Academic literature on the topic 'LC3 associated phagocytosis (LAP)'
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Journal articles on the topic "LC3 associated phagocytosis (LAP)"
Yuan, Jin, Qiuyu Zhang, Shihua Chen, Min Yan, and Lei Yue. "LC3-Associated Phagocytosis in Bacterial Infection." Pathogens 11, no. 8 (July 30, 2022): 863. http://dx.doi.org/10.3390/pathogens11080863.
Full textDuan, Zhimin, Qing Chen, Leilei Du, Jianbo Tong, Song Xu, Rong Zeng, Yuting Ma, Xu Chen, and Min Li. "Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/4938649.
Full textGalais, Mathilde, Baptiste Pradel, Isabelle Vergne, Véronique Robert-Hebmann, Lucile Espert, and Martine Biard-Piechaczyk. "La phagocytose associée à LC3 (LAP)." médecine/sciences 35, no. 8-9 (August 2019): 635–42. http://dx.doi.org/10.1051/medsci/2019129.
Full textLai, Shu-chin, and Rodney J. Devenish. "LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy." Cells 1, no. 3 (July 30, 2012): 396–408. http://dx.doi.org/10.3390/cells1030396.
Full textMorita, Maya, Mayu Kajiye, Chiye Sakurai, Shuichi Kubo, Miki Takahashi, Daiki Kinoshita, Naohiro Hori, and Kiyotaka Hatsuzawa. "Characterization of MORN2 stability and regulatory function in LC3-associated phagocytosis in macrophages." Biology Open 9, no. 6 (May 15, 2020): bio051029. http://dx.doi.org/10.1242/bio.051029.
Full textMartinez, Jennifer, Andrew Oberst, Thirumala Devi-Kanneganti, and Douglas Green. "LC3-associated phagocytosis is a critical regulator of innate immunity. (P1261)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 56.13. http://dx.doi.org/10.4049/jimmunol.190.supp.56.13.
Full textWen, Haitao, Tianliang Li, Xinghui Li, Yu Lei, and Douglas R. Green. "Mitochondrial Calcium Signaling Facilitates Bacterial Survival by Restraining LC3-associated Phagocytosis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 227.1. http://dx.doi.org/10.4049/jimmunol.204.supp.227.1.
Full textInomata, Megumi, Shuying Xu, Pallavi Chandra, Simin N. Meydani, Genzou Takemura, Jennifer A. Philips, and John M. Leong. "Macrophage LC3-associated phagocytosis is an immune defense against Streptococcus pneumoniae that diminishes with host aging." Proceedings of the National Academy of Sciences 117, no. 52 (December 21, 2020): 33561–69. http://dx.doi.org/10.1073/pnas.2015368117.
Full textWan, JingHong, Emmanuel Weiss, Sanae Ben Mkaddem, Morgane Mabire, Pierre-Marie Choinier, Olivia Picq, Tristan Thibault-Sogorb, et al. "LC3-associated phagocytosis protects against inflammation and liver fibrosis via immunoreceptor inhibitory signaling." Science Translational Medicine 12, no. 539 (April 15, 2020): eaaw8523. http://dx.doi.org/10.1126/scitranslmed.aaw8523.
Full textLi, Xuelei, Mark Prescott, Ben Adler, John D. Boyce, and Rodney J. Devenish. "Beclin 1 Is Required for Starvation-Enhanced, but Not Rapamycin-Enhanced, LC3-Associated Phagocytosis of Burkholderia pseudomallei in RAW 264.7 Cells." Infection and Immunity 81, no. 1 (October 31, 2012): 271–77. http://dx.doi.org/10.1128/iai.00834-12.
Full textDissertations / Theses on the topic "LC3 associated phagocytosis (LAP)"
Gluschko, Alexander [Verfasser], and Thorsten [Gutachter] Hoppe. "LC3-associated Phagocytosis induced by the ß2 integrin Mac-1 enhances Immunity to Infection with Listeria monocytogenes / Alexander Gluschko ; Gutachter: Thorsten Hoppe." Köln : Universitäts- und Stadtbibliothek Köln, 2018. http://d-nb.info/1165772752/34.
Full textStetter, Maurice [Verfasser], Antje [Gutachter] Gohla, Wolfgang [Gutachter] Kastenmüller, and Ann [Gutachter] Wehman. "LC3-associated phagocytosis seals the fate of the second polar body in \(Caenorhabditis\) \(elegans\) / Maurice Stetter ; Gutachter: Antje Gohla, Wolfgang Kastenmüller, Ann Wehman." Würzburg : Universität Würzburg, 2021. http://d-nb.info/123075864X/34.
Full textLigeon, Laure-Anne. "Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie." Thesis, Lille 2, 2013. http://www.theses.fr/2013LIL2S043/document.
Full textYersinia pseudotuberculosis is a member of the Enterobacteriaceae family. In human, Y. pseudotuberculosis infection is responsible for enteric and, in rare cases, erythema nodosum. During host colonization, a minor part of Y. pseudotuberculosis presents an intracellular replication step. Y. pseudotuberculosis can replicate inside macrophages by hijacking the autophagy pathway. The bacteria are able to block autophagosome maturation by acidification impairment, which allows to create a replicative niche. The membrane traffic during internalization of Yersinia remains poorly characterized. First, we highlighted that in epithelial cells, Y. pseudotuberculosis replicates mainly in vacuoles positive for LC3, a hallmark of autophagy. Surprisingly, this LC3-positive-vacuole presents only single limiting membrane. Second, we showed that SNARE proteins play a role in Y. pseudotuberculosis intracellular traffic. VAMP3 and VAMP7 are sequentially recruited to Yersinia-containing vacuoles (YCVs). VAMP7 is involved in the LC3 recruitment to YCVs with single- and double-membrane. We proposed that VAMP3 is a component of the molecular checkpoint for bacterial commitment to either single- or double-membrane LC3-positive pathway. Third, we characterized the traffic of endosomal proteins recruited to LC3-positive-YCV with single membrane in epithelial cells. We showed that markers of early endosome and proteins involved in autophagosome formation, are recruited to YCVs during the early stage of infection. Then, the vacuole acquire late endosomal and lysosomal proteins but acidification is not observed. Finally, we initiated a high-content screening approach for the identification of SNARE partners.Overall this work illustrates the importance of LC3-positive compartment ultrastructure analysis. Our result demonstrate how bacterial subvert the molecular machinery of the host in order to create a replicative niche. Finally, we present the importance of autophagy regulation by highlighting for the first times the existence of a molecular checkpoint between two LC3-positive vacuoles with different morphologies
Asare, Patrick. "An investigation of the Rubicon/LC3 associated phagocytosis (LAP) dysregulation as a therapeutic target in chronic obstructive pulmonary diseases (COPD) and in response to cigarette smoke exposure." Thesis, 2021. https://hdl.handle.net/2440/135321.
Full textThesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2022
Viegas, Michelle. "The role of the endocytic and autophagic molecular machineries in the removal of apoptotic cells." Doctoral thesis, 2014. http://hdl.handle.net/10316/25251.
Full textEvery day the human body turns over billions of cells ensuring the disposal of unwanted targets that die by apoptosis. The prompt and efficient removal of apoptotic cells by cell line (vascular SMC). The maturation of phagosomes containing dying cells was compared with the processing of phagosomes loaded with IgG-opsonized particles, which are internalized via Fcγ-receptors and are the best characterized phagocytic model. At the present work, we provide evidence that the nature of the cargo modulates the phagocytic response, since phagosomes carrying apoptotic particles reach the lysosomes with a delay when compared to those containing IgG-opsonized particles. Furthermore, for the first time, we have identified some canonical autophagy effectors in phagolysosome formation, suggesting that LC3-Associated Phagocytosis (LAP), a process involved in phagosome maturation, implies more than the phagosomal recruitment of LC3 (Sanjuan et al., 2007). Indeed, experiments performed in bone marrow-derived macrophages from p62-KO mice clearly suggest that p62, despite not being required for LC3 recruitment, is important for phagolysosome biogenesis. In summary, this data will improve our knowledge on the molecular machinery and mechanisms involved in efferocytosis. In the end, we hope to contribute to a better understanding of efferocytosis and the ways to modulate this process, which could culminate with the discovery of therapies that may benefit patients with atherosclerosis and other type of diseases in which efferocytosis is not efficient.phagocytes, referred as to efferocytosis, plays an essential role during development, tissue repair and in the maintenance of homeostasis, triggering an immunological tolerance (Henson and Hume, 2006). On the other hand, defective clearance promote dying cell accumulation, converting harmless apoptotic cells into a risky secondary necrotic state that, eventually, expose self-antigens, which has been linked to the onset of several human disorders, including autoimmunity and chronic inflammatory diseases, such as atherosclerosis (Elliott and Ravichandran, 2010). Atherosclerosis remains the biggest cause of mortality and disabilities worldwide, especially in developing countries. The formation of the atheroma starts with the retention of low-density lipoproteins (LDL) inside the wall of blood vessels, where they become subjected to several chemical modifications. These modified-LDL induce the recruitment of monocyte-derived macrophages, which internalize the deposited fatty material. Over time, these lipid-loaded macrophages are no longer able to process the cholesterol, forming foam-cells that eventually undergo apoptosis. In early stages of atherogenesis, efferocytosis is very efficient; however in advanced lesions this process somehow fails, triggering an inflammatory response that, in turn, recruits more cells, including neighboring smooth muscle cells (SMC). Besides macrophages, SMC, the major cell type in the blood vessels wall, play an essential role by dealing with the dying cell accumulation, thus preventing atheroma progression (Moore and Tabas, 2011). Although many efforts have been done to understand the machinery involved in the recognition of apoptotic cells by phagocytic cells (receptors and ligands), as well as the immune response elicited, very little is known about the intracellular transport of phagosomes containing apoptotic cells and its subsequent digestion into phagolysosomes, the final degradative compartment of the host cell (Hochreiter-Hufford and Ravichandran, 2013). Beyond that, C. elegans has been the model organism in studies of engulfment and degradation of apoptotic cells, which reinforce the need to have more information about the development of this process in mammalian systems. Thus, it is crucial to our understanding, to figure out the causes of the inefficient efferocytosis and how it contributes to the pathogenesis of certain diseases. In this thesis, we have performed a detailed study on the maturation of phagosomes containing human aged red blood cells, our apoptotic cell model, using a mammalian phagocytic
Stetter, Maurice. "LC3-associated phagocytosis seals the fate of the second polar body in \(Caenorhabditis\) \(elegans\)." Doctoral thesis, 2021. https://doi.org/10.25972/OPUS-23198.
Full textUm besser zu verstehen, wie undifferenzierte pluripotente Zellen mit abgestorbenen Zellen umgehen, wird in dieser Dissertation die Phagozytose und der Abbau des 2. Polkörpers der weiblichen Meiose im Fadenwurm C. elegans untersucht. Mithilfe von fluorenzenzmikroskopischen Aufnahmen wird in dieser Arbeit gezeigt, dass beide Polkörper schon früh ihre Membranintegrität verlieren. Der 2. Polkörper, welcher direkten Kontakt zu embryonischen Zellen hat, wird daraufhin mithilfe des Rac1-Orthologs CED-10 phagozytiert. Es wird gezeigt, dass es sich bei dem Abbauprozess um LC3-assoziierte Phagozytose handelt. Die RAB-7 GTPase ist notwendig für die Rekrutierung von Lysosomen, während LC3 darauf keinen Einfluss hat, aber trotzdem den Abbau des Polkörpers beschleunigt. Mit dieser Arbeit konnte ein genetisches Modell für die Erforschung von Zelltod und der LC3-assoziierten Phagozytose entwickelt werden und weitere Aspekte der Phagosomreifung und des -abbaus aufgedeckt werden
Book chapters on the topic "LC3 associated phagocytosis (LAP)"
Ligeon, Laure-Anne, Susana Romao, and Christian Münz. "Analysis of LC3-Associated Phagocytosis and Antigen Presentation." In Methods in Molecular Biology, 145–68. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6581-6_10.
Full textJacquin, Elise, Katherine Fletcher, and Oliver Florey. "Imaging Noncanonical Autophagy and LC3-Associated Phagocytosis in Cultured Cells." In Methods in Molecular Biology, 295–303. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_19.
Full textHolownia, A., A. Niechoda, J. Lachowicz, E. Golabiewska, and U. Baranowska. "Phagocytosis and Autophagy in THP-1 Cells Exposed to Urban Dust: Possible Role of LC3-Associated Phagocytosis and Canonical Autophagy." In Advances in Medicine and Medical Research, 55–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/5584_2018_323.
Full textWong, Sing-Wai, Sandeep Upadhyay, and Jennifer Martinez. "LC3-associated phagocytosis." In Non-Canonical Autophagy, 69–91. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820538-9.00005-3.
Full textCunha, Larissa D., and Jennifer Martinez. "Autophagy and LC3-Associated Phagocytosis Mediate the Innate Immune Response." In Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging, 303–19. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-805420-8.00016-0.
Full textConference papers on the topic "LC3 associated phagocytosis (LAP)"
Asare, P. F., E. Roscioli, P. R. Hurtado, H. B. Tran, S. Maiolo, and S. Hodge. "THP-1 Macrophages Exposed to the Factors in Cigarette Smoke Exhibit Dysregulation of LC3-Associated Phagocytosis (LAP)." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4752.
Full textGreen, Douglas R. "Abstract IA13: LC3-associated phagocytosis in inflammation and anticancer immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-ia13.
Full textMoore, Jamie Aaron, Jayna J. Mistry, Charlotte Hellmich, Aisha Jibril, Tom Wileman, Angela Collins, Kristian M. Bowles, and Stuart A. Rushworth. "Abstract 2752: LC3-associated phagocytosis in bone marrow macrophages suppresses AML progression through TIM-4 mediated STING activation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2752.
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