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1

Da, Silva Alison. "Étude de la reconnaissance des Escherichia coli adhérents et invasifs (AIEC) associés à la maladie de Crohn par l'autophagie : identification des récepteurs autophagiques et des facteurs de virulence." Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://www.theses.fr/2023UCFA0117.

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La maladie de Crohn (MC) est une maladie inflammatoire chronique de l'intestin, dont l'étiologie est multifactorielle. Elle résulte de l'interaction complexe entre des prédispositions génétiques, des facteurs environnementaux et des altérations de la composition du microbiote intestinal, induisant une dérégulation du système immunitaire intestinal. À ce jour, la MC est incurable, seuls des traitements visant à soulager les symptômes et à prévenir les récidives et complications sont disponibles. Chez les patients atteints de la MC, une augmentation de la prévalence de souches particulières d'Es
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2

Verlhac, Pauline. "Rôle des récepteurs autophagiques dans la maturation des autophagosomes." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1138/document.

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La xénophagie est une forme d'autophagie sélective permettant de capture des pathogènes dans les autophagosomes et de les dégrader dans les autolysosomes. Cette sélectivité est assurée par une famille de protéines ; les récepteurs autophagiques qui reconnaissent des substrats cytosoliques d'un côté et les membres de la famille LC3 ancrés dans la membrane de l'autophagosome de l'autre. Parmi ces récepteurs, NDP52 cible la bactérie Salmonella Typhimurium vers l'autophagie.Nous décrivons un rôle nouveau et inattendu pour NDP52 ; assurer la maturation d'autophagosomes durant l'infection par Salmon
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3

Petkova, Denitsa. "Étude du rôle de récepteurs autophagiques lors de l'infection par le virus de la rougeole." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10311/document.

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La macroautophagie assure l'homéostasie cellulaire en recyclant du matériel cytosolique obsolète ou délétère et sa dérégulation est associée à plusieurs pathologies. Elle constitue aussi un mécanisme de défense car elle peut éliminer des pathogènes intracellulaires. L'étape cruciale de l'autophagie est la maturation lors de laquelle la vésicule renfermant des substrats cytosoliques, l'autophagosome, fusionne avec des lysosomes et la dégradation a lieu. Nous nous intéressons à la régulation de l'autophagie et aux conséquences de sa perturbation lors des infections, notamment par le virus de la
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4

Negulescu, Ana-Maria. "Caractérisation des récepteurs à dépendance Notch3 et Kremen1 dans les cancers." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1265.

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Les récepteurs membranaires sont des acteurs majeurs des interactions entre la cellule et son environnement. Ils peuvent être à l'origine des signaux de survie, de différentiation, de migration ou bien de mort cellulaire. Les travaux de ce manuscrit ont été faits sur une famille de récepteurs nommés "récepteurs à dépendance". Ils sont caractérisés par leur fonctionnement dans la cellule plutôt que par leur structure: en présence de leurs ligands ces récepteurs induisent un signal de survie et en l'absence de ces mêmes ligands ils induisent un signal actif de mort cellulaire. Deux nouveaux réce
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5

Runwal, Gautam. "The study of two transmembrane autophagy proteins and the autophagy receptor, p62." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290149.

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Autophagy is an evolutionarily conserved process across eukaryotes that is responsible for degradation of cargo such as aggregate-prone proteins, pathogens, damaged organelles, macromolecules etc. via its delivery to lysosomes. The process is known to involve the formation of a double-membraned structure, called autophagosome, that engulfs the cargo destined for degradation and delivers its contents by fusing with lysosomes. This process involves several proteins at its core which include two transmembrane proteins, ATG9 and VMP1. While ATG9 and VMP1 has been discovered for about a decade and
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6

Coly, Pierre-Michaël. "Régulation de l'activité autophagique par les récepteurs chimiotactiques couplés aux protéines G : rôle essentiel dans la migration directionnelle." Thesis, Normandie, 2017. http://www.theses.fr/2017NORMR004/document.

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L’autophagie est un processus catabolique par lequel certaines protéines cytosoliquessont dirigées vers le compartiment lysosomial, afin d’y être dégradées. Ce processus débutepar la séquestration de constituants cytoplasmiques par une structure multimembranaireappelée phagophore. La fermeture du phagophore donne naissance à une vésicule à doublemembrane nommée autophagosome, qui fusionne avec les lysosomes, ce qui conduit à ladégradation du contenu de sa lumière. Ainsi, la modulation de l’autophagie permet unremodelage dynamique du protéome cellulaire. Bien que des données récentes ont permis
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7

Bigford, Gregory E. "Activation of NR2B and Autophagy Signaling Pathways Following Traumatic Brain Injury." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/204.

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Hyper-activation of N-methyl-D-aspartate receptors (NRs) is associated with excitotoxic cell death during secondary injury following traumatic brain injury (TBI). The efficiency of the NR is dependent on the location of receptors in membrane raft microdomains that provide a platform for coupling of NRs and effector proteins. In many neurodegenerative diseases, activation of the autophagy pathway has been suggested to contribute to glutamate excitotoxicity, but whether increased autophagy signaling contributes to pathology after TBI has not been defined. In these studies, I investigate wheth
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8

Tian, Ailing. "IGF1 Receptor Inhibition Amplifies the Effects of Cancer Drugs by Autophagy and Immune-Dependent Mechanisms." Electronic Thesis or Diss., université Paris-Saclay, 2022. http://www.theses.fr/2022UPASL040.

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Un certain nombre de produits végétaux naturels induisent l'autophagie et interviennent sur la durée de vie et la durée de vie dépendantes de l'autophagie dans des modèles de souris appropriés. Ici, nous avons identifié la picropodophylline (PPP) comme un inducteur non toxique du flux autophagique qui agit sur les cellules humaines et de souris in vitro, ainsi que sur les organes de souris in vivo. Mécaniquement, PPP inhibe IGF1R ainsi qu'en aval d'AKT, la cible mécaniste du complexe de rapamycine 1 (mTORC1), couplé à l'activation des facteurs de transcription pro-autophagiques EB (TFEB) et E3
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9

Manni, Diego. "Oxidation-dependent regulation of the selective autophagy receptor SQSTM1/p62." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3675.

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Oxidative stress and impairment of autophagy can lead to the accumulation and aggregation of damaged proteins, a common feature of most age-related neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. SQSTM1/p62, a receptor and a substrate of selective autophagy, is implicated in the degradation of damaged and polyubiquitinated substrates. Importantly, p62 has been detected in many types of protein inclusions found in neurodegenerative diseases, together with other disease-related proteins. However, the mechanisms allowing p62 to selectively recruit and degrade auto
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10

Vicencio, Bustamante José Miguel. "The inositol-1,4,5-trisphosphate receptor regulates autophagy through its interaction with Beclin 1." Paris 11, 2009. http://www.theses.fr/2009PA11T045.

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11

Singh, Madhu [Verfasser]. "Autophagy and Listeria monocytogenes : the role(s) of cargo receptors / Madhu Singh." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/1068773235/34.

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12

Walinda, Erik. "Structural Study of Proteins Involved in Autophagy." 京都大学 (Kyoto University), 2015. http://hdl.handle.net/2433/202720.

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13

BRILLANTE, SIMONA. "THE OFD1 PROTEIN CONTROLS AUTOPHAGOSOME BIOGENESIS THROUGH SELECTIVE AUTOPHAGY." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/793410.

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Cilia are cellular projections that serve a wide variety of essential functions in mammals. Defects in cilia structure or function have emerged as etiological mechanisms underpinning human diseases called ciliopathies. The OFD1 gene, defective in a rare developmental ciliopathy known as Oral facial digital syndrome type I, encodes for a centrosomal/basal body protein required for cilia formation. Recent data link ciliary structures to autophagy, the major intracellular degradation system, although the mechanisms and the main players underlying this connection are still to be determined. Autop
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14

Ellison, Cara Jane. "Sphingomyelin as a danger signal in cell-autonomous immunity." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267993.

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Individual cells employ mechanisms of cell-autonomous immunity to defend their cytosol against bacterial invasion. One such mechanism involves indirect detection of the pathogen through recognition of pathogen-induced disturbances causing the appearance of specific host molecules in an abnormal location. For example, glycans, which are located on the extracellular leaflet of the plasma membrane under homeostatic conditions, become hidden inside bacteria-containing vacuoles (BCVs) during bacterial entry into the cell. Upon BCV rupture, glycans become exposed to the cytosol where they act as a d
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15

Äijälä, M. (Meiju). "Studies about contribution of leptin receptor in cardiovascular risk." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526203058.

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Abstract Leptin is a hormone secreted by adipose tissue. It is involved in the regulation of appetite and energy expenditure. Leptin binds to its receptor (LEPR) that is expressed in the central nervous system as well as in other tissues including adipocytes and endothelial cells. Plasma leptin level reflects the amount of adipose tissue and previously, it has been shown to be associated with the risk for coronary artery disease. Two LEPR polymorphisms, Lys109Arg and Gln223Arg, have been extensively studied and they have been associated with several risk factors of atherosclerosis. Earlier stu
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LE, Thi Yen Loan. "Role of mineralocorticoid receptor regulation during experimental myocardial infarction." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10270.

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Ischaemic heart disease remains the leading cause of death worldwide. Following an ischaemic event, the primary strategy is to restore blood flow (reperfusion). However, this triggers release of reactive oxygen species, activation of stress-related gene transcription, autophagy and cell death processes leading to further injury (reperfusion injury). Elevated plasma aldosterone levels produce adverse cardiac effects, while mineralocorticoid receptor (MR) antagonists (spironolactone or eplerenone) reduce mortality, although mechanisms have not been defined. The aim of this thesis was to determin
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17

Blasi, Beriain Ignacio. "Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway." Doctoral thesis, Universitat Internacional de Catalunya, 2017. http://hdl.handle.net/10803/461098.

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Resum: Porphyromonas gingivalis often subverts host cell autophagic processes for its own survival. Our previous studies document the association of the cargo sorting protein, melanoregulin (MREG), with its binding partner, the autophagic protein, microtubule-associated protein 1 light chain 3 (LC3) in macrophages incubated with P. gingivalis (strain 33277). Differences in the lipid A moiety of lipopolysaccharide (LPS) affect the virulence of P. gingivalis; penta-acylated LPS1690 is a weak Toll-like receptor 4 agonist compared with Escherichia coli LPS, whereas tetra-acylated LPS1435/1449 act
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18

Rohatgi, Rasika. "Autophagy-Independent Role for Beclin 1 in the Regulation of Growth Factor Receptor Signaling: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/873.

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Beclin 1 is a haplo-insufficient tumor suppressor that is decreased in many human tumors. The function of Beclin 1 in cancer has been attributed primarily to its role in the degradative process of autophagy. However, the role of autophagy itself in tumorigenesis is context-dependent and can be both preventive and promoting. Due to its dual function in cancer a better understanding of this process is necessary to develop potential novel cancer therapies. To gain insight into the role of autophagy in breast carcinoma, I analyzed the autophagydependency of different subtypes of breast cancer. My
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19

Lin, Ching-Yu. "LAMTOR2/LAMTOR1 complex is required for TAX1BP1-mediated xenophagy." Kyoto University, 2020. http://hdl.handle.net/2433/253144.

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20

Chen, Jinyun. "REGULATION OF INTRACELLULAR ARYL HYDROCARBON RECEPTOR PROTEIN LEVELS." Scholarly Commons, 2020. https://scholarlycommons.pacific.edu/uop_etds/3675.

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The aryl hydrocarbon receptor (AHR) is a ligand-activated signaling molecule which controls tumor growth and metastasis, T cell differentiation, and liver development. Expression levels of this receptor protein are sensitive to the cellular p23 protein levels in immortalized cancer cell lines. As little as 30% reduction of the p23 cellular content can suppress the AHR function. Here we reported that down-regulation of the p23 protein content in normal, untransformed human bronchial/tracheal epithelial cells to 48% of its content also suppresses the AHR protein levels to 54% of its content. Thi
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21

Ruddy, Samantha. "Preferential Estrogen Receptor β Ligands Inhibit Proliferation and Reduce Bcl-2 Expression in Fulvestrant-resistant Breast Cancer Cells". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23669.

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Endocrine resistance is a significant clinical problem in the treatment of estrogen (E2) receptor positive breast cancers. There are two ER subtypes, ERα and ERβ, which promote and inhibit breast cancer cell proliferation respectively. While ER positive breast cancers typically express a high ratio of ERα to ERβ, the acquisition of antiestrogen resistance in vitro and in vivo is associated with increased relative expression of the ERβ. On some gene enhancers ERβ has been shown to function in opposition to the ERα in the presence of E2. Here we demonstrate that exposure to two different ERβ ag
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Lopez, Corcino Yalitza Z. "Inhibition of Epidermal Growth Factor Receptor (EGFR) Leads to Autophagy-mediated Killing of Toxoplasma gondii and Control of Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560350001767936.

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23

Gao, Jianqun. "TLR2 and α-synuclein mediated pathology in human neuronal cell models". Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20502.

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Parkinson’s disease (PD) is a progressively debilitating neurodegenerative disorder with the formation and development of Lewy bodies (LBs) and Lewy neurites (LNs) as its pathological characteristics. The most prominent and well-studied component of LBs and LNs is α-synuclein, which is thought to propagate through PD brain and contribute to neural dysfunction and clinical symptoms. The α-synuclein protein invades vulnerable neurons in the PD brain in a predictable, staged pattern. Recent evidence suggests that this propagation has some characteristics similar to the propagation of the prion pr
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Giorgetti, E. "DIFFERENT APPROACHES TO UNDERSTAND AND COUNTERACT SPINAL AND BULBAR MUSCOLAR ATROPHY (SBMA)." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/246561.

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Spinal and Bulbar Muscular Atrophy (SBMA), or Kennedy’s disease, is a hereditary neuromuscular disorder that affect only men and is characterized by slowly progressive weakness and atrophy of bulbar, facial, and limb muscles, which are attributable to degeneration of lower motor neurons in the spinal cord and brainstem. The disease is associated with an abnormally expanded CAG repeat in the androgen receptor (AR) gene which results in a longer polyglutamine tract (polyQ) at the N-terminus of the protein. PolyQ tract triggers AR protein misfolding and aggregation and leads to nuclear toxicity a
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Janota, Danielle Marie. "Alpha1-Adrenergic Receptor Activation Mimics Ischemic Postconditioning in Cardiac Myocytes." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1406562863.

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Wang, Qian, and 王倩. "Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206750.

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Autophagy is a major catabolic pathway for maintaining cell homeostasis through degradation and recycle of macromolecules and organelles. Autophagy can be activated under environmental stress conditions, including reactive oxygen species (ROS). TRPM2, a non-selective trans-membrane calcium channel, can be activated by ROS that, in turn, leads to intracellular 〖Ca〗^(2+) increase through 〖Ca〗^(2+) influx. It is well known that ROS regulates autophagy, and vice versa. Yet, the molecular mechanisms underlying the interplay between ROS and autophagy remain elusive. Here we studied the role of TRPM
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Nguyen, The Duy [Verfasser], Rolf [Gutachter] Marschalek, and Christian [Gutachter] Brandts. "The role of the selective autophagy receptor p62 in acute myeloid leukemia / The Duy Nguyen ; Gutachter: Rolf Marschalek, Christian Brandts." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2018. http://d-nb.info/1157097979/34.

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28

Lajoie, Patrick. "Regulation of receptor signaling and membrane trafficking by beta1,6-branched n-glycans and caveolin-1/cholesterol membrane domain organization." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/336.

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Modification by glycosylation gives proteins a range of diverse functions reflecting their structural variability. N-glycans regulate many biological outcomes in mammalian cells under both normal and pathological conditions. They play a major role in various pathologies such as cancer and lysosomal storage diseases. Interplay between N-glycans and other regulators, such as membrane lipid domains, in the control of signaling pathways remains poorly understood. My thesis therefore focuses on how N-glycans and membrane lipid domains oppose and/or work together at different cellular levels to regu
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Schuh, Mélanie. "Caractérisation des voies de signalisation contrôlées par les androgènes dans le muscle strié chez la souris." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ106/document.

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Les muscles permettent de générer force et mouvements et ont des fonctions métaboliques importantes. Mon travail a consisté à caractériser le rôle et les mécanismes d’actions des androgènes dans le muscle strié. Nous avons montré que l’ablation du récepteur des androgènes dans les myofibres n’affecte pas la masse musculaire car à la fois les voies anaboliques (IGF1) et cataboliques (myostatine) sont dérégulées. Cependant, l’absence du récepteur dans les myofibres diminue l’hypertrophie musculaire induite par une surcharge mécanique et limite l’atrophie induite par les glucocorticoïdes. Son abl
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Yang, Yujie. "POST-TRANSLATIONAL MODIFICATION AND DEGRADATION MECHANISMS OF THE ARYL HYDROCARBON RECEPTOR." Scholarly Commons, 2021. https://scholarlycommons.pacific.edu/uop_etds/3753.

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The aryl hydrocarbon receptor (AHR) is a transcription factor first discovered to be activated by exogenous ligands, such as dioxins, and helps promote downstream gene (e.g. CYP1A1) transcription to metabolize the toxicants. With the reports of various AHR targets genes, the expression levels and activities of AHR have been implicated in many physiological and pathological situations. Understanding how AHR protein level is regulated would provide more information to target AHR. AHR stays in the cytosol in the absence of ligand in a complex with HSP90, p23 and XAP2. After ligand activation, AHR
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Eimer, Sandrine. "Etude des réponses induites par l’erlotinib dans des cellules de lignées de glioblastome." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21822/document.

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Le glioblastome (GBM), tumeur de plus haut grade du système nerveux central (OMS grade 4) a un pronostic très sombre, quelque soit le traitement, lié à une résistance à l’apoptose. L’erlotinib (Tarceva®, OSI 774) est un inhibiteur de la tyrosine kinase du récepteur au facteur de croissance épithélial (EGFR). L’hyper-expression et l’amplification du gène de l’EGFR dans 40 à 60% des GBM, fourni un rationnel pour utiliser l’erlotinib. Nous avons montré sur U87-MG et DBTRG-05MG, deux lignées de GBM, l’absence d’apoptose avec l’erlotinib, liée soit à un déficit en pro-caspase 3, soit à une accumula
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Ségala, Grégory. "Caractérisation des mécanismes moléculaires impliqués dans l'activité anti-cancéreuse du Tamoxifène et de la Dendrogénine A." Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1694/.

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Le tamoxifène (Tam) est l'un principaux médicament utilisé pour le traitement des cancers du sein exprimant les récepteurs des œstrogènes (ER). Des résistances au Tam limitent son utilisation thérapeutique et l'identification des mécanismes responsables de ces résistances nécessite une connaissance approfondie de la pharmacologie du Tam. L'ER est la cible la mieux connue du Tam mais d'autres cibles existent parmi lesquelles le site de liaison des anti-oestrogènes (AEBS : AntiEstrogen Binding Site). L'équipe de Marc Poirot a montré qu'AEBS est impliqué dans les effets anti-cancéreux du Tam par
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Peng, Luo-Gen [Verfasser]. "Urokinase-type plasminogen activator receptor contributes to chemosensitivity and epithelial-to-mesenchymal transition in PDAC : uPAR and p38 regulate autophagy dependent gemcitabine resistance in AsPC1: autophagy inhibitors and gemcitabine as a potential combined therapy for a subgroup of pancreastic cancers / Luogen Peng." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1221802313/34.

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Peng, Luogen [Verfasser]. "Urokinase-type plasminogen activator receptor contributes to chemosensitivity and epithelial-to-mesenchymal transition in PDAC : uPAR and p38 regulate autophagy dependent gemcitabine resistance in AsPC1: autophagy inhibitors and gemcitabine as a potential combined therapy for a subgroup of pancreastic cancers / Luogen Peng." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1221802313/34.

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Berleth, Niklas [Verfasser], Björn [Akademischer Betreuer] Stork, and Thomas [Gutachter] Klein. "NRBF2, a novel component of the class III PtdIns3K complex, regulates starvation-induced autophagy and nuclear receptor-mediated gene expression / Niklas Berleth ; Gutachter: Thomas Klein ; Betreuer: Björn Stork." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2018. http://d-nb.info/1172968012/34.

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36

Laurent, Anne-Coline. "Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T044/document.

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Les catécholamines induisent la synthèse d’AMPc par une stimulation des récepteurs β-adrénergiques et contrôlent ainsi la fonction cardiaque en activant une pléiade de voies de signalisation intracellulaires. Les protéines Epac sont des facteurs d’échange pour les petites protéines G et sont directement activés par l’AMPc. Devant l’importance de la voie β-adrénergique dans la physiopathologie cardiaque et dans le but de mieux comprendre la régulation des processus cellulaires dépendants de l’AMPc dans le cœur, il apparaît essentiel de caractériser le rôle des facteurs d’échange Epac dans le my
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Sahin, Katherine B. "Evaluation of cell division cycle associated protein 3 (CDCA3) as a novel prognostic/therapeutic target for EGFR-mutant non-small cell lung cancer." Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/231468/1/Katherine_Sahin_Thesis.pdf.

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This thesis defined a unique role for the protein cell division cycle associated protein-3 (CDCA3) in epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer (NSCLC). This thesis has established an association between the levels of CDCA3 expression and the tumour response to tyrosine kinase inhibitors (TKI), which are the front-line therapy for EGFR-mutant NSCLC. In this disease, CDCA3 functions to modulate cellular growth pathways to impact sensitivity towards TKI therapy. Future work might enable development of a clinical stratification tool to discern TKI responsive from n
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Weng, Shu-Chuan. "Preclinical exploration of novel small molecules as anticancer agents in triple-negative and HER2/neu-positive breast cancers." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1227727553.

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Morelli, E. "NOVEL FUNCTIONS OF THE SNARE PROTEIN SNAP29IN MEMBRANE TRAFFICKING AND CELL DIVISION." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/265475.

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Vesicular trafficking within cells is an important process for tissue development and homeostasis. A key step of vesicular trafficking is the fusion between two membranes, a process in which SNARE (Soluble NSF Attachment Protein Receptors) proteins play a fundamental role. SNAP29 (SyNaptosomal Associated Proteins 29) is a ubiquitous SNARE, regulating membrane fusion in different trafficking compartments and in different contexts in non dividing cells. We isolated a loss of function mutant in usnp, the gene encoding the Drosophila homolog of the human protein SNAP29 (Snap29 hereafter), that, wh
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"Expression patterns of estrogen receptor isoforms in thyroid cancer and the role of estrogen receptor alpha in autophagy of thyroid cancer cells." 2013. http://library.cuhk.edu.hk/record=b5884401.

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Fan, Dahua.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2013.<br>Includes bibliographical references (leaves 117-155).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Abstracts also in Chinese.
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Rocha, Mariana Botelho da. "Autophagy in the hypothalamus: role of Neuropeptide Y and impact on Synaptic Plasticity." Doctoral thesis, 2016. http://hdl.handle.net/10316/29288.

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Tese de doutoramento em Ciências Farmacêuticas, na especialidade Farmacologia e Farmacoterapia, apresentada à Faculdade de Farmácia da Universidade de Coimbra<br>O hipotálamo é uma região do cérebro que regula o desenvolvimento, o crescimento e o metabolismo. Recentemente, foi também demonstrado que o hipotálamo desempenha um papel chave no desenvolvimento generalizado do envelhecimento. A autofagia é um processo intracelular envolvido na reciclagem dos constituintes da célula e na manutenção da homeostase celular. Durante o envelhecimento e em doenças associadas ao envelhecimento ocorre dimin
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Balounová, Jana. "Toll like receptory a myeloidní buňky ve vývoji a nemoci." Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-342350.

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Toll like receptors (TLRs) are germline-encoded pattern recognition receptors (PRRs) that play a central role in host cell recognition and responses to pathogens. Primarily they are responsible for induction and regulation of the innate and adaptive immune responses whereby the effector function is executed chiefly by differentiated myeloid cells. Somewhat unexpectedly, TLRs have been also shown to be involved in direct pathogen sensing by bone marrow-derived hematopoietic stem cells (HSCs) and hematopoietic progenitors when, under inflammatory conditions, the rapid generation of innate immune
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Lin, Yi-Sheng, and 林易陞. "Mechanism study on autophagy cargo receptor Joka2-involved chloroplast degradation." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/68929480746577128696.

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碩士<br>國立中興大學<br>生物化學研究所<br>105<br>Plant selective autophagy plays a significant role in stress responses, delay aging and nutrient shortage. The main function of selective autophagy is to recycle the specific elements like organelles, aggregated proteins or specific proteins. Previous studies indicated that phytoene desaturase (pds) silencing not only lead to the decrease of carotenoid and chlorophyll contents, but also cause an albino phenotype. Here, we characterized the relationship between pds silencing and leaf albino were characterized. We observed the number of chloroplasts was reduced
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Tung, Ying-Tsen, and 董盈岑. "The role of the autophagic cargo receptor p62 in the clearance of aggregation-prone proteins." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/80367896685135791504.

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博士<br>國立臺灣大學<br>動物學研究所<br>101<br>The accumulation of certain misfolded protein aggregates in the brain is a common feature in various neurodegenerative diseases, and is accepted as a major causative factor of neurodegeneration. Aggrephagy, the process by which protein aggregates are selectively degraded through macroautophagy, plays an essential role in protecting neurons from aggregate-induced neurotoxicity. Recent findings have identified p62/sequestosome1 as a cargo receptor that interacts with the autophagosomal membrane associated protein LC3, and recruits ubiquitin-positive protein aggre
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Pascoal, Jorge Filipe da Conceição. "Autophagy in hypothalamic cells: role of Neuropeptide Y." Master's thesis, 2011. http://hdl.handle.net/10400.1/2259.

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Dissertação de mest.Ciências Biomédicas. Departamento de Ciências Biomédicas e Medicina, Univ. do Algarve, 2011<br>A autofagia é um mecanismo celular, presente em todas as células eucariotas, responsável pela degradação e reciclagem de proteínas de longa vida e organelos danificados. É caracterizada pela formação de uma vesícula de membrana dupla, designada autofagossoma, que captura as proteínas ou os organelos a degradar e, posteriormente, se funde com lisossomas, levando à degradação dos substratos. Embora ocorra ao nível basal, a sua estimulação é normalmente provocada por sinais de priva
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Peng, Kuan-Jen, and 彭冠蓁. "TIM-1 receptor-mediated dengue virus-induced autophagy facilitates virus production." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/zrx3xn.

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Liang, Jing-Zhang, and 梁晉彰. "Functional Studies of Rice Autophagy Cargo Receptor Under Abiotic Stress Conditions." Thesis, 2019. http://ndltd.ncl.edu.tw/cgi-bin/gs32/gsweb.cgi/login?o=dnclcdr&s=id=%22107NCHU5107008%22.&searchmode=basic.

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碩士<br>國立中興大學<br>生物化學研究所<br>107<br>Plants frequently encounter adverse environmental conditions, such as heat stress or salt stress. Autophagy not only plays an important role in nutrient recycling and utilization, but also can reduce energy consumption during stress conditions. Next to BRCA1 gene 1 (NBR1), a selective autophagy cargo receptor, is to recognize degraded protein.ACR1 is a homologous protein of NBR1.However, the function of ACR1 in rice is still unknown. In this study, the role of ACR1 in rice was explored. We found that the expression levels (protein and mRNA) of ACR1 were induce
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Lai, Yi-Ping, та 賴益平. "Regulatory Mechanisms of Estrogen Receptor β on Hypoxia-induced Autophagic and Apoptotic Pathways in Myocardial Cells". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/87922722926966670275.

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碩士<br>中國醫藥大學<br>基礎醫學研究所碩士班<br>100<br>Myocardial infarction (MI) is the common cause of cardiomyocyte death. Even hypoxia alone is sufficient to induce apoptosis of cardiomyocytes. In hearts, autophagy play important roles in hypoxia-mediated cardioprotection or myocardial injury effects. To date, the hypoxia-inducible factor-1α (HIF-1α) transcriptional factor and the BH-3 only protein, Bcl-2 adenovirus E1B 19 kDa interacting protein 3 (BNIP3), are known to play fundamental roles in adaptive or death process in response to hypoxia. In addition, hypoxia induces insulin-like growth factor binding
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Conlon, Donna Marie. "Role of Autophagy and Peroxisome Proliferator-Activated Receptor Gamma2 in Hepatic Lipid Homeostasis." Thesis, 2014. https://doi.org/10.7916/D81C1V2R.

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The liver maintains lipid homeostasis by regulating hepatic uptake of circulating fatty acids (FA) and triglycerides (TG), de novo lipogenesis (DNL), FA, and secretion of TG in very low density lipoproteins (VLDL). To investigate the effects of reduced VLDL secretion on hepatic lipid homeostasis, we examined the effects of knockdown of either apolipoproteinB (apoB) or microsomal triglyceride transfer protein (MTP) using antisense oligonucleotides (ASO) for 6 weeks in apobec-1 knockout mice. Despite a similar decrease in VLDL secretion in mice treated with either apoB ASO or MTP ASO, there was
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Yueh, Yi-Mei, and 樂以梅. "Toll-like Receptor 7 Ligands Induce Autophagy and Their Effects on B cell Antigen Receptor Mediated Apoptosis in Ramos B cells." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/72030476377955515377.

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碩士<br>國立中興大學<br>生物醫學研究所<br>99<br>Autophagy is a highly conserved degradative process for cellular maintenance in all eukaryotic cells and its functional relationship with apoptosis is complex. Recent studies have shown that autophagy is important for the regulation of innate immunity and Toll-like receptor ( TLR ) ligands are potent autophagy inducers in macrophage. In addition, TLR ligands have been demonstrated to protect B cells from B cell antigen receptor ( BCR ) mediated apoptosis, an important mechanism to eliminate the autoreactive B cells. However, whether the TLR ligands could induce
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