Relevant bibliographies by topics / Autophagic receptors

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Autophagic receptors'

Author: Grafiati
Published: 13 April 2024
Last updated: 31 July 2025

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Journal articles on the topic "Autophagic receptors"

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Pino-Belmar, Camila, Rayén Aguilar, Guillermo E. Valenzuela-Nieto, et al. "An Intrinsic Host Defense against HSV-1 Relies on the Activation of Xenophagy with the Active Clearance of Autophagic Receptors." Cells 13, no. 15 (2024): 1256. http://dx.doi.org/10.3390/cells13151256.

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Autophagy engulfs cellular components in double-membrane-bound autophagosomes for clearance and recycling after fusion with lysosomes. Thus, autophagy is a key process for maintaining proteostasis and a powerful cell-intrinsic host defense mechanism, protecting cells against pathogens by targeting them through a specific form of selective autophagy known as xenophagy. In this context, ubiquitination acts as a signal of recognition of the cargoes for autophagic receptors, which direct them towards autophagosomes for subsequent breakdown. Nevertheless, autophagy can carry out a dual role since n
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Kimura, Tomonori, Ashish Jain, Seong Won Choi, et al. "TRIM-mediated precision autophagy targets cytoplasmic regulators of innate immunity." Journal of Cell Biology 210, no. 6 (2015): 973–89. http://dx.doi.org/10.1083/jcb.201503023.

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The present paradigms of selective autophagy in mammalian cells cannot fully explain the specificity and selectivity of autophagic degradation. In this paper, we report that a subset of tripartite motif (TRIM) proteins act as specialized receptors for highly specific autophagy (precision autophagy) of key components of the inflammasome and type I interferon response systems. TRIM20 targets the inflammasome components, including NLRP3, NLRP1, and pro–caspase 1, for autophagic degradation, whereas TRIM21 targets IRF3. TRIM20 and TRIM21 directly bind their respective cargo and recruit autophagic
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Kim, Eun Young, and Jae Man Lee. "Liver Metabolism at the Crossroads: The Reciprocal Control of Nutrient-Sensing Nuclear Receptors and Autophagy." International Journal of Molecular Sciences 26, no. 12 (2025): 5825. https://doi.org/10.3390/ijms26125825.

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Peroxisome proliferator-activated receptor α (PPARα, encoded by NR1C1) and farnesoid X receptor (FXR, encoded by NR1H4) are the two prominent nutrient-sensing nuclear receptors essential for maintaining hepatic metabolism during fasting and fed states, respectively. These nuclear receptors comprehensively regulate the transcription of numerous genes involved in fatty acid oxidation (FAO), ketogenesis, bile acid (BA) biosynthesis, and other metabolic processes critical for liver energy homeostasis. These receptors have been shown to have opposite impacts on autophagy, which is triggered by PPAR
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Lin, Long, Peiguo Yang, Xinxin Huang, Hui Zhang, Qun Lu, and Hong Zhang. "The scaffold protein EPG-7 links cargo–receptor complexes with the autophagic assembly machinery." Journal of Cell Biology 201, no. 1 (2013): 113–29. http://dx.doi.org/10.1083/jcb.201209098.

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The mechanism by which protein aggregates are selectively degraded by autophagy is poorly understood. Previous studies show that a family of Atg8-interacting proteins function as receptors linking specific cargoes to the autophagic machinery. Here we demonstrate that during Caenorhabditis elegans embryogenesis, epg-7 functions as a scaffold protein mediating autophagic degradation of several protein aggregates, including aggregates of the p62 homologue SQST-1, but has little effect on other autophagy-regulated processes. EPG-7 self-oligomerizes and is degraded by autophagy independently of SQS
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Luo, Shuwei, Xifeng Li, Yan Zhang, et al. "Cargo Recognition and Function of Selective Autophagy Receptors in Plants." International Journal of Molecular Sciences 22, no. 3 (2021): 1013. http://dx.doi.org/10.3390/ijms22031013.

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Autophagy is a major quality control system for degradation of unwanted or damaged cytoplasmic components to promote cellular homeostasis. Although non-selective bulk degradation of cytoplasm by autophagy plays a role during cellular response to nutrient deprivation, the broad roles of autophagy are primarily mediated by selective clearance of specifically targeted components. Selective autophagy relies on cargo receptors that recognize targeted components and recruit them to autophagosomes through interaction with lapidated autophagy-related protein 8 (ATG8) family proteins anchored in the me
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Chang, Chunmei, Xiaoshan Shi, Liv E. Jensen, et al. "Reconstitution of cargo-induced LC3 lipidation in mammalian selective autophagy." Science Advances 7, no. 17 (2021): eabg4922. http://dx.doi.org/10.1126/sciadv.abg4922.

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Selective autophagy of damaged mitochondria, protein aggregates, and other cargoes is essential for health. Cargo initiates phagophore biogenesis, which entails the conjugation of LC3 to phosphatidylethanolamine. Current models suggest that clustered ubiquitin chains on a cargo trigger a cascade from autophagic cargo receptors through the core complexes ULK1 and class III phosphatidylinositol 3-kinase complex I, WIPI2, and the ATG7, ATG3, and ATG12ATG5-ATG16L1 machinery of LC3 lipidation. This was tested using giant unilamellar vesicles (GUVs), GST-Ub4 as a model cargo, the cargo receptors NDP
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Valenzuela, Cristián A., Marco Azúa, Claudio A. Álvarez, Paulina Schmitt, Nicolás Ojeda, and Luis Mercado. "Evidence of the Autophagic Process during the Fish Immune Response of Skeletal Muscle Cells against Piscirickettsia salmonis." Animals 13, no. 5 (2023): 880. http://dx.doi.org/10.3390/ani13050880.

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Autophagy is a fundamental cellular process implicated in the health of the cell, acting as a cytoplasmatic quality control machinery by self-eating unfunctional organelles and protein aggregates. In mammals, autophagy can participate in the clearance of intracellular pathogens from the cell, and the activity of the toll-like receptors mediates its activation. However, in fish, the modulation of autophagy by these receptors in the muscle is unknown. This study describes and characterizes autophagic modulation during the immune response of fish muscle cells after a challenge with intracellular
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Papandreou, Margarita-Elena, and Nektarios Tavernarakis. "Selective Autophagy as a Potential Therapeutic Target in Age-Associated Pathologies." Metabolites 11, no. 9 (2021): 588. http://dx.doi.org/10.3390/metabo11090588.

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Progressive accumulation of damaged cellular constituents contributes to age-related diseases. Autophagy is the main catabolic process, which recycles cellular material in a multitude of tissues and organs. Autophagy is activated upon nutrient deprivation, and oncogenic, heat or oxidative stress-induced stimuli to selectively degrade cell constituents and compartments. Specificity and accuracy of the autophagic process is maintained via the precision of interaction of autophagy receptors or adaptors and substrates by the intricate, stepwise orchestration of specialized integrating stimuli. Pol
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Skendros, Panagiotis, and Ioannis Mitroulis. "Host Cell Autophagy in Immune Response to Zoonotic Infections." Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/910525.

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Autophagy is a fundamental homeostatic process in which cytoplasmic targets are sequestered within double-membraned autophagosomes and subsequently delivered to lysosomes for degradation. Accumulating evidence supports the pivotal role of autophagy in host defense against intracellular pathogens implicating both innate and adaptive immunity. Many of these pathogens cause common zoonotic infections worldwide. The induction of the autophagic machinery by innate immune receptors signaling, such as TLRs, NOD1/2, and p62/SQSTM1 in antigen-presenting cells results in inhibition of survival and elimi
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Li, Hongli, Celien Lismont, Cláudio F. Costa, Mohamed A. F. Hussein, Myriam Baes, and Marc Fransen. "Enhanced Levels of Peroxisome-Derived H2O2 Do Not Induce Pexophagy but Impair Autophagic Flux in HEK-293 and HeLa Cells." Antioxidants 12, no. 3 (2023): 613. http://dx.doi.org/10.3390/antiox12030613.

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Peroxisomes are functionally specialized organelles that harbor multiple hydrogen peroxide (H2O2)-producing and -degrading enzymes. Given that this oxidant functions as a major redox signaling agent, peroxisomes have the intrinsic ability to mediate and modulate H2O2-driven processes, including autophagy. However, it remains unclear whether changes in peroxisomal H2O2 (po-H2O2) emission impact the autophagic process and to which extent peroxisomes with a disturbed H2O2 metabolism are selectively eliminated through a process called “pexophagy”. To address these issues, we generated and validate
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Dissertations / Theses on the topic "Autophagic receptors"

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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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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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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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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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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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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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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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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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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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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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Books on the topic "Autophagic receptors"

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Conlon, Donna Marie. Role of Autophagy and Peroxisome Proliferator-Activated Receptor Gamma2 in Hepatic Lipid Homeostasis. [publisher not identified], 2014.

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Book chapters on the topic "Autophagic receptors"

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Viret, Christophe, and Mathias Faure. "Autophagy and Pattern Recognition Receptors." In Autophagy Networks in Inflammation. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30079-5_2.

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Juretschke, Thomas, Petra Beli, and Ivan Dikic. "Quantitative Phosphoproteomics of Selective Autophagy Receptors." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_46.

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Olsvik, Hallvard Lauritz, Trond Lamark, and Terje Johansen. "Autophagy Receptors Couple Cargo Destined to Be Degraded with the Core Autophagy Machinery." In Learning Materials in Biosciences. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-88121-3_4.

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Abert, Christine, and Sascha Martens. "Studies of Receptor-Atg8 Interactions During Selective Autophagy." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_11.

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MacLean, Jessica, and Kishore B. S. Pasumarthi. "Adrenergic Receptor Signaling Pathways in the Regulation of Apoptosis and Autophagy in the Heart." In Biochemistry of Apoptosis and Autophagy. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78799-8_2.

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Zhu, Yun, Jian Deng, Mei-Ling Nan, et al. "The Interplay Between Pattern Recognition Receptors and Autophagy in Inflammation." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0606-2_6.

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Wu, Yaoxing, and Jun Cui. "Selective Autophagy Regulates Innate Immunity Through Cargo Receptor Network." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0606-2_9.

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Singh, Aru, Megha Chagtoo, Bandana Chakravarti, and Madan M. Godbole. "Role of Inositol Triphosphate Receptor in Cancer and Its Targeting Through Autophagy." In Multi-Targeted Approach to Treatment of Cancer. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12253-3_19.

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Datan, Emmanuel, and Shaima Salman. "Autophagic cell death in viral infection: Do TAM receptors play a role?" In TAM Receptors in Health and Disease. Elsevier, 2020. http://dx.doi.org/10.1016/bs.ircmb.2020.10.001.

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Driscoll, Paul C. "Structural Studies of Death Receptors." In Regulated Cell Death Part B - Necroptotic, Autophagic and other Non-apoptotic Mechanisms. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-801430-1.00009-3.

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Conference papers on the topic "Autophagic receptors"

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Maher, Christina M., Jane Y. Tong, Charles G. Longen, et al. "Abstract 3023: Cytoplasmic sequestration and autophagic degradation of ErbB receptors in HER2-driven cancer cells by small molecule Sigma1 modulators." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3023.

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McCallum, K., L. Dunning, L. McGarvey, et al. "S75 Proteinase activated receptor-2 induced autophagy dysregulation." In British Thoracic Society Winter Meeting 2019, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 4 to 6 December 2019, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2019. http://dx.doi.org/10.1136/thorax-2019-btsabstracts2019.81.

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Bell, Emily S., Dongmei Zuo, and Morag Park. "Abstract 3453: Autophagic regulation of the Met receptor tyrosine kinase in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3453.

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Bonilla, Diana L., N. T. Eissa, and Youbao Sha. "Linking Autophagy And Phagocytosis: A Role For Class A Scavenger Receptors." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5055.

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Mccallum, K., L. Dunning, L. Mcgarvey, et al. "Regulation of lung autophagy by proteinase-activated receptor 2 activation." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.75.

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Wen, Yun-Fei, Whitney Spannuth Graybill, and Anil Sood. "Abstract 1330: Immunotherapy targeting folate receptor induces autophagy in ovarian cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1330.

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Wen, Yun-Fei, and Anil Sood. "Abstract 3529: Immunotherapy targeting folate receptor induces autophagy in ovarian cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3529.

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Wen, Yun-Fei, and Anil K. Sood. "Abstract 3817: Suicidal autophagy induced by immunotherapy targeting folate receptor in ovarian cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3817.

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Carey, Gregory B., Sanjit K. Roy, and Alphius Sesay. "Abstract 1728: Bcl-XL overexpression prevents B Cell receptor driven autophagy in IgM+ lymphoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1728.

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Tazawa, Hiroshi, Shuya Yano, Ryosuke Yoshida, Yasuo Urata, and Toshiyoshi Fujiwara. "Abstract 2862: Bioengineered oncolytic adenovirus induces autophagic cell death through an E2F1-microRNA-7-epidermal growth factor receptor axis." 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.am2011-2862.

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