Autophagy reports最新文献_第4页

Autophagy in the endothelium commands flow-mediated vascular reactivity and remodelling, and regulates VEGFR2 subcellular localization and signalling 内皮细胞中的自噬可以控制血流介导的血管反应性和重塑，并调节VEGFR2亚细胞定位和信号传导

Autophagy reports Pub Date : 2023-11-13 DOI: 10.1080/27694127.2023.2277585

Pierre-Louis Tharaux, Olivia Lenoir

引用次数: 0

Structural biology of the Atg8 and Atg12 conjugation systems at8和Atg12偶联体系的结构生物学

Autophagy reports Pub Date : 2023-11-10 DOI: 10.1080/27694127.2023.2277582

Nobuo N. Noda

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MALT-1 shortens lifespan by inhibiting autophagy in the intestine of C. elegans MALT-1通过抑制秀丽隐杆线虫肠道内的自噬而缩短寿命

Autophagy reports Pub Date : 2023-11-09 DOI: 10.1080/27694127.2023.2277584

Julie Vérièpe-Salerno, Silvia Podavini, Marcus J.C. Long, Irina Kolotuev, Muriel Cuendet, Margot Thome

引用次数: 0

Dual function of the Leon/USP5 deubiquitinase in the ubiquitin-proteasome and autophagic pathways Leon/USP5去泛素酶在泛素-蛋白酶体和自噬途径中的双重功能

Autophagy reports Pub Date : 2023-11-09 DOI: 10.1080/27694127.2023.2278299

Yuchieh Jay Lin, Guang-Chao Chen

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TRIMming down Mycobacterium tuberculosis replication: TRIM32 is required for bacterial ubiquitination and autophagy induction in macrophages 修剪结核分枝杆菌的复制:TRIM32是巨噬细胞中细菌泛素化和自噬诱导所必需的

Autophagy reports Pub Date : 2023-11-05 DOI: 10.1080/27694127.2023.2278120

Alessandra Romagnoli, Martina Di Rienzo, Mauro Piacentini, Gian Maria Fimia

{"title":"TRIMming down Mycobacterium tuberculosis replication: TRIM32 is required for bacterial ubiquitination and autophagy induction in macrophages","authors":"Alessandra Romagnoli, Martina Di Rienzo, Mauro Piacentini, Gian Maria Fimia","doi":"10.1080/27694127.2023.2278120","DOIUrl":"https://doi.org/10.1080/27694127.2023.2278120","url":null,"abstract":"Mycobacterium tuberculosis (Mtb) promotes its intracellular persistence by subverting defense mechanisms, such as autophagy. Remarkably, enhancing autophagy is sufficient to trigger intracellular Mtb killing and effective immune response, making this process a valid target of host-directed therapies. However, several aspects of autophagy regulation during Mtb infection remain unsolved. Tripartite motif (TRIM) proteins are a large family of ubiquitin ligases primarily involved in innate immunity by regulating inflammation and autophagy. By combining transcriptomic and infectivity screens, we recently identified a set of TRIMs that modulate Mtb replication. In detail, overexpression of TRIM22 and TRIM32 reduces Mtb growth in THP1 macrophages, while that of TRIM36 and TRIM56 promotes Mtb replication. Analysis of the molecular mechanisms underlying inhibition of Mtb replication by TRIM32 showed that its overexpression promote xenophagy, a selective autophagy of pathogens, by increasing Mtb ubiquitination and the recruitment of CALCOCO2/NDP52 (calcium binding and coiled-coil domain 2) and MAP1LC3B (microtubule-associated protein 1 light chain 3B) to intracellular bacteria. Consistently, TRIM32 downregulation reduces the xenophagic response, resulting in increased Mtb replication. Altogether, we characterized a novel role for TRIM32 in the host response to pathogen infections and identify TRIM36 and TRIM56 as possible host factors required for Mtb infection.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"61 10","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135726256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AeiA, an Atg8-interacting protein in Aspergillus oryzae , promotes peroxisome degradation by pexophagy AeiA是米曲霉中一种与atg8相互作用的蛋白，通过噬酶促进过氧化物酶体降解

Autophagy reports Pub Date : 2023-10-23 DOI: 10.1080/27694127.2023.2271281

Takashi Kikuma, Joichiro Nishio

引用次数: 0

MTFP1 is a mitophagy receptor that operates in PINK1/PRKN-dependent mitophagy and promotes oral cancer cell survival MTFP1是一种线粒体自噬受体，在PINK1/ prkn依赖性的线粒体自噬中起作用，并促进口腔癌细胞的存活

Autophagy reports Pub Date : 2023-10-16 DOI: 10.1080/27694127.2023.2267882

Debasna P Panigrahi, Sujit K Bhutia

{"title":"MTFP1 is a mitophagy receptor that operates in PINK1/PRKN-dependent mitophagy and promotes oral cancer cell survival","authors":"Debasna P Panigrahi, Sujit K Bhutia","doi":"10.1080/27694127.2023.2267882","DOIUrl":"https://doi.org/10.1080/27694127.2023.2267882","url":null,"abstract":"MTFP1 (mitochondrial fission process 1), an inner mitochondrial membrane protein, plays a crucial role in mitochondrial fission to maintain mitochondrial morphology. Our study found that MTFP1 contains a LIR (LC3-interacting region) to interact with MAP1LC3B (microtubule-associated protein 1 light chain 3 beta) and serves as a mitophagy receptor to eliminate damaged mitochondria. Interestingly, mutation of MTFP1 LIR motif (MTFP1mLIR) inhibits this interaction, decreasing mitophagy in oral cancer cells. Moreover, knockdown of PRKN (parkin RBR E3 ubiquitin protein ligase) or PINK1 (PTEN-induced kinase 1) abolished mitophagy in MTFP1-overexpressing oral cancer cells. In this setting, we observed that MTFP1mLIR-expressing cells display a decrease in TOMM20 (translocase of outer mitochondrial membrane 20) levels without affecting those of COX4 (cytochrome c oxidase subunit 4). In contrast, loss of PRKN or PINK1 caused inhibition of both TOMM20 and COX4 degradation in MTFP1mLIR-expressing cells exposed to cellular stress, suggesting that PRKN may activate the rupture of outer mitochondrial membrane in MTFP1-overexpressing cells for effective mitophagy. We also observed that MTFP1 is beneficial to oral cancer cell survival exposed to anticancer drugs, such as cisplatin, through mitophagy, since inhibition of MTFP1-dependent mitophagy induced cell death. Thus, targeting MTFP1-associated mitophagy could represent a strategy for oral cancer therapy.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"86 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136142802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ouabain promotes claudin-1, -2, and -4 autophagic degradation through oxidative stress and AMPK activation in MDCK cells 瓦巴因通过氧化应激和AMPK激活促进MDCK细胞中claudin-1、-2和-4的自噬降解

Autophagy reports Pub Date : 2023-10-02 DOI: 10.1080/27694127.2023.2256146

Jessica P. Campos-Blázquez, Catalina Flores-Maldonado, Juan M. Gallardo, José Bonilla-Delgado, Alan A. Pedraza-Ramírez, Octavio López-Méndez, Enoc M. Cortés-Malagón, Rubén G. Contreras

{"title":"Ouabain promotes claudin-1, -2, and -4 autophagic degradation through oxidative stress and AMPK activation in MDCK cells","authors":"Jessica P. Campos-Blázquez, Catalina Flores-Maldonado, Juan M. Gallardo, José Bonilla-Delgado, Alan A. Pedraza-Ramírez, Octavio López-Méndez, Enoc M. Cortés-Malagón, Rubén G. Contreras","doi":"10.1080/27694127.2023.2256146","DOIUrl":"https://doi.org/10.1080/27694127.2023.2256146","url":null,"abstract":"Epithelial cells transport substances through the cellular and paracellular pathways. The last one depends on tight junctions, particularly on claudins, the family of integral membrane proteins responsible for the permeability and selectivity of these junctions. 300 nM ouabain (OUA) induces endocytosis and lysosomal degradation of claudin-2 and -4 in an Src and ERK1/2 kinases-dependent manner. Here we investigate whether OUA-induced lysosomal degradation of claudins implicates autophagy in renal epithelial Madin-Darby canine kidney cells. During autophagy, LC3 protein binds phosphatidylethanolamine and incorporates, together with protein p62, into the phagophore. Subsequently, the autolysosome degrades both LC3 and p62 proteins. OUA’s occupancy of its site in the Na⁺/K⁺ATPase (300 nM, 10 h) increases autophagic flux because of degradation of LC3 and p62 and an increase in the number of autophagosomes, as detected by fluorescent LC3 and p62 puncta and the rise in autolysosomes seen by the GFP-LC3-RFP probe. Finally, OUA increases the colocalisation of claudin-1, -2, or -4 with p62 in these puncta. OUA induces autophagy increasing reactive oxygen species generation that activates AMP-activated protein kinase, phosphorylating ULK1 at S555. The autophagy inducer rapamycin causes a degradation of the studied claudins comparable to the one generated by OUA. Furthermore, the autophagy inhibitor dorsomorphin blocks OUA-induced autophagy and claudin-1, -2, and -4 degradation. These results demonstrated that OUA induces claudin-1, -2, and -4 autophagy through oxidative stress.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"97 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135899242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

INPP5D inhibits anti-malarial immunity by promoting IRF3 degradation through selective autophagy INPP5D通过选择性自噬促进IRF3降解，从而抑制抗疟疾免疫

Autophagy reports Pub Date : 2023-09-18 DOI: 10.1080/27694127.2023.2254614

Hongyu Li, Xiao Yu

{"title":"INPP5D inhibits anti-malarial immunity by promoting IRF3 degradation through selective autophagy","authors":"Hongyu Li, Xiao Yu","doi":"10.1080/27694127.2023.2254614","DOIUrl":"https://doi.org/10.1080/27694127.2023.2254614","url":null,"abstract":"As a member of the inositol polyphosphate-5-phosphatase family, INPP5D (inositol polyphosphate-5-phosphatase D) is an important regulator of immune cell activation. To date, the mechanisms underlying anti-malarial immunity have not been elucidated. We recently identified INPP5D as a negative regulator of IFN-I (type I interferon) signaling by promoting autophagic degradation of IRF3 (interferon regulatory factor 3) during malaria infection. Mechanistically, INPP5D enhances the association between IRF3 and the autophagy receptor CALCOCO2/NDP52 (calcium binding and coiled-coil domain 2), which promotes the K63-linked ubiquitination of IRF3 at K313 and serves as a signal for CALCOCO2-dependent selective macroautophagy (hereafter autophagy). Moreover, INPP5D is downregulated by IFN-I-induced miR-155-5p after Plasmodium yoelii (P. yoelii) nigeriensis N67 infection and plays a role as a feedback loop between IFN-I signaling and autophagy. Thus, our study reveals the key role of INPP5D in mediating the crosstalk between IFN-I response and autophagy during anti-malarial immune responses, and suggests that INPP5D may be a potential therapeutic target to control malaria.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135203607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Improved volume CLEM revealed that aberrant phagophores and RB1CC1/FIP200-containing clusters appear surround SQSTM1/p62 aggregates in Atg9a-deficient cells 改进的体积CLEM显示，在atg9a缺陷细胞中，在SQSTM1/p62聚集体周围出现了异常的吞噬团和RB1CC1/FIP200-containing团

Autophagy reports Pub Date : 2023-09-15 DOI: 10.1080/27694127.2023.2256599

Soichiro Kakuta, Junji Yamaguchi, Chigure Suzuki, Isei Tanida, Yasuo Uchiyama

{"title":"Improved volume CLEM revealed that aberrant phagophores and RB1CC1/FIP200-containing clusters appear surround SQSTM1/p62 aggregates in <i>Atg9a</i>-deficient cells","authors":"Soichiro Kakuta, Junji Yamaguchi, Chigure Suzuki, Isei Tanida, Yasuo Uchiyama","doi":"10.1080/27694127.2023.2256599","DOIUrl":"https://doi.org/10.1080/27694127.2023.2256599","url":null,"abstract":"ATG9A is an important membrane protein in mammalian macroautophagy. The formation of autophagosomes and phagophores is blocked in atg9a KO cells. However, it remains possible that residual membrane formation activity exists in these cells. These precursor structures that precede phagophores are, if they exist, rare and may be difficult to find. Here, we introduce the modified volume correlative light and electron microscopy (CLEM) method to analyze these structures three-dimensionally. In addition to target proteins, mitochondria were labeled as a landmark for precise correlation of slice images by a confocal fluorescence microscope and a focused ion beam scanning electron microscope. We found phagophores and small membrane vesicles near SQSTM1/p62 aggregates in atg9a KO cells, indicating that phagophores could be formed in atg9a-deficient cells, although they were immature and inefficient. Furthermore, we found that RB1CC1/FIP200-positive structures formed clusters around SQSTM1/p62 with ferritin and TAX1BP1. Taken together, our method contributes to the understanding of undiscovered fine structures.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135395744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0