC-specific deletion of Atf6a limits fibrogenesis in vivo despite increased IRE1α signaling. Conditional deletion of Ire1α from HSCs limits fibrogenic gene transcription without impacting overall fibrosis. This could be due in part to observed upregulation of the ATF6α pathway. Dual loss of Atf6a and Ire1a from HSCs worsens fibrosis in vivo through enhanced HSC activation.
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Stauffer, Winston T., Adrian Arrieta, Erik A. Blackwood та Christopher C. Glembotski. "Sledgehammer to Scalpel: Broad Challenges to the Heart and Other Tissues Yield Specific Cellular Responses via Transcriptional Regulation of the ER-Stress Master Regulator ATF6α". International Journal of Molecular Sciences 21, № 3 (2020): 1134. http://dx.doi.org/10.3390/ijms21031134.

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There are more than 2000 transcription factors in eukaryotes, many of which are subject to complex mechanisms fine-tuning their activity and their transcriptional programs to meet the vast array of conditions under which cells must adapt to thrive and survive. For example, conditions that impair protein folding in the endoplasmic reticulum (ER), sometimes called ER stress, elicit the relocation of the ER-transmembrane protein, activating transcription factor 6α (ATF6α), to the Golgi, where it is proteolytically cleaved. This generates a fragment of ATF6α that translocates to the nucleus, where
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Azuma, Yoshinori, Daisuke Hagiwara, Wenjun Lu та ін. "Activating Transcription Factor 6α Is Required for the Vasopressin Neuron System to Maintain Water Balance Under Dehydration in Male Mice". Endocrinology 155, № 12 (2014): 4905–14. http://dx.doi.org/10.1210/en.2014-1522.

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Activating transcription factor 6α (ATF6α) is a sensor of endoplasmic reticulum (ER) stress and increases the expression of ER chaperones and molecules related to the ER-associated degradation of unfolded/misfolded proteins. In this study, we used ATF6α knockout (ATF6α−/−) mice to clarify the role of ATF6α in the arginine vasopressin (AVP) neuron system. Although urine volumes were not different between ATF6α−/− and wild-type (ATF6α+/+) mice with access to water ad libitum, they were increased in ATF6α−/− mice compared with those in ATF6α+/+ mice under intermittent water deprivation (WD) and a
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Dissertations / Theses on the topic "ATF6α"

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Forouhan, Mitra. "The role of ATF6α and ATF6β in the UPR associated with an ER stress-induced skeletal chondrodysplasia". Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-atf6alpha-and-atf6-in-the-upr-associated-with-an-er-stressinduced-skeletal-chondrodysplasia(9e26ce51-f188-454c-8ee1-3832845ee014).html.

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Mutations in the COL10A1 gene cause metaphyseal chondrodysplasia type Schmid (MCDS) by triggering ER stress and unfolded protein response (UPR). MCDS is characterised by a mild short-limb dwarfism accompanied by expansion of the cartilage growth plate hypertrophic zone (HZ) and altered differentiation of hypertrophic chondrocytes (HCs). ATF6 is one of the UPR mediators, which exists in two isoforms, ATF6α and ATF6β. Activation and up-regulation of ATF6α was a prominent biochemical sign of ER stress in a mouse model of MCDS, COL10a1 p.N617K. Although ATF6β is induced and activated in response t
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Egawa, Naohiro. "The endoplasmic reticulum stress sensor, ATF6α, protects against neurotoxin-induced dopaminergic neuronal death". Kyoto University, 2011. http://hdl.handle.net/2433/142092.

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Giroud, Joëlle. "Impact of the UPR pathway on the establishment of the senescent phenotype induced by UVB." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS036.

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Contexte : En France, la prévalence des modifications corporelles apparentes augmente, y compris chez les médecins généralistes. Il n’existe actuellement pas d’étude sur le vécu des médecins porteurs de modifications corporelles apparentes dans leur relation avec le patient.Méthode : Etude qualitative par IPA par entretiens semi-directifs entre janvier et juin 2024. Le recrutement a eu lieu au cours du CNGE de 2022, par « effet boule de neige » et via la diffusion d’annonces sur les réseaux sociaux. 6 médecins ont été interrogés sur la base d’un guide d’entretien révisé après chaque entretien.
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Felden, Julia Verfasser], and Bernd [Akademischer Betreuer] [Wissinger. "Die Bedeutung von Atf6 für die Zebrafischretina : Generierung und Charakterisierung eines atf6-/- - Zebrafischmodells / Julia Felden ; Betreuer: Bernd Wissinger." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/1199929522/34.

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SICARI, DARIA. "Unveiling a role for mutant p53 in regulation of Unfolded Protein Response." Doctoral thesis, Università degli Studi di Trieste, 2018. http://hdl.handle.net/11368/2924770.

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Disturbances in the homeostasis of endoplasmic reticulum (ER) referred to as ER stress is involved in a variety of human diseases. Tumor progression is strictly related to ER stress, while cancer cells are prone to tolerate unfolded protein accumulation and to take advantages from ER stress-related pro-survival pathways. Mutation of Tp53 gene is a frequent event in human tumor and a significant factor in cancer development and progression. We report that cancer cells bearing mutant p53 respond to ER stress insult by dampening ER-stress associated pro-apoptotic factor and by sustaining survival
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Santinelli, Raphaël. "Inhibition de la voie ATF6 de la réponse aux protéines mal formées comme nouvelle approche thérapeutique dans le cadre de la mucoviscidose." Electronic Thesis or Diss., Brest, 2024. http://www.theses.fr/2024BRES0009.

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La mucoviscidose est la maladie génétique létale à transmission autosomale récessive la plus fréquemment retrouvée dans la population européenne. Elle est due à des mutations altérant le gène CFTR, dont la plus fréquente est la mutation induisant la délétion d’une phénylalanine en position 508 de la séquence polypeptidique de cette protéine (p.Phe508del-CFTR). Ces mutations altèrent la viscosité du mucus présent à la surface apicale des cellules épithéliales des systèmes respiratoire, digestif et génital. Cela entraîne une baisse de la clairance mucociliaire, rendant difficile le renouvellemen
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Huguet, Florentin. "Impact de la modulation de TRPM7 et ATF6 sur le cystic fibrosis transmembrane conductance regulator." Thesis, Brest, 2017. http://www.theses.fr/2017BRES0058/document.

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La mucoviscidose est une maladie causée par des mutations du gène cftr entraînant des défauts importants de la protéine CFTR. La mutation la plus fréquente (F508del) est caractérisée par un repliement incorrect conduisant à la rétention de la protéine dans le RE.L’accumulation de CFTR-F508del dans le RE, l’inflammation et les infections vont déclencher un stress du RE dans les cellules épithéliales ainsi que l’UPR. Cette dernière est une réponse adaptative déclenchée par le stress du RE et permet de rétablir l’homéostasie de ce compartiment. L’UPR est constituée de trois voies majeures dont l’
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Papaioannou, Alexandra. "Fine-tuning UPR signals and subsequent cellular outputs." Thesis, Rennes 1, 2019. http://www.theses.fr/2019REN1B013.

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La présente thèse explore le monde de la biologie du stress du RE (réticulum endoplasmique). Une vue globale du RE et du stress du RE est d'abord fournie en commençant par les mécanismes de base impliqués pour aller vers de possibles applications cliniques. L'accent est ensuite mis sur le rôle crucial de l'UPR dans la cancérogénèse, qui est activée en réponse au stress du RE dans la micro-environnement de la tumeur. Après avoir passé en revue ces aspects, nous mettons en évidence des éléments manquants dans notre compréhension de la façon dont les signaux UPR sont affinés et conduisent soit à
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Martindale, Joshua J. "Protecting the myocardium from ischemia and reperfusion injury via inducible activation of ATF6 or constitutive expression of MKK6 /." Diss., Connect to a 24 p. preview or request complete full text in PDF formate. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3236641.

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Lyle, Chimera. "Super Low Dose Endotoxin Exacerbates Low Grade Inflammation through Modulating Cell Stress and Decreasing Cellular Homeostatic Protein Expression." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/86360.

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The establishment of non-resolving inflammation underlies the pathogenesis of chronic inflammatory diseases in humans. Super low dose (SLD) endotoxin has been associated with exacerbating inflammation and the pathogenesis of chronic inflammatory diseases. However, the underlying molecular mechanisms are not well studied. In this study, I tested the hypothesis that SLD endotoxin may potentiate non-resolving innate immune cell inflammation through disrupting cellular endoplasmic reticulum (ER) homeostasis. We chose to study the dynamics of ER homeostasis in macrophages stimulated with SLD end
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Book chapters on the topic "ATF6α"

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Chiang, Wei-Chieh Jerry, Heike Kroeger, Lulu Chea, and Jonathan H. Lin. "Pathomechanisms of ATF6-Associated Cone Photoreceptor Diseases." In Retinal Degenerative Diseases. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_50.

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Jerry Chiang, Wei-Chieh, and Jonathan H. Lin. "The Effects of IRE1, ATF6, and PERK Signaling on adRP-Linked Rhodopsins." In Retinal Degenerative Diseases. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_83.

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Bradley, Allyssa, Masako Le, Soyeon Park, et al. "Dysregulation of Retinal and Photoreceptor Structural Integrity Genes in ATF6−/− Retinal Organoids." In Advances in Experimental Medicine and Biology. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-76550-6_66.

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"ATF6." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_430.

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Kohl, Susanne, Stylianos Michalakis, and Katarina Stingl. "Achromatopsia—Rod Monochromacy." In Genetic Diseases of the Eye, 3rd ed. Oxford University PressNew York, 2025. https://doi.org/10.1093/med/9780197659403.003.0031.

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Abstract Achromatopsia is also referred to as rod monochromacy (or rod monochromatism), complete (or total) color blindness (OMIM #216900, #262300, #139340, #613093, #610024, #616517), or day blindness (hemeralopia) with pronounced photophobia, and is inherited as an autosomal recessive trait. This chapter covers clinical description and diagnosis (including psychophysics, electrophysiology, and retinal imaging), management and visual aids, prevalence, and the genetic basis (CNGA3, CNGB3, GNAT2, PDE6C, PDE6H, and ATF6) of achromatopsia. In addition, available animal models carrying disease-ass
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Conference papers on the topic "ATF6α"

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Mekhael, O., H. Patel, J. Imani та ін. "Assessing the Role of ATF6α in the Alternative Activation of Macrophages in the Progression of Fibrotic Lung Diseases". У American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7232.

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Edmondson, Jacob L., Megan R. Reed, Daniel Fil, et al. "538 ATF6 activation in melanoma promotes anti-tumor immunity and improves ICB therapy response." In SITC 39th Annual Meeting (SITC 2024) Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-sitc2024.0538.

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McMellen, Alexandra N., and Benjamin G. Bitler. "Abstract A51: The role of ATF6-mediate AP-1 signaling in promoting PARP inhibitor-resistant ovarian cancer." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a51.

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Yan, Xiao Hong, Yuan Wang, Ya Lan Ding, Min Hu, Gui Mei Wang, and Xiao Min Guo. "ATF6 activated endoplasmic reticulum stress involved in cardioprotection of hydrogen sulfide postconditioning against cardiac myocytes apoptosis by ischemia reperfusion in vivo." In Annual International Conference on Advanced Research: Physiology. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-607x_arp14.16.

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Carvajal, Patricia, Sergio Aguilera, María-José Barrera, et al. "THU0203 PROMOTER DNA METHYLATION AND HSA-MIR-424-5P REGULATE ATF6 ALPHA EXPRESSION IN SALIVARY GLANDS OF PATIENTS WITH SJÖGREN’S SYNDROME." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4712.

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Guan, Min. "Abstract 2653: Nelfinavir induces apoptosis in hormone-resistant prostate cancer cells through inhibition of regulated intramembrane proteolysis of SREBP-1 and ATF6." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2653.

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