3,305 results match your criteria Autophagy[Journal]


Using Reactome to build an autophagy mechanism knowledgebase.

Autophagy 2020 Jun 2:1-12. Epub 2020 Jun 2.

European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus , Cambridge, UK.

The 21st century has revealed much about the fundamental cellular process of autophagy. Autophagy controls the catabolism and recycling of various cellular components both as a constitutive process and as a response to stress and foreign material invasion. There is considerable knowledge of the molecular mechanisms of autophagy, and this is still growing as new modalities emerge. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761659DOI Listing

Corrigendum.

Authors:

Autophagy 2020 May 31. Epub 2020 May 31.

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http://dx.doi.org/10.1080/15548627.2020.1770431DOI Listing

Selective autophagy controls the stability of transcription factor IRF3 to balance type I interferon production and immune suppression.

Autophagy 2020 May 31:1-14. Epub 2020 May 31.

State Key Laboratory of Oncology in South China, MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University , Guangzhou, GD, China.

IRF3 (interferon regulatory factor 3) is one of the most critical transcription factors in antiviral innate immune signaling, which is ubiquitously expressed in a variety of cells. Although it has been demonstrated that IRF3 can provoke multiple cellular processes during viral infection, including type I interferon (IFN) production, the mechanisms underlying the precise regulation of IRF3 activity are still not completely understood. Here, we report that selective macroautophagy/autophagy mediated by cargo receptor CALCOCO2/NDP52 promotes the degradation of IRF3 in a virus load-dependent manner. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761653DOI Listing

TNFAIP8L2/TIPE2 impairs autolysosome reformation via modulating the RAC1-MTORC1 axis.

Autophagy 2020 May 28:1-16. Epub 2020 May 28.

Department of Immunology, School of Basic Medical Science, Shandong University , Jinan, China.

Macroautophagy/autophagy is an evolutionarily conserved process that involves the selective degradation of cytoplasmic components within lysosomes in response to starvation. Autophagy is an ancient defense mechanism that has been closely integrated with the immune system and has multiple effects on innate and adaptive immunity. The pro-inflammatory and anti-inflammatory cytokines can activate and inhibit autophagy, respectively. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761748DOI Listing

Selective autophagy of MHC-I promotes immune evasion of pancreatic cancer.

Autophagy 2020 May 27:1-2. Epub 2020 May 27.

Department of Radiation Oncology, Perlmutter Cancer Center, New York University School of Medicine , New York, NY, USA.

Major histocompatibility complex class I (MHC-I) is a key molecule in anti-tumor adaptive immunity. MHC-I is essential for endogenous antigen presentation by cancer cells and subsequent recognition and clearance by CD8 T cells. Defects in MHC-I expression occur frequently in several cancers, leading to impaired antigen presentation, immune evasion and/or resistance to immune checkpoint blockade (ICB) therapy. Read More

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http://dx.doi.org/10.1080/15548627.2020.1769973DOI Listing

A location, location, location mutation impairs DNM2-mediated release of nascent autophagosomes from recycling endosomes.

Autophagy 2020 May 26:1-2. Epub 2020 May 26.

Department of Medical Genetics, Cambridge Institute for Medical Research , Cambridge, UK.

Elucidation of the membranes contributing to autophagosomes has been a critical question in the field, and an area of active research. Recently, we showed that key events in autophagosome formation, from PtdIns3P formation/WIPI2 recruitment to LC3-GABARAP membrane conjugation, occur on the RAB11A-positive compartment (recycling endosomes). This observation raised the question of how the LC3-positive autophagosome precursors detach from the recycling endosome. Read More

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http://dx.doi.org/10.1080/15548627.2020.1764210DOI Listing

High-throughput screening of functional deubiquitinating enzymes in autophagy.

Autophagy 2020 May 26:1-12. Epub 2020 May 26.

The Third Affiliated Hospital, MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University , Guangzhou, China.

Macroautophagy/autophagy, a eukaryotic homeostatic process that sequesters cytoplasmic constituents for lysosomal degradation, is orchestrated by a number of autophagy-related (ATG) proteins tightly controlled by post-translational modifications. However, the involvement of reversible ubiquitination in the regulation of autophagy remains largely unclear. Here, we performed a single-guide RNA-based screening assay to investigate the functions of deubiquitinating enzymes (DUBs) in regulating autophagy. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761652DOI Listing

Synucleinphagy: a microglial "community cleanup program" for neuroprotection.

Autophagy 2020 May 26. Epub 2020 May 26.

Departments of Neurology and Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY, 10029, USA.

SNCA/α-synuclein is a major component in the Lewy body (LB), a pathological hallmark of Parkinson disease (PD) and dementia with Lewy body (DLB), collectively known as synucleinopathies. SNCA/α-synuclein can be secreted from neurons and transmitted to neighboring cells including neurons and glia, which underlie the spreading of LB pathology as described by Braak and colleagues. We recently have investigated the mechanism and significance for microglia, a prototypic phagocyte in the brain, in engulfing and controlling SNCA/α-synuclein homeostasis in the brain. Read More

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http://dx.doi.org/10.1080/15548627.2020.1774149DOI Listing

Autophagy and post-ischemic conditioning in retinal ischemia.

Autophagy 2020 May 26:1-21. Epub 2020 May 26.

Department of Anesthesiology, And College of Medicine, University of Illinois at Chicago , Chicago, IL, USA.

Retinal ischemia is a major cause of vision loss and a common underlying mechanism associated with diseases, such as diabetic retinopathy and central retinal artery occlusion. We have previously demonstrated the robust neuroprotection in retina induced by post-conditioning (post-C), a brief period of ischemia, 24 h, following a prolonged and damaging initial ischemia. The mechanisms underlying post-C-mediated retinal protection are largely uncharacterized. Read More

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http://dx.doi.org/10.1080/15548627.2020.1767371DOI Listing

Restoration of CTSD (cathepsin D) and lysosomal function in stroke is neuroprotective.

Autophagy 2020 May 25:1-19. Epub 2020 May 25.

Departments of Pharmacology and Toxicology, University of Alabama School of Medicine , Birmingham, AL, USA.

Stroke is a leading cause of death and disability. The pathophysiological mechanisms associated with stroke are very complex and not fully understood. Lysosomal function has a vital physiological function in the maintenance of cellular homeostasis. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761219DOI Listing

LC3-associated phagocytosis in myeloid cells, a fireman that restrains inflammation and liver fibrosis, via immunoreceptor inhibitory signaling.

Autophagy 2020 May 31:1-3. Epub 2020 May 31.

Centre de Recherche Sur l'Inflammation (CRI), INSERM, Université de Paris , Paris, France.

Control of systemic and hepatic inflammation, in particular originating from monocytes/macrophages, is crucial to prevent liver fibrosis and its progression to end-stage cirrhosis. LC3-associated phagocytosis (LAP) is a non-canonical form of autophagy that shifts the monocyte/macrophage phenotype to an anti-inflammatory phenotype. In a recent study, we uncovered LAP as a protective mechanism against inflammation-driven liver fibrosis and systemic inflammation in the context of cirrhosis. Read More

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http://dx.doi.org/10.1080/15548627.2020.1770979DOI Listing

Discovery of a potent SCAP degrader that ameliorates HFD-induced obesity, hyperlipidemia and insulin resistance via an autophagy-independent lysosomal pathway.

Autophagy 2020 May 20:1-22. Epub 2020 May 20.

State Key Laboratory of Natural Medicines, China Pharmaceutical University , Nanjing, Jiangsu, China.

SCAP (SREBF chaperone) regulates SREBFs (sterol regulatory element binding transcription factors) processing and stability, and, thus, becomes an emerging drug target to treat dyslipidemia and fatty liver disease. However, the current known SCAP inhibitors, such as oxysterols, induce endoplasmic reticulum (ER) stress and NR1H3/LXRα (nuclear receptor subfamily 1 group H member 3)-SREBF1/SREBP-1 c-mediated hepatic steatosis, which severely limited the clinical application of this inhibitor. In this study, we identified a small molecule, lycorine, which binds to SCAP, which suppressed the SREBF pathway without inducing ER stress or activating NR1H3. Read More

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http://dx.doi.org/10.1080/15548627.2020.1757955DOI Listing

Regulation of autophagy by DNA G-quadruplexes.

Autophagy 2020 May 18. Epub 2020 May 18.

Department of Neurology, the University of Texas McGovern Medical School at Houston , TX.

Guanine-rich DNA strands can form secondary structures known as G-quadruplexes (G4-DNA). G4-DNA is important for the regulation of replication and transcription. We recently showed that the expression of , a gene that is critical for macroautophagy/autophagy, is controlled by G4-DNA in neurons. Read More

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http://dx.doi.org/10.1080/15548627.2020.1769991DOI Listing

MLKL contributes to Western diet-induced liver injury through inhibiting autophagy.

Autophagy 2020 May 13:1-2. Epub 2020 May 13.

Department of Inflammation and Immunity, Cleveland Clinic, Center for Liver Disease Research , Cleveland, OH, USA.

Macroautophagy/autophagy is critical in maintaining cellular functions and homeostasis. Dynamic regulation of autophagy is associated with development of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH); however, the mechanisms involved in the regulation of autophagy in NAFLD/NASH are not well understood. Here we discuss our recent work identifying MLKL as an important nexus between autophagy and necroptosis in models of NAFLD/NASH. Read More

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http://dx.doi.org/10.1080/15548627.2020.1760624DOI Listing

Autophagy in the physiological endometrium and cancer.

Autophagy 2020 May 13:1-19. Epub 2020 May 13.

Laboratory of Precision Medicine, Oncobell Program. Bellvitge Biomedical Research Institute (IDIBELL), Gran via De l'Hospitalet , Barcelona, Spain.

Autophagy is a highly conserved catabolic process and a major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. An increasing body of evidence has unveiled autophagy as an indispensable biological function that helps to maintain normal tissue homeostasis and metabolic fitness that can also lead to severe consequences for the normal cellular functioning when altered. Recent accumulating data point to autophagy as a key player in a wide variety of physiological and pathophysiological conditions in the human endometrium, one of the most proficient self-regenerating tissues in the human body and an instrumental player in placental species reproductive function. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752548DOI Listing

BHRF1, a BCL2 viral homolog, disturbs mitochondrial dynamics and stimulates mitophagy to dampen type I IFN induction.

Autophagy 2020 May 13:1-20. Epub 2020 May 13.

Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC) , 91198, Gif-sur-Yvette, France.

Mitochondria respond to many cellular functions and act as central hubs in innate immunity against viruses. This response is notably due to their role in the activation of interferon (IFN) signaling pathways through the activity of MAVS (mitochondrial antiviral signaling protein) present at the mitochondrial surface. Here, we report that the BHRF1 protein, a BCL2 homolog encoded by Epstein-Barr virus (EBV), inhibits IFNB/IFN-β induction by targeting the mitochondria. Read More

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http://dx.doi.org/10.1080/15548627.2020.1758416DOI Listing

CYBB/NOX2 in conventional DCs controls T cell encephalitogenicity during neuroinflammation.

Autophagy 2020 May 13:1-15. Epub 2020 May 13.

Department of Neurology with Institute of Translational Neurology, University of Münster , Münster, Germany.

Whereas central nervous system (CNS) homeostasis is highly dependent on tissue surveillance by immune cells, dysregulated entry of leukocytes during autoimmune neuroinflammation causes severe immunopathology and neurological deficits. To invade the CNS parenchyma, encephalitogenic T helper (T) cells must encounter their cognate antigen(s) presented by local major histocompatibility complex (MHC) class II-expressing antigen-presenting cells (APCs). The precise mechanisms by which CNS-associated APCs facilitate autoimmune T cell reactivation remain largely unknown. Read More

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http://dx.doi.org/10.1080/15548627.2020.1756678DOI Listing

The LC3-conjugation machinery specifies cargo loading and secretion of extracellular vesicles.

Autophagy 2020 May 13:1-3. Epub 2020 May 13.

Life Sciences Institute, University of Michigan , Ann Arbor, MI, USA.

Classical macroautophagy/autophagy functions to maintain cell health during stressful conditions by targeting cytosolic components for degradation and recycling through the lysosomal pathway. In contrast, nondegradative secretory autophagy functions as an alternative autophagy mechanism to mediate extracellular secretion. A recent study published in from the laboratory of Jayanta Debnath has identified components of the LC3-conjugation machinery as mediators in the selection of cargo for nonclassical secretion. Read More

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http://dx.doi.org/10.1080/15548627.2020.1760057DOI Listing

New tricks of an old autophagy regulator: AMPK-dependent regulation of autophagy through CCNY (cyclin Y)-CDK16.

Autophagy 2020 Jun;16(6):973-974

Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan , Ann Arbor, MI, USA.

AMPK is one of the main regulators of energy homeostasis in the cell, achieving this role in part by upregulating autophagy in times of nutrient deprivation. Previous reports have described several AMPK substrates involved in autophagy regulation; however, there are still undiscovered AMPK downstream effectors that could play an important role in autophagy. In a new article, Dohmen et al. Read More

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http://dx.doi.org/10.1080/15548627.2020.1756665DOI Listing

Stabilization of MORC2 by estrogen and antiestrogens through GPER1- PRKACA-CMA pathway contributes to estrogen-induced proliferation and endocrine resistance of breast cancer cells.

Autophagy 2020 Jun 6;16(6):1061-1076. Epub 2019 Sep 6.

Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University , Shanghai, China.

Aberrant activation of estrogen signaling through three ESR (estrogen receptor) subtypes, termed ESR1/ERα, ESR2/ERβ, and GPER1 (G protein-coupled estrogen receptor 1), is implicated in breast cancer pathogenesis and progression. Antiestrogens tamoxifen (TAM) and fulvestrant (FUL) are effective for treatment of ESR1-positive breast tumors, but development of resistance represents a major clinical challenge. However, the molecular mechanisms behind these events remain largely unknown. Read More

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http://dx.doi.org/10.1080/15548627.2019.1659609DOI Listing

Mitophagy deficiency increases NLRP3 to induce brown fat dysfunction in mice.

Autophagy 2020 May 13:1-17. Epub 2020 May 13.

Biomedical Research Center, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine , Seoul, Korea.

Although macroautophagy/autophagy deficiency causes degenerative diseases, the deletion of essential autophagy genes in adipocytes paradoxically reduces body weight. Brown adipose tissue (BAT) plays an important role in body weight regulation and metabolic control. However, the key cellular mechanisms that maintain BAT function remain poorly understood. Read More

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http://dx.doi.org/10.1080/15548627.2020.1753002DOI Listing

Involvement of CASP9 (caspase 9) in IGF2R/CI-MPR endosomal transport.

Autophagy 2020 May 25:1-17. Epub 2020 May 25.

Departments of Pathology, University of Pittsburgh School of Medicine and the University of Pittsburgh Cancer Institute , Pittsburgh, PA, USA.

Recently, we reported that increased expression of CASP9 pro-domain, at the endosomal membrane in response to HSP90 inhibition, mediates a cell-protective effect that does not involve CASP9 apoptotic activity. We report here that a non-apoptotic activity of endosomal membrane CASP9 facilitates the retrograde transport of IGF2R/CI-MPR from the endosomes to the trans-Golgi network, indicating the involvement of CASP9 in endosomal sorting and lysosomal biogenesis. CASP9-deficient cells demonstrate the missorting of CTSD (cathepsin D) and other acid hydrolases, accumulation of late endosomes, and reduced degradation of bafilomycin A-sensitive proteins. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761742DOI Listing

The anti-cancer drug ABTL0812 induces ER stress-mediated cytotoxic autophagy by increasing dihydroceramide levels in cancer cells.

Autophagy 2020 May 25:1-18. Epub 2020 May 25.

Protein Kinases and Signal Transduction Laboratory, Departament De Bioquímica I Biologia Molecular and Institut De Neurociències, Universitat Autònoma De Barcelona (UAB) , Barcelona, Spain.

ABTL0812 is a first-in-class small molecule with anti-cancer activity, which is currently in clinical evaluation in a phase 2 trial in patients with advanced endometrial and squamous non-small cell lung carcinoma (NCT03366480). Previously, we showed that ABTL0812 induces TRIB3 pseudokinase expression, resulting in the inhibition of the AKT-MTORC1 axis and macroautophagy/autophagy-mediated cancer cell death. However, the precise molecular determinants involved in the cytotoxic autophagy caused by ABTL0812 remained unclear. Read More

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http://dx.doi.org/10.1080/15548627.2020.1761651DOI Listing

An integrative multi-omics approach uncovers the regulatory role of CDK7 and CDK4 in autophagy activation induced by silica nanoparticles.

Autophagy 2020 May 23:1-22. Epub 2020 May 23.

Key Laboratory of Molecular Biophysics of Ministry of Education, Hubei Bioinformatics and Molecular Imaging Key Laboratory, Center for Artificial Intelligence Biology, College of Life Science and Technology, Huazhong University of Science and Technology , Wuhan, China.

Dysfunction of macroautophagy/autophagy has been postulated as a major cellular toxicological response to nanomaterials. It has been reported that excessive autophagy activation, induced by silica nanoparticles (SiNPs), contributes to autophagy dysfunction, whereas little is known how SiNPs trigger autophagy activation. Here, we treated normal rat kidney (NRK) cells using 3 different sizes of SiNPs (16, 29, and 51 nm) and observed that 16-nm SiNPs, with a final concentration of 60 μg/mL, dramatically induce autophagy activation without reducing cell viability. Read More

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http://dx.doi.org/10.1080/15548627.2020.1763019DOI Listing

Impact of differential and time-dependent autophagy activation on therapeutic efficacy in a model of Huntington disease.

Autophagy 2020 May 6:1-14. Epub 2020 May 6.

Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University , Lund, Sweden.

Activation of macroautophagy/autophagy, a key mechanism involved in the degradation and removal of aggregated proteins, can successfully reverse Huntington disease phenotypes in various model systems. How neuronal autophagy impairments need to be considered in Huntington disease progression to achieve a therapeutic effect is currently not known. In this study, we used a mouse model of HTT (huntingtin) protein aggregation to investigate how different methods and timing of autophagy activation influence the efficacy of autophagy-activating treatment . Read More

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http://dx.doi.org/10.1080/15548627.2020.1760014DOI Listing

Autophagy suppresses TRP53/p53 and oxidative stress to enable mammalian survival.

Autophagy 2020 May 23:1-3. Epub 2020 May 23.

Rutgers Cancer Institute of New Jersey , New Brunswick, NJ, USA.

Macroautophagy (hereafter autophagy) plays an important role in maintaining cellular homeostasis under stress conditions. We previously demonstrated that conditional autophagy deficiency in adult mice causes selective tissue damage, is lethal upon fasting, and shortens lifespan to less than three months primarily due to neurodegeneration, but not all the mechanisms are known. We conditionally deleted and/or the essential autophagy gene throughout adult mice to test whether TRP53 is responsible for any of these phenotypes. Read More

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http://dx.doi.org/10.1080/15548627.2020.1765522DOI Listing
May 2020
11.753 Impact Factor

LC3-dependent extracellular vesicle loading and secretion (LDELS).

Autophagy 2020 Jun 24;16(6):1162-1163. Epub 2020 Apr 24.

Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco , San Francisco, CA, USA.

Accumulating evidence implicates various autophagy-related (ATG) proteins in cellular secretion. Recently, we identified a new secretory autophagy pathway in which components of LC3 conjugation machinery specify the incorporation of RNA binding proteins (RBPs) and small non-coding RNAs into extracellular vesicles (EVs), resulting in their secretion outside of cells. We term this process C3-ependent V oading and ecretion (LDELS). Read More

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http://dx.doi.org/10.1080/15548627.2020.1756557DOI Listing

Autophagy induction by thiostrepton for the improvement of anticancer therapy.

Autophagy 2020 Jun 24;16(6):1166-1167. Epub 2020 Apr 24.

Equipe Labellisée Par La Ligue Contre Le Cancer, Université De Paris, Sorbonne Université , Paris, France.

Macroautophagy/autophagy induction by caloric restriction mimetics (CRMs) is a strategy to stimulate anticancer immune responses of immunogenic cell death (ICD)-inducing chemotherapeutics. We designed a phenotypic screening campaign in which we identified pharmacological agents that have CRM properties (i.e. Read More

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http://dx.doi.org/10.1080/15548627.2020.1758417DOI Listing

Autophagy triggers CTSD (cathepsin D) maturation and localization inside cells to promote apoptosis.

Autophagy 2020 Apr 23:1-23. Epub 2020 Apr 23.

Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, China.

CTSD/CathD/CATD (cathepsin D) is a lysosomal aspartic protease. A distinguishing characteristic of CTSD is its dual functions of promoting cell proliferation via secreting a pro-enzyme outside the cells as a ligand, and promoting apoptosis via the mature form of this enzyme inside cells; however, the regulation of its secretion, expression, and maturation is undetermined. Using the lepidopteran insect , a serious agricultural pest, as a model, we revealed the dual functions and regulatory mechanisms of CTSD secretion, expression, and maturation. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752497DOI Listing

ATG13 dynamics in nonselective autophagy and mitophagy: insights from live imaging studies and mathematical modeling.

Autophagy 2020 Apr 22:1-11. Epub 2020 Apr 22.

The Babraham Institute, Babraham Research Campus, Cambridge, UK.

During macroautophagy/autophagy, the ULK complex nucleates autophagic precursors, which give rise to autophagosomes. We analyzed, by live imaging and mathematical modeling, the translocation of ATG13 (part of the ULK complex) to the autophagic puncta in starvation-induced autophagy and ivermectin-induced mitophagy. In nonselective autophagy, the intensity and duration of ATG13 translocation approximated a normal distribution, whereas wortmannin reduced this effect and shifted to a log-normal distribution. Read More

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http://dx.doi.org/10.1080/15548627.2020.1749401DOI Listing

Methylmalonyl acidemia: from mitochondrial metabolism to defective mitophagy and disease.

Autophagy 2020 Jun 22;16(6):1159-1161. Epub 2020 Apr 22.

Institute of Physiology, Mechanisms of Inherited Kidney Disorders Group, University of Zurich , Zurich, Switzerland.

Methylmalonic acidemia (MMA) is an autosomal recessive inborn error of metabolism due to the deficiency of mitochondrial MMUT (methylmalonyl-CoA mutase) - an enzyme that mediates the cellular breakdown of certain amino acids and lipids. The loss of MMUT leads to the accumulation of toxic organic acids causing severe organ dysfunctions and life-threatening complications. The mechanisms linking MMUT deficiency, mitochondrial alterations and cell toxicity remain uncharacterized. Read More

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http://dx.doi.org/10.1080/15548627.2020.1753927DOI Listing

On-demand autophagic network adaptations upon limited lipid availability.

Autophagy 2020 Apr 16:1-3. Epub 2020 Apr 16.

Institute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.

The synthesis of autophagic vesicles is strongly dependent on sufficient lipid supply. Recently, the RAB GTPase RAB18 was shown to affect autophagy by mediating fatty acid release from lipid droplets, which are lipid sources for autophagosome formation. The stable loss of RAB18 interfered with fatty acid release from the lipid reservoirs and provoked autophagy network adaptations aiming to maintain autophagic activity under lipid limiting conditions. Read More

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http://dx.doi.org/10.1080/15548627.2020.1753926DOI Listing

TORC2-SGK-1 signaling integrates external signals to regulate autophagic turnover of mitochondria via mtROS.

Autophagy 2020 Jun 15;16(6):1154-1156. Epub 2020 Apr 15.

Bioinformatics and Molecular Genetics, Faculty of Biology, University of Freiburg , Freiburg, Germany.

Macroautophagy/autophagy is an evolutionarily conserved cellular degradation and recycling process that is tightly regulated by external stimuli, diet, and stress. Our recent findings suggest that in , a nutrient sensing pathway mediated by MTORC2 (mechanistic target of rapamycin kinase complex 2) and its downstream effector kinase SGK-1 (serum- and glucocorticoid-inducible kinase homolog 1) suppresses autophagy, involving mitophagy. Induced autophagy/mitophagy in MTORC2-deficient animals slows down development and impairs reproduction independently of the SGK-1 effectors DAF-16/FOXO and SKN-1/NFE2L2/NRF2. Read More

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http://dx.doi.org/10.1080/15548627.2020.1749368DOI Listing

Dimerization of mitophagy receptor BNIP3L/NIX is essential for recruitment of autophagic machinery.

Autophagy 2020 Apr 24:1-12. Epub 2020 Apr 24.

School of Medicine, University of Split, Split, Croatia.

Mitophagy is a conserved intracellular catabolic process responsible for the selective removal of dysfunctional or superfluous mitochondria to maintain mitochondrial quality and need in cells. Here, we examine the mechanisms of receptor-mediated mitophagy activation, with the focus on BNIP3L/NIX mitophagy receptor, proven to be indispensable for selective removal of mitochondria during the terminal differentiation of reticulocytes. The molecular mechanisms of selecting damaged mitochondria from healthy ones are still very obscure. Read More

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http://dx.doi.org/10.1080/15548627.2020.1755120DOI Listing

1-phenyl 2-thiourea (PTU) activates autophagy in zebrafish embryos.

Autophagy 2020 Apr 22:1-10. Epub 2020 Apr 22.

Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.

1-phenyl 2-thiourea (PTU) is a Tyr (tyrosinase) inhibitor that is extensively used to block pigmentation and improve optical transparency in zebrafish () embryo. Here, we reported a previously undescribed effect of PTU on macroautophagy/autophagy in zebrafish embryos. Upon 0. Read More

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http://dx.doi.org/10.1080/15548627.2020.1755119DOI Listing

Correction.

Authors:

Autophagy 2020 Apr 14. Epub 2020 Apr 14.

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http://dx.doi.org/10.1080/15548627.2020.1751979DOI Listing

A monolayer hiPSC culture system for autophagy/mitophagy studies in human dopaminergic neurons.

Autophagy 2020 Apr 14:1-17. Epub 2020 Apr 14.

Cell Biology Laboratories, School of Biochemistry, University of Bristol, Bristol, UK.

Macroautophagy/autophagy cytoplasmic quality control pathways are required during neural development and are critical for the maintenance of functional neuronal populations in the adult brain. Robust evidence now exists that declining neuronal autophagy pathways contribute to human neurodegenerative diseases, including Parkinson disease (PD). Reliable and relevant human neuronal model systems are therefore needed to understand the biology of disease-vulnerable neural populations, to decipher the underlying causes of neurodegenerative disease, and to develop assays to test therapeutic interventions . Read More

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http://dx.doi.org/10.1080/15548627.2020.1739441DOI Listing

Correction.

Authors:

Autophagy 2020 Apr 10. Epub 2020 Apr 10.

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http://dx.doi.org/10.1080/15548627.2020.1753431DOI Listing

Correction.

Authors:

Autophagy 2020 Apr 10. Epub 2020 Apr 10.

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http://dx.doi.org/10.1080/15548627.2020.1752074DOI Listing

Autophagy-related protein PIK3C3/VPS34 controls T cell metabolism and function.

Autophagy 2020 Apr 16:1-12. Epub 2020 Apr 16.

Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA.

The PIK3C3/VPS34 subunit of the class III phosphatidylinositol 3-kinase (PtdIns3K) complex is a key early player in macroautophagy/autophagy. In this study, we assessed the contribution of PIK3C3 to T cell metabolism and function. We found that -deficient T cells exhibited impaired cellular metabolism, and -deficient CD4 T cells failed to differentiate into T helper 1 cells. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752979DOI Listing

COST1 balances plant growth and stress tolerance via attenuation of autophagy.

Autophagy 2020 Jun 14;16(6):1157-1158. Epub 2020 Apr 14.

Department of Genetics, Development and Cell Biology, Iowa State University , Ames, IA, USA.

In plants, macroautophagy/autophagy has been reported to function in various biotic and abiotic stress-response pathways, but few direct regulators linking stress and autophagy have yet been identified. Other than the conserved nutrient sensing kinase TOR (Target of Rapamycin), negative regulators that can directly modulate plant autophagy are unknown. We recently identified a mutant, termed (Constitutively Stressed 1), which has strong drought tolerance with constitutive induction of autophagy and broad expression of normally stress-responsive genes. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752981DOI Listing

Autophagy: an essential but limited cellular process for timely skeletal muscle recovery from injury.

Autophagy 2020 Apr 17:1-4. Epub 2020 Apr 17.

Department of Kinesiology, University of Georgia, Athens, GA, USA.

Macroautophagy/autophagy induction, i.e., the formation of autophagosomes, is robust following many forms of muscle injury. Read More

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http://dx.doi.org/10.1080/15548627.2020.1753000DOI Listing

Autophagy suppresses breast cancer metastasis by degrading NBR1.

Autophagy 2020 Jun 14;16(6):1164-1165. Epub 2020 Apr 14.

Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco , San Francisco, CA, USA.

Macroautophagy/autophagy plays complex, context-dependent roles in cancer. How autophagy governs the emergence of metastatic disease has been incompletely understood. We recently uncovered that genetic autophagy inhibition strongly attenuates primary tumor growth in mammary cancer models, yet paradoxically promotes spontaneous metastasis to the lung and enables the outgrowth of disseminated tumor cells (DTCs) into overt macro-metastases. Read More

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http://dx.doi.org/10.1080/15548627.2020.1753001DOI Listing

Acetylation of STX17 (syntaxin 17) controls autophagosome maturation.

Autophagy 2020 Apr 15:1-13. Epub 2020 Apr 15.

Department of Biochemistry and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

The fusion of autophagosomes and endosomes/lysosomes, also called autophagosome maturation, ensures the degradation of autophagic cargoes. It is an important regulatory step of the macroautophagy/autophagy process. STX17 is the key autophagosomal SNARE protein that mediates autophagosome maturation. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752471DOI Listing
April 2020
11.753 Impact Factor

Sex differences in autophagy-mediated diseases: toward precision medicine.

Autophagy 2020 Apr 17:1-12. Epub 2020 Apr 17.

Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan, China.

Nearly all diseases in humans, to a certain extent, exhibit sex differences, including differences in the onset, progression, prevention, therapy, and prognosis of diseases. Accumulating evidence shows that macroautophagy/autophagy, as a mechanism for development, differentiation, survival, and homeostasis, is involved in numerous aspects of sex differences in diseases such as cancer, neurodegeneration, and cardiovascular diseases. Advances in our knowledge regarding sex differences in autophagy-mediated diseases have enabled an understanding of their roles in human diseases, although the underlying molecular mechanisms of sex differences in autophagy remain largely unexplored. Read More

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http://dx.doi.org/10.1080/15548627.2020.1752511DOI Listing

The functions of Atg8-family proteins in autophagy and cancer: linked or unrelated?

Autophagy 2020 Apr 19:1-13. Epub 2020 Apr 19.

Univ. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon, France.

The Atg8-family proteins are subdivided into two subfamilies: the GABARAP and LC3 subfamilies. These proteins, which are major players of the autophagy pathway, present a conserved glycine in their C-terminus necessary for their association to the autophagosome membrane. This family of proteins present multiple roles from autophagy induction to autophagosome-lysosome fusion and have been described to play a role during cancer progression. Read More

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http://dx.doi.org/10.1080/15548627.2020.1749367DOI Listing

The AMPK-MFN2 axis regulates MAM dynamics and autophagy induced by energy stresses.

Autophagy 2020 Apr 19:1-15. Epub 2020 Apr 19.

Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.

Energy deprivation activates the cellular energy sensor AMP-activated protein kinase (AMPK), which in turn induces macroautophagy/autophagy. The mitochondrial-associated ER membrane (MAM) plays a key role in mitochondrial division and autophagy, and the mitochondrial fusion protein MFN2 (mitofusin 2) tethers the MAM, but the mechanism by which AMPK and MFN2 regulate autophagy in response to energy stress remains unclear. Here, we found that energy stress not only triggers mitochondrial fission and autophagy, but more importantly increases the number of MAMs, a process that requires AMPK. Read More

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http://dx.doi.org/10.1080/15548627.2020.1749490DOI Listing

The trehalose-6-phosphate phosphatase Tps2 regulates transcription and autophagy in .

Autophagy 2020 Apr 2:1-15. Epub 2020 Apr 2.

School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.

Macroautophagy/autophagy is an important catabolic process for maintaining cellular homeostasis by adapting to various stress conditions. Autophagy is mediated by a double-membrane autophagosome, which sequesters a portion of cytoplasmic components for delivery to the vacuole. Several autophagy-related () genes play crucial roles in autophagosome formation. Read More

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http://dx.doi.org/10.1080/15548627.2020.1746592DOI Listing

Corrigendum.

Authors:

Autophagy 2020 Mar 31. Epub 2020 Mar 31.

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http://dx.doi.org/10.1080/15548627.2020.1744941DOI Listing

Nucleoporin TPR (translocated promoter region, nuclear basket protein) upregulation alters MTOR-HSF1 trails and suppresses autophagy induction in ependymoma.

Autophagy 2020 Mar 24:1-12. Epub 2020 Mar 24.

WPI Nano Life Science Institute (WPI-nanoLSI) & Cell-Bionomics Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.

Children with ependymoma have high mortality rates because ependymoma is resistant to conventional therapy. Genomic and transcriptomic studies have identified potential targets as significantly altered genes in ependymoma patients. Although several candidate oncogenes in ependymoma were recently reported, the detailed mechanisms for the roles of these candidate oncogenes in ependymoma progression remain unclear. Read More

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http://dx.doi.org/10.1080/15548627.2020.1741318DOI Listing