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Teses / dissertações sobre o tema "ATF6α"

Autor: Grafiati

Publicado: 7 de dezembro de 2024

Última modificação: 19 de julho de 2025

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Baier, Katrin Maria [Verfasser]. "Modulation der Unfolded Protein Response (UPR) bei Überexpression der Hepatitis-B-Oberflächenantigene unter Berücksichtigung des Transkriptionsfaktors ATF6 / Katrin Maria Baier." Gießen : Universitätsbibliothek, 2018. http://d-nb.info/1173086838/34.

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12

Baier, Katrin [Verfasser]. "Modulation der Unfolded Protein Response (UPR) bei Überexpression der Hepatitis-B-Oberflächenantigene unter Berücksichtigung des Transkriptionsfaktors ATF6 / Katrin Maria Baier." Gießen : Universitätsbibliothek, 2018. http://d-nb.info/1173086838/34.

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13

DI, CRISTINO FRANCESCA. "The stress-activated kinase p38MAPK contributes to ATF6 activation and resistance to ER stress in cancer cells with mutant p53." Doctoral thesis, Università degli Studi di Trieste, 2022. http://hdl.handle.net/11368/3030938.

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Endoplasmic Reticulum Stress (ERS) is one hallmark of cancer cells: tumor hypoxia, glucose reduction and genome instability all promote accumulation of misfolded proteins in the endoplasmic reticulum. ER stress triggers the Unfolded Protein Response (UPR), a conserved pathway initiated by three ER-resident receptors, IRE1α, PERK, and ATF6, that activate specific and overlapping transcriptional programs aimed to overcome the stress or induce cell death. Accumulating evidence suggest a role for UPR in cancer progression, therefore uncovering functional interactions of this pathway with the oncog

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14

Nozaki, Junichi. "The endoplasmic reticulum stress response is stimulated through the continuous activation of transcription factors ATF6 and XBP1 in Ins2[+/Akita] pancreatic β cells". 京都大学 (Kyoto University), 2004. http://hdl.handle.net/2433/147911.

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15

古場, 玲. "ジスルフィド結合を介して構成的に形成される小胞体ストレスセンサーATF6多量体の解析". Kyoto University, 2020. http://hdl.handle.net/2433/253127.

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16

Fu, Yanlin. "Proteostasis Maintenance of γ-aminobutyric Acid Type A Receptors (GABAARs)". Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1554993220214253.

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17

松居, 利江. "哺乳動物小胞体ストレス応答を制御する転写因子ATF6とXBP1の作用機作に関する研究". 京都大学 (Kyoto University), 2007. http://hdl.handle.net/2433/137023.

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18

堀本, 賢. "膜タンパク質小胞体ストレスセンサーATF6を基質とした小胞体関連分解因子SEL1LおよびEDEMの機能解析". 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/215356.

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This research was originally published in The Journal of Biological Chemistry. Satoshi Horimoto, Satoshi Ninagawa, Tetsuya Okada, Hibiki Koba, Takehiro Sugimoto, Yukiko Kamiya, Koichi Kato, Shunichi Takeda, and Kazutoshi Mori. The Unfolded Protein Response Transducer ATF6 Represents a Novel Transmembrane-type Endoplasmic Reticulum-associated Degradation Substrate Requiring Both Mannose Trimming and SEL1L Protein. The Journal of Biological Chemistry. 2013. 288:31517-31527. © the American Society for Biochemistry and Molecular Biology<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(理学)<br>甲第

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19

Snyder, Jarin T. "ER Stress and ATF6alpha potently induce S-Phase in Old Mouse Beta Cells Cultured Ex-Vivo in High Glucose." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1125.

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Aging is associated with a loss of proliferation of the insulin-secreting beta cell, a possible contributing factor to the greatly increased rate of type-2 diabetes in the elderly. A landmark study from our lab previously illustrated that mild endoplasmic reticulum (ER) stress drives beta cell proliferation specifically through ATF6α, one arm of the tripartite Unfolded Protein Response (UPR). It is unknown if old beta cells differ from young beta cells in UPR signaling or proliferative response to ER stress or ATF6α activation. To investigate, young and old mouse islets were cultured ex vivo i

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20

土師, 京介. "哺乳動物の小胞体ストレス応答に関与する転写調節因子ATF6の活性発現機構に関する研究". 京都大学 (Kyoto University), 2002. http://hdl.handle.net/2433/150107.

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21

佐藤, 吉美. "哺乳動物小胞体ストレス応答を制御する小胞体膜結合性転写因子ATF6の活性化機構に関する研究". 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/142424.

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22

岡田, 徹也. "哺乳動物小胞体ストレス応答を制御する膜結合性転写因子ATF6の標的ならびに活性化プロセスに関する研究". 京都大学 (Kyoto University), 2004. http://hdl.handle.net/2433/147908.

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23

山本, 敬祐. "哺乳動物小胞体ストレス応答に関与するシス配列ERSE-IIの解析ならびに転写因子ATF6のターゲティングに関する研究". 京都大学 (Kyoto University), 2004. http://hdl.handle.net/2433/68781.

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24

LISTI', Angela. "UNRAVELLING THE ROLES OF THE NUCLEAR PROTEIN 1 DURING ER-STRESS INDUCTION." Doctoral thesis, Università degli Studi di Palermo, 2020. http://hdl.handle.net/10447/400605.

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Background: NUPR1 was described as a transcriptional factor involved in the regulation of various cellular stress-response genes, playing a crucial role in the condition of the endoplasmic-reticulum (ER) stress, thus emerging as a common molecular factor of different pathologies, obesity, hepatic steatosis, and cancer. In the present work we aim to explore how NUPR1 interacts with some pivotal genes that are the major modulators of the ER stress and metabolic cell functions. In particular we investigated the biochemical and molecular effects arising from the loss of NUPR1 in ER stress phy

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25

安達, 雄亮. "哺乳動物小胞体ストレス応答を制御する小胞体膜結合性転写因子ATF6の活性化制御機構ならびに標的遺伝子に関する研究". 京都大学 (Kyoto University), 2008. http://hdl.handle.net/2433/124349.

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26

Ortet, Cortada Laura. "Signalling of ciclyn o complexes through EIF2alpha phosphorylation." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/7259.

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We have identified a novel Cyclin, called Cyclin O, which is able to bind and activate Cdk2 in response to intrinsic apoptotic stimuli. We have focused on the study of Cyclin Oα and Cyclin Oβ, alternatively spliced products of the gene. Upon treatment with different stress stimuli, transfected Cyclin Oα accumulates in dense aggregations in the cytoplasm compatible with being Stress Granules (SGs). Furthermore, we have seen that Cyclin Oβ and a point mutant of the N-terminal part of the protein constitutively localize to the SGs. Although both alpha and beta isoforms are pro

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27

Odisho, Tanya. "Investigating the Role of ATF6Beta in the ER Stress Response of Pancreatic Beta-cells." Thesis, 2013. http://hdl.handle.net/1807/43275.

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Endoplasmic reticulum (ER) stress has been implicated as a causative factor in the development of pancreatic beta-cell dysfunction and death resulting in type 2 diabetes. This thesis examined the role of ATF6beta in the ER stress response of beta-cells. Using an ATF6beta-specific antibody, expression of full-length ATF6beta was detected in various insulinoma cell lines and rodent islets and the induction of the active form (ATF6beta-p60) under ER stress conditions. Knock-down of ATF6beta in INS-1 832/13 cells did not affect mRNA induction of known ER stress response genes in response to tun

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28

Resende, Daniel Marcos da Silva. "Impact of ER stress and its reversion via chemical chaperones, on age- and proteostasis-associated pathways." Master's thesis, 2019. http://hdl.handle.net/10773/28430.

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Aging remains to this day one of the unresolved biology areas of upmost importance and many age-related diseases are on the rise worldwide. One of aging major hallmarks, proteostasis, has several associated pathways across different segments which have not yet been fully detailed in various cell lines and are needed to better understand the underlying aging problem. Here, using a neuronal-like cell line such as SH-SY5Y, several ER stress biomarkers and proteostasis associated targets are evaluated under ER stress-induced environment through tunicamycin (TUN) or thapsigargin (TG) presence. The

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29

Chang, Jin-Ling, and 張金鈴. "Transactivation of GRP94 by ER stress induced by GA in 9L rat brain tumor cells - Activation of the grp94 promoter mainly through ERSEs by transcription factor ATF6." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/17950088837799507083.

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碩士<br>國立清華大學<br>生物科技研究所<br>95<br>Geldanamycin (GA), a benzoquinone ansamycin, is an inhibitor of heat shock protein 90 (HSP90)/ glucose-regulated protein 94 (GRP94) and has been implicated as a potent anti-cancer drug. In our previous study, we found that GA with sublethal dose provoked the ER stress in 9L rat brain tumor (RBT) cells and induced glucose-regulated proteins under unfold protein response (UPR) at transcriptional level. The promoter of grp genes contain multiple copies of the ER stress response element (ERSE), with a consensus of CCAAT(N9)CCACG, which is critical and necessary for

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30

Teodoro, Tracy. "Examining the Role of Endoplasmic Reticulum Stress in Pancreatic Beta-cell Biology." Thesis, 2012. http://hdl.handle.net/1807/32825.

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Pancreatic beta-cells are responsible for secreting insulin into the circulation to maintain whole body glucose homeostasis. While pancreatic beta-cells have a large capacity to secrete insulin, their function progressively deteriorates during the pathogenesis of type 2 diabetes as a result of both genetic predisposition and environmental factors. Obesity is the largest risk factor for developing type 2 diabetes and is associated with various conditions that can impair normal beta-cell function, including excess free fatty acids, inflammation and insulin resistance. Accumulating evidence in th

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31

Amyot, Julie. "Rôles du stress du réticulum endoplasmique et de l'immunité innée dans l'inhibition de la transcription du gène de l'insuline : étude du facteur de transcription ATF6 et du récepteur TLR4." Thèse, 2011. http://hdl.handle.net/1866/6961.

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Le diabète de type 2 (DT2) est caractérisé par une résistance des tissus périphériques à l’action de l’insuline et par une insuffisance de la sécrétion d’insuline par les cellules β du pancréas. Différents facteurs tels que le stress du réticulum endoplasmique (RE) et l’immunité innée affectent la fonction de la cellule β-pancréatique. Toutefois, leur implication dans la régulation de la transcription du gène de l’insuline demeure imprécise. Le but de cette thèse était d’identifier et de caractériser le rôle du stress du RE et de l’immunité innée dans la régulation de la transcription du gène

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