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Готові списки джерел за темами / Autophagic receptors

Добірка наукової літератури з теми "Autophagic receptors"

Автор: Grafiati

Опубліковано: 13 квітня 2024

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Статті в журналах з теми "Autophagic receptors":

1

Kimura, Tomonori, Ashish Jain, Seong Won Choi, Michael A. Mandell, Kate Schroder, Terje Johansen, and Vojo Deretic. "TRIM-mediated precision autophagy targets cytoplasmic regulators of innate immunity." Journal of Cell Biology 210, no. 6 (September 7, 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 machinery to execute degradation. The autophagic function of TRIM20 is affected by mutations associated with familial Mediterranean fever. These findings broaden the concept of TRIMs acting as autophagic receptor regulators executing precision autophagy of specific cytoplasmic targets. In the case of TRIM20 and TRIM21, precision autophagy controls the hub signaling machineries and key factors, inflammasome and type I interferon, directing cardinal innate immunity response systems in humans.

2

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 (March 25, 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 SQST-1. SQST-1 directly interacts with EPG-7 and colocalizes with EPG-7 aggregates in autophagy mutants. Mutations in epg-7 impair association of SQST-1 aggregates with LGG-1/Atg8 puncta. EPG-7 interacts with multiple ATG proteins and colocalizes with ATG-9 puncta in various autophagy mutants. Unlike core autophagy genes, epg-7 is dispensable for starvation-induced autophagic degradation of substrate aggregates. Our results indicate that under physiological conditions a scaffold protein endows cargo specificity and also elevates degradation efficiency by linking the cargo–receptor complex with the autophagic machinery.

3

Luo, Shuwei, Xifeng Li, Yan Zhang, Yunting Fu, Baofang Fan, Cheng Zhu, and Zhixiang Chen. "Cargo Recognition and Function of Selective Autophagy Receptors in Plants." International Journal of Molecular Sciences 22, no. 3 (January 20, 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 membrane of the forming autophagosomes. In mammals and yeast, a large collection of selective autophagy receptors have been identified that mediate the selective autophagic degradation of organelles, aggregation-prone misfolded proteins and other unwanted or nonnative proteins. A substantial number of selective autophagy receptors have also been identified and functionally characterized in plants. Some of the autophagy receptors in plants are evolutionarily conserved with homologs in other types of organisms, while a majority of them are plant-specific or plant species-specific. Plant selective autophagy receptors mediate autophagic degradation of not only misfolded, nonactive and otherwise unwanted cellular components but also regulatory and signaling factors and play critical roles in plant responses to a broad spectrum of biotic and abiotic stresses. In this review, we summarize the research on selective autophagy in plants, with an emphasis on the cargo recognition and the biological functions of plant selective autophagy receptors.

4

Chang, Chunmei, Xiaoshan Shi, Liv E. Jensen, Adam L. Yokom, Dorotea Fracchiolla, Sascha Martens, and James H. Hurley. "Reconstitution of cargo-induced LC3 lipidation in mammalian selective autophagy." Science Advances 7, no. 17 (April 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 NDP52, TAX1BP1, and OPTN, and the autophagy core complexes. All three cargo receptors potently stimulated LC3 lipidation on GUVs. NDP52- and TAX1BP1-induced LC3 lipidation required all components, but not ULK1 kinase activity. However, OPTN bypassed the ULK1 requirement. Thus, cargo-dependent stimulation of LC3 lipidation is common to multiple autophagic cargo receptors, yet the details of core complex engagement vary between the different receptors.

5

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 (February 28, 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 pathogen Piscirickettsia salmonis. For this, primary cultures of muscle cells were challenged with P. salmonis, and the expressions of immune markers il-1β, tnfα, il-8, hepcidin, tlr3, tlr9, mhc-I and mhc-II were analyzed through RT-qPCR. The expressions of several genes involved in autophagy (becn1, atg9, atg5, atg12, lc3, gabarap and atg4) were also evaluated with RT-qPCR to understand the autophagic modulation during an immune response. In addition, LC3-II protein content was measured via Western blot. The challenge of trout muscle cells with P. salmonis triggered a concomitant immune response to the activation of the autophagic process, suggesting a close relationship between these two processes.

6

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 (March 2, 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 validated HEK-293 and HeLa pexophagy reporter cell lines in which the production of po-H2O2 can be modulated. We demonstrate that (i) po-H2O2 can oxidatively modify multiple selective autophagy receptors and core autophagy proteins, (ii) neither modest nor robust levels of po-H2O2 emission act as a prime determinant of pexophagy, and (iii) high levels of po-H2O2 impair autophagic flux by oxidative inhibition of enzymes involved in LC3II formation. Unexpectedly, our analyses also revealed that the autophagy receptor optineurin can be recruited to peroxisomes, thereby triggering pexophagy. In summary, these findings lend support to the idea that, during cellular and organismal aging, peroxisomes with enhanced H2O2 release can escape pexophagy and downregulate autophagic activity, thereby perpetuating the accumulation of damaged and toxic cellular debris.

7

Papandreou, Margarita-Elena, and Nektarios Tavernarakis. "Selective Autophagy as a Potential Therapeutic Target in Age-Associated Pathologies." Metabolites 11, no. 9 (August 31, 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. Polymorphisms in genes regulating selective autophagy have been linked to aging and age-associated disorders. The involvement of autophagy perturbations in aging and disease indicates that pharmacological agents balancing autophagic flux may be beneficial, in these contexts. Here, we introduce the modes and mechanisms of selective autophagy, and survey recent experimental evidence of dysfunctional autophagy triggering severe pathology. We further highlight identified pharmacological targets that hold potential for developing therapeutic interventions to alleviate cellular autophagic cargo burden and associated pathologies.

8

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 elimination of invading pathogens. Furthermore, Th1 cytokines induce the autophagic process, whereas autophagy also contributes to antigen processing and MHC class II presentation, linking innate to adaptive immunity. However, several pathogens have developed strategies to avoid autophagy or exploit autophagic machinery to their advantage. This paper focuses on the role of host cell autophagy in the regulation of immune response against intracellular pathogens, emphasizing on selected bacterial and protozoan zoonoses.

9

Wang, Wang-sheng, Wen-jiao Li, Ya-wei Wang, Lu-yao Wang, Ya-bing Mi, Jiang-wen Lu, Yi Lu, Chu-yue Zhang, and Kang Sun. "Involvement of serum amyloid A1 in the rupture of fetal membranes through induction of collagen I degradation." Clinical Science 133, no. 3 (February 2019): 515–30. http://dx.doi.org/10.1042/cs20180950.

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Abstract The de novo synthesis of serum amyloid A1 (SAA1) is augmented in human fetal membranes at parturition. However, its role in parturition remains largely unknown. Here, we investigated whether SAA1 was involved in the rupture of fetal membranes, a crucial event in parturition accompanied with extensive degradation of collagens. Results showed that SAA1 decreased both intracellular and extracellular COL1A1 and COL1A2 abundance, the two subunits of collagen I, without affecting their mRNA levels in human amnion fibroblasts. These reductions were completely blocked only with inhibition of both matrix metalloproteases (MMPs) and autophagy. Consistently, SAA1 increased MMP-2/9 abundance and the markers for autophagic activation including autophagy related (ATG) 7 (ATG7) and the microtubule-associated protein light chain 3 β (LC3B) II/I ratio with the formation of LC3 punctas and autophagic vacuoles in the fibroblasts. Moreover, the autophagic degradation of COL1A1/COL1A2 and activation of MMP-2/9 by SAA1 were blocked by inhibitors for the toll-like receptors 2/4 (TLR2/4) or NF-κB. Finally, reciprocal corresponding changes of SAA1 and collagen I were observed in the amnion following spontaneous rupture of membranes (ROM) at parturition. Conclusively, SAA1 may participate in membrane rupture at parturition by degradating collagen I via both autophagic and MMP pathways. These effects of SAA1 appear to be mediated by the TLR2/4 receptors and the NF-κB pathway.

10

Cheng, Li-sha, Jing Li, Yun Liu, Fu-ping Wang, Si-qi Wang, Wei-min She, Sheng-di Wu, Xiao-long Qi, Yong-ping Zhou, and Wei Jiang. "HMGB1-induced autophagy: a new pathway to maintain Treg function during chronic hepatitis B virus infection." Clinical Science 131, no. 5 (February 15, 2017): 381–94. http://dx.doi.org/10.1042/cs20160704.

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High-mobility group box-1 (HMGB1) protein, as one of the well-known damage-associated molecular pattern molecules (DAMPs), is enriched in chronic hepatitis B virus (HBV) infection and has a context-dependent role in autophagy, a highly conserved self-digestive process in response to environmental stress. Recent mouse studies indicate that autophagy is highly active in regulatory T (Treg)-cells. In the present study, we evaluated spontaneous and induced autophagy of peripheral Treg cells from 98 patients with chronic hepatitis B (CHB), by measuring levels of lipidated form of microtubule-associated light chain 3 (LC3-II, marker for closed autophagosomes) and observing autophagic vacuoles (AV) with transmission electron microscope. No significant difference was found in spontaneous autophagy of either Treg or CD4+ naive cells when comparing CHB patients with healthy subjects, apart from CHB-Treg showed significantly higher autophagic activity after activation by anti-CD3–CD28 beads. Besides, incubation of CHB-Treg cells with CHB-serum greatly maintained their autophagic behaviour, which could be significantly diminished by blocking HMGB1 with the neutralizing antibody. Further, we characterized time- and dose-dependent effects by recombinant HMGB1 protein on autophagy of CHB-Treg cells. We also documented a significant up-regulation of HMGB1 and its receptors [toll-like receptor (TLR4), receptor for advanced glycation end-product (RAGE)] in both peripheral and intra-hepatic microenvironments of CHB patients. Moreover, the RAGE–extracellular regulated protein kinases (ERK) axis and rapamycin-sensitive components of mammalian target of rapamycin (mTOR) pathways were demonstrated in vitro to be involved in HMGB1-induced autophagy of Treg cells. Additionally, HMGB1-induced autophagy could maintain cell survival and functional stability of CHB-Treg cells. Our findings could open new perspectives in developing therapeutic strategies to activate specific anti-HBV immunity by diminishing Treg autophagy.

Більше джерел

Дисертації з теми "Autophagic receptors":

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'Escherichia coli, appelées les AIEC (adherent-invasive E. coli), a été rapportée. Les AIEC sont des pathobiontes capables d'adhérer et d'envahir les cellules épithéliales intestinales ainsi que de se répliquer en macrophages sans induire la mort cellulaire, entraînant une réponse immunitaire dérégulée. Par ailleurs, des études ont montré que plusieurs polymorphismes dans les gènes de l'autophagie (ATG16L1, IRGM, ULK1, etc.) sont associés à un risque augmenté de développer la MC. L'autophagie est un processus essentiel au maintien de l'homéostasie cellulaire permettant la dégradation et le recyclage de composants cytoplasmiques et de pathogènes via le lysosome. Toutefois, certains pathogènes intracellulaires développent diverses stratégies pour échapper à la dégradation par l'autophagie. Dans ce contexte, l'objectif de mes travaux de thèse était d'identifier les récepteurs autophagiques responsables de la reconnaissance des AIEC, ainsi que les gènes nécessaires aux AIEC pour échapper à l'autophagie.Le 1er axe de mes travaux de thèse a montré que la déficience de p62 ou NDP52 dans les cellules HeLa entraîne une augmentation de la réplication intracellulaire de la souche de référence AIEC LF82 et de la production de cytokines pro-inflammatoires. L'analyse par microscopie confocale a révélé la colocalisation de p62 ou NDP52 avec la bactérie AIEC LF82 et la protéine LC3, un marqueur de l'autophagie. Ainsi, nos résultats suggèrent que p62 et NDP52 agiraient comme des récepteurs autophagiques pour contrôler la réplication intracellulaire des AIEC. De plus, nous avons étudié l'impact d'un polymorphisme du gène NDP52 associé à une susceptibilité augmentée de développer la MC, appelé NDP52Val248Ala, sur le contrôle des AIEC. Aucune différence n'a été observée dans le nombre de bactéries AIEC LF82 intracellulaires entre les cellules HeLa exprimant le variant à risque NDP52Val248Ala et celles exprimant l'allèle sauvage, suggérant un autre rôle de ce variant, probablement dans le contrôle de l'inflammation.Le 2ème axe de mes travaux de thèse s'est concentré sur l'identification de gènes nécessaires aux AIEC pour échapper au contrôle par l'autophagie en utilisant la technique Transposon Sequencing (Tn-Seq). Brièvement, une banque de mutants de la souche AIEC LF82 a été créée de manière « saturée », c'est-à-dire que chacun des gènes du génome bactérien a été interrompu par au moins un transposon, conduisant à son invalidation. Cette banque de mutants a été utilisée pour infecter des cellules HeLa contrôles et déficientes pour l'autophagie. À 24h post-infection, l'ADN des mutants a été extrait et les sites d'insertion du transposon déterminés par séquençage ont permis d'identifier 68 gènes différentiellement représentés entre nos deux conditions. Les gènes sur-représentés dans les cellules HeLa déficientes pour l'autophagie par rapport aux cellules contrôles, sont les gènes potentiellement nécessaires aux AIEC pour échapper à l'autophagie. Ainsi, cette étude permettrait d'identifier de nouvelles cibles pour limiter la virulence des AIEC.En conclusion, ces travaux contribuent à la compréhension des divers aspects de l'interaction entre les cellules hôtes et les bactéries AIEC associées à la MC et permettront, à l'avenir, de mieux caractériser la pathogenèse de cette maladie
Crohn's disease (CD) is a chronic inflammatory bowel disease, of which the etiology is multifactorial. It results from the complex interaction between genetic predispositions, environmental factors and alterations in the intestinal microbiota composition, inducing a deregulation of the intestinal immune system. To date, CD is incurable, only treatments aimed at alleviating symptoms and preventing recurrences and complications are available. In CD patients, an increase in the prevalence of particular strains of Escherichia coli, called AIEC (adherent-invasive E. coli) strains, has been reported. AIEC are the pathobionts able to adhere to and to invade intestinal epithelial cells as well as replicate inside macrophages without inducing cell death, leading to a dysregulated immune response. Furthermore, it has been shown that several polymorphisms in autophagy-related genes (ATG16L1, IRGM, ULK1, etc.) are associated with an increased risk to develop CD. Autophagy is an essential process for maintaining cellular homeostasis, which allows the degradation and recycling of cytoplasmic components and pathogens via the lysosome. However, some intracellular pathogens develop various strategies to escape autophagy degradation. In this context, the aim of my thesis was to identify the autophagic receptors responsible for AIEC recognition, as well as the genes necessary for AIEC to escape autophagy.The first part of my thesis showed that the depletion of p62 or NDP52 in HeLa cells leads to an increase in the intracellular replication of the AIEC LF82 reference strain and the production of pro-inflammatory cytokines. Confocal microscopy analysis revealed the colocalization of p62 or NDP52 with AIEC LF82 bacteria and LC3 protein, a marker of autophagy. Thus, our results suggest that p62 and NDP52 could act as autophagic receptors to control AIEC intracellular replication. Additionally, we investigated the impact of a polymorphism in the NDP52 gene associated with increased susceptibility to develop CD, called NDP52Val248Ala, on the control of AIEC. No difference was observed in the AIEC LF82 intracellular number between HeLa cells expressing the NDP52Val248Ala risk variant and those expressing the wild-type allele, suggesting another role for this variant, probably in the control of inflammation.The second part of my thesis focused on the identification of the genes necessary for AIEC to escape from autophagy control by the Transposon Sequencing (Tn-Seq) technique. Briefly, a mutant library of the AIEC LF82 strain was created in a “saturated” manner, meaning that each gene of the bacterial genome was inserted by at least one transposon, leading to its invalidation. This mutant library was used to infect control and autophagy-deficient HeLa cells. At 24 hours post-infection, the mutants DNA was extracted and transposon insertion sites determined by sequencing allowed the identification of 68 genes differentially represented between our two conditions. The genes over-represented in autophagy-deficient HeLa cells compared to control cells, are potential genes necessary for AIEC to escape from autophagy control. Thus, this study could allow the identification of new targets to limit the virulence of AIEC.In conclusion, this work contributes to the understanding of various aspects of the interaction between host cells and CD-associated AIEC bacteria and, in the future, will aide to better characterize the etiopathogenesis of this disease

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 Salmonella mais aussi durant l'autophagie basale. De manière intéressante, ce rôle de NDP52 dans la maturation est indépendant de son rôle dans le ciblage de la bactérie puisque ces fonctions nécessitent des domaines et des partenaires moléculaires de NDP52 distincts. Nous montrons aussi que d'autres récepteurs peuvent participer à la maturation comme Optineurine. Ce travail montre donc que NDP52 assure deux rôles durant la xénophagie en ciblant les bactéries vers les autophagosomes en formation puis en promouvant la maturation de l'autophagosome. De plus, nous proposons aussi un possible mécanisme de régulation de ces deux fonctions par des modifications post-traductionnelles des récepteurs autophagiques.Ce travail démontre que les récepteurs autophagiques jouent des rôles au-delà du ciblage des pathogènes qui sont aussi cruciaux pour une xénophagie efficace. De plus, les récepteurs autophagiques sont aussi nécessaires pour le déroulement de l'autophagie basale. Ces travaux offrent une nouvelle compréhension de la régulation moléculaire de l'autophagie et de la xénophagie
Xenophagy relies on the ability of the autophagy process to selectively entrap intracellular pathogens within autophagosomes to degrade them into autolysosomes. The selectivity of the process relies on proteins named autophagy receptors that share the ability to recognise cytosolic cargos on one hand and autophagosome-bound members of the ATG8 family on the other. Among autophagy receptors NDP52 has been described to target Salmonella Typhimurium to the growing autophagosome. We describe a new unexpected role for NDP52, as this receptor also regulates the maturation of Salmonella-containing autophagosomes and during ongoing autophagy. Interestingly, the role of NDP52 in maturation is independent from its role in targeting as they rely on different binding domains and protein partners. We also show that other autophagy receptors also mediate autophagosome maturation such as Optineurin. Therefore, our work shows that NDP52 plays a dual function during xenophagy first by targeting bacteria to growing autophagosomes and then by assuring autophagosome maturation. Moreover, we also provide insights as to how these dual roles are regulated by post-translational modifications of autophagy receptors.This work demonstrates that autophagy receptors have other roles beyond pathogen targeting that are also crucial for an efficient xenophagy. Moreover, autophagy receptors are also necessary for autophagy completion in uninfected cells. These results strengthen our understanding of both ongoing autophagy and xenophagy molecular mechanisms

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 rougeole (VR). Les données de l'équipe montrent qu'il induit et utilise toutes les étapes de l'autophagie, afin de se répliquer efficacement. Mes travaux montrent que des protéines du virus peuvent interagir avec au moins deux protéines cellulaires NDP52 et T6BP qui sont des récepteurs autophagiques (protéines cytosoliques ayant un domaine de liaison aux autophagosomes et un domaine de liaison au substrat à dégrader, par exemple des pathogènes). J'ai alors étudié le rôle des récepteurs autophagiques T6BP, NDP52 et Optineurine dans la réplication virale. J'ai aussi participé à une étude décrivant que NDP52 et Optineurine régulent en plus la maturation. Mes travaux de thèse démontrent un tel double rôle pour T6BP. Cependant, seuls T6BP et NDP52 sont nécessaires à la réplication du VR bien qu'elle requiert la maturation autophagique. Ainsi mes résultats suggèrent d'une part que les trois récepteurs puissent réguler la maturation d'autophagosomes distincts.D'autre part, le VR pourrait exploiter individuellement les autophagosomes dont la maturation dépend de T6BP et NDP52 pour se répliquer
Macroautophagy ensures cell homeostasis through the recycling of obsolete or deleterious cytosolic components and its deregulation is associated with several pathologies. It is also a defense mechanism as it allows the elimination of intracellular pathogens. The most important autophagic step is maturation, during which the cytosolic substrate-containing vesicle, the autophagosome, fuses with lysosomes and the degradation occurs. We study autophagy regulation and the consequences of its disruption during infections and in particular by measles virus (MeV). Our team has shown that MeV induces and exploits all steps of autophagy, to replicate more efficiently. My results indicate that viral proteins can interact with at least two cellular proteins, NDP52 and T6BP, which are autophagy receptors (cytosolic proteins that carry an autophagosome-binding domain and a domain binding substrates that would be degraded, such as intracellular pathogens). I then studied the role of autophagic receptors T6BP, NDP52 and OPTINEURIN in viral replication. I also took part in a study describing NDP52 and OPTINEURIN as autophagosome maturation regulators. My work depicts the same dual role for T6BP. However, only T6BP and NDP52 are necessary for MeV replication even though it requires autophagosome maturation. Thus, my results suggest that the three autophagy receptors might regulate distinct autophagosome maturation on one hand. On the other, MeV could individually exploit autophagosomes, the maturation of which is regulated by T6BP or NDP2 to replicate efficiently

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 récepteurs à dépendance ont été étudiés: Notch3 et Kremen1 dans le contexte du contrôle de l'homéostasie et plus particulièrement dans le contrôle de la tumorigenèse du cancer du sein. Nous montrons que le récepteur à dépendance Notch3 est perdu dans le cancer du sein, dû à un gain significatif de méthylation, entre le tissu normal et le tissu tumoral dans les patients. Notch3 a également un rôle pro-apoptotique dans les cellules endothéliales dans le cancer du poumon. Des études effectuées sur des cohortes de cancer nous ont permis de voir que le ligand Dickkopf1 (Dkk1), qui lie le récepteur Kremen1, est sur-exprimé dans plusieurs cancers tandis que le récepteur il est perdu dans les cancers. Rétablir l'expression de Kremen1 ou invalider Dkk1 dans la lignée de cancer du sein de type basal MDA-MB 231 conduit à une forte mort cellulaire de type autophagique. En ce qui concerne les enjeux thérapeutiques de ces travaux, nous avons pu sélectionner plusieurs anticorps dirigés contre le domaine extracellulaire de Kremen1, qui induisent la mort des cellules cancéreuses
Membrane receptors are major actors of the interaction between a cell and its environment. They are able to trigger different types of signals such as survival, differentiation, migration or cell death. The work presented in this manuscript has been done on a particular family of receptors called dependence receptors. They are characterized by their function rather than by their structure. In the presence of their ligand they induce a survival signal whereas in the absence of the ligand they induce an active signal of cell death. Two new dependence receptors have been studied: Notch3 and Kremen1, in the context of homeostasis control, and more particularly in the control of breast cancer tumorigenesis. We show that Notch3 dependence receptor is lost in breast cancer, because of a significant gain of methylation observed between the normal tissu and the tumoral tissue within the same patient. Notch3 plays also a pro-apoptotic role in endothelial cells of lung cancer. Experiences carried on cancer cohorts have allowed us to notice that the Dickkopf (Dkk1) ligand, which links the Kremen1 receptor, is over-expressed in several cancers whereas the receptor is lost in different cancers. Restoring Kremen1 expression or disabling Dkk1 in breast cancer basal type MDA-MB 231 cells, leads to large autophagic cell death. Concerning therapeutic approaches, we selected several antibodies against Kremen1 extra-cellular domain, which induce the death of cancer cells

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 half, the trafficking and function of these proteins remain relatively unclear. My work in this thesis identifies and characterises a novel trafficking route for ATG9 and VMP1 and shows that both these proteins traffic via the dynamin-independent ARF6-associated pathway. Moreover, I also show that these proteins physically interact with each other. In addition, the tools developed during these studies helped me identify a new role for the most common autophagy receptor protein, p62. I show that p62 can specifically associate with and sequester LC3-I in autophagy-impaired cells (ATG9 and ATG16 null cells) leading to formation of LC3-positive structures that can be misinterpreted as mature autophagosomes. Perturbations in the levels of p62 were seen to affect the formation of these LC3-positive structures in cells. This observation, therefore, questions the reliability of LC3-immunofluorescence assays in autophagy-impaired cells as method of assessing autophagy and points towards the homeostatic function played by p62 in autophagy-impaired cells.

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 dedémontrer la dégradation autophagique de protéines impliquées dans la migration cellulaire,telles que des intégrines, ou encore les protéines RhoA et Src, l'impact fonctionnel del'autophagie sur la migration cellulaire demeure sujet à controverse. Alors que l'autophagie estdécrite comme un processus pro-migratoire et pro-invasif dans certaines études, d'autrestravaux indiquent que l'inactivation des protéines pro-autophagiques stimule l'invasion descellules cancéreuses. De plus, l'effet fonctionnel des RCPG chimiotactiques sur l’activitéautophagique reste totalement inexploré. Sur la base de ces données, les objectifs de mon travail de thèse ont été i) d’évaluer les effets des RCPG chimiotactiques, le CXCR4 et l’UT,sur le processus autophagique et ii) d’étudier l’impact de cette modulation sur la migrationcellulaire. Pour ce faire, nous avons utilisé des cellules HEK-293, transfectées à l’aide deconstruits permettant l’expression des RCPG CXCR4 et UT, ainsi que la lignée deglioblastome humain U87, exprimant ces deux récepteurs de manière endogène.Nous avons dans un premier temps évalué l’activité autophagique à l’aide de laprotéine de fusion EGFP-LC3, marqueur des autophagosomes. Nous avons ainsi démontréque l’activation du CXCR4 et de l’UT provoque une diminution significative de la biogénèsedes autophagosomes. Une étape essentielle de cette biogenèse est le recrutement des protéinesAtg16L1 et Atg5 à la membrane plasmique, conduisant à la formation d'endosomes Atg16L1-Atg5-positifs, appelés « endosomes pré-autophagiques ». Cette population d’endosomesconstitue une source importante de phospholipides nécessaire à l’expansion du phagophore etla formation d’un autophagosome mature. Afin d’évaluer l’impact des RCPG chimiotactiquessur le recrutement de la protéine Atg16L1 à la membrane plasmique, nous avons bloqué leprocessus d’endocytose par l’utilisation d’un inhibiteur de la dynamine, le Dynasore. Cettemolécule provoque une accumulation marquée de la protéine Atg16L1 dans les endosomespré-autophagiques en formation, retenus à la membrane plasmique
Autophagy is a catabolic process by which certain cytosolic proteins are directed to thelysosomal compartment to be degraded. This process begins with the sequestration ofcytoplasmic components, by a multimembrane structure called the phagophore. The closure ofthe phagophore gives rise to a double membrane vesicle called autophagosome, which thenmerges with lysosomes in order to degrade its luminal content. Autophagy modulation allowsa dynamic remodeling of the cellular proteome. Although recent evidence has demonstratedautophagic degradation of key proteins involved in cell migration, such as integrins, RhoAand the Src kinase, the functional impact of autophagy on cell migration remainscontroversial. While autophagy is described as a pro-migratory and pro-invasive process insome studies, others indicate that the inactivation of pro-autophagic proteins stimulates thecancer cell invasion. In addition, the functional effect of chemotactic GPCR on autophagicactivity remains unexplored. On the basis of these data, the objectives of my thesis were i) toevaluate the effects of the chemotactic GPCRs for SDF-1 (CXCR4) and for the vasoactivepeptide urotensin II (UT), on the autophagic process and ii) to study the impact of thismodulation on cell migration. In order to do this, we used HEK-293 cells, transfected with constructs allowing the expression of CXCR4 and UT, as well as the human glioblastomaline, U87, which endogenously expresses these two receptors. Previous studies have demonstrated a direct interaction of Atg5 with membranes,suggesting that recruitment of Atg16L1 to the plasma membrane may depend on Atg5. This prompted us to evaluate the formation of Atg16L1-positive pre-autophagic endosomes,following depletion of Atg5 levels. Several interfering RNAs, targeting the transcriptencoding Atg5, have been tested and, as expected, these interfering RNAs completely blockedthe recruitment of Atg16L1 to forming pre-autophagic endosomes. We then tested the effectsof chemotactic GPCRs on the subcellular localization of the Atg5 protein. By confocalmicroscopy, we found that a significant fraction of Atg5 localized to the plasma membraneunder basal conditions. The activation of CXCR4 or UT is accompanied by a marked decreaseof the Atg5 pool localized at the plasma membrane. Furthermore, we have demonstrated thatthe anti-autophagic effects of chemotactic GPCRs are completely abrogated byoverexpression of a recombinant Atg5 protein, suggesting that chemotactic GPCRs exert theiranti-autophagic effects by reducing the membrane pool of Atg5, necessary for the productionof pre-autophagic endosomes, and the expansion of the phagophore

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 whether membrane rafts mediate NR signaling and autophagy in cortices of adult male rats subjected to moderate TBI and in sham-operated controls. These studies demonstrate that membrane rafts of the normal rat cortex contain a novel multi-protein signaling complex that links the NR2B glutamate receptor and the autophagic protein Beclin 1. TBI caused a rapid disruption of this complex in which NR2B and pCaMKII were recruited to membrane microdomains. Alteration in NR2B-Beclin 1 association in membrane rafts resulted in activation of autophagy as demonstrated by increased expression of key autophagic proteins Beclin 1, ATG 5 and ATG 7, and significant increases in autophagic vacuoles in neurons of traumatized brains. Administration of the NR2B antagonist RO 25-6981 significantly blocked TBI-induced redistribution of NR2B signaling intermediates and Beclin 1 and delayed the increase in autophagy protein expression in traumatized cortices. Thus, stimulation of autophagy by NR2B signaling may be regulated by redistribution of Beclin 1 in membrane rafts after TBI.

8

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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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 autophagic substrates in conditions of oxidative stress remain unknown. The aim of this thesis work is to understand the mechanisms underlying the oligomerisation and the aggregation of p62 during oxidation, looking at post-translational modifications that can lead to the formation of protein aggregates. We found that p62 senses and is regulated by oxidative stress. In response to oxidation, two cysteine (Cys) residues C105 and C113 of p62 mediate the formation of disulphide-linked conjugates (DLC). The formation of p62 DLC was reduced upon antioxidants addition, while inhibitors of the antioxidant system enhanced their development. This feature was critical for the function of p62 as an autophagy receptor as well as for the accumulation of polyubiquitinated aggregates. Indeed, the accumulation and degradation of p62 and its substrates was impaired following mutation of the Cys residues implicated in DLC formation, while the interaction between p62 and polyubiquitinated substrates was not affected. Oxidation of p62 was also required for cell survival in conditions of oxidative stress, indicating the physiological importance of the correct function of p62 in selective autophagy. In addition, formation of p62 DLC was increased in ageing and age-related neurodegenerative diseases, possibly as a compensatory mechanism to protect cells in increased oxidative conditions. In conclusion, we reveal a new mechanism of p62 oligomerisation aiding the selective autophagy of dysfunctional proteins under oxidative stress conditions.

10

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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Книги з теми "Autophagic receptors":

1

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

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Частини книг з теми "Autophagic receptors":

1

Viret, Christophe, and Mathias Faure. "Autophagy and Pattern Recognition Receptors." In Autophagy Networks in Inflammation, 21–41. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30079-5_2.

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2

Juretschke, Thomas, Petra Beli, and Ivan Dikic. "Quantitative Phosphoproteomics of Selective Autophagy Receptors." In Methods in Molecular Biology, 691–701. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_46.

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3

Abert, Christine, and Sascha Martens. "Studies of Receptor-Atg8 Interactions During Selective Autophagy." In Methods in Molecular Biology, 189–96. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_11.

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4

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, 23–36. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78799-8_2.

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5

Zhu, Yun, Jian Deng, Mei-Ling Nan, Jing Zhang, Akinkunmi Okekunle, Jiang-Yuan Li, Xiao-Qiang Yu, and Pei-Hui Wang. "The Interplay Between Pattern Recognition Receptors and Autophagy in Inflammation." In Advances in Experimental Medicine and Biology, 79–108. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0606-2_6.

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6

Wu, Yaoxing, and Jun Cui. "Selective Autophagy Regulates Innate Immunity Through Cargo Receptor Network." In Advances in Experimental Medicine and Biology, 145–66. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0606-2_9.

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7

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, 311–21. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12253-3_19.

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8

Datan, Emmanuel, and Shaima Salman. "Autophagic cell death in viral infection: Do TAM receptors play a role?" In TAM Receptors in Health and Disease, 123–68. Elsevier, 2020. http://dx.doi.org/10.1016/bs.ircmb.2020.10.001.

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9

Driscoll, Paul C. "Structural Studies of Death Receptors." In Regulated Cell Death Part B - Necroptotic, Autophagic and other Non-apoptotic Mechanisms, 201–42. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-801430-1.00009-3.

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10

Echeverría-Valencia, Gabriela. "Phagocytosis of Mycobacterium tuberculosis: A Narrative of the Uptaking and Survival." In Phagocytosis - Main Key of Immune System [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.110067.

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Mycobacterium tuberculosis is the causal agent of human tuberculosis. The initial events of the establishment of the infection include the phagocytosis by several innate immune response cells. This chapter will discuss the immune cells involved, the phagocytic pattern recognition receptors (PPRs) that recognize and mediate bacteria phagocytosis (such as C-type lectin receptors, Toll-like receptors, complement receptors, and scavenger receptors), and the outcome of this initial interaction. Additionally, the bacterial strategies to evade the immune response—which includes the inhibition of the phagosome maturation and arresting of phagosome acidification, the mechanisms to survive to the reactive nitrogen species and reactive oxygen species, and finally, the resistance to the apoptosis and autophagy—will be reviewed. Finally, the host-pathogen interaction of M. tuberculosis with the phagocytic human cells during the primary events of the tuberculosis infection will also be reviewed.

Тези доповідей конференцій з теми "Autophagic receptors":

1

Maher, Christina M., Jane Y. Tong, Charles G. Longen, Mercedes I. Lioni, Jeffrey D. Thomas, Xing Tan, Logan Tyler, Fernando U. Garcia, and Felix J. Kim. "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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2

McCallum, K., L. Dunning, L. McGarvey, M. Hollywood, J. Brzeszczynska, A. Crilly, JC Lockhart, and GJ Litherland. "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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3

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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4

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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5

Mccallum, K., L. Dunning, L. Mcgarvey, M. Hollywood, J. Brzeszczynska, C. Goodyear, J. Lockhart, A. Crilly, and G. Litherland. "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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6

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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7

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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8

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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9

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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10

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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