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651 results for “autophagy”
Dataset for genome-wide profiling of autophagy dynamics under nutrient availability in <em>Saccharomyces cerevisiae</em>
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Activation of autophagy during normothermic machine perfusion of discarded livers is associated with improved hepatocellular function
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Data from: Role of Atg3, Atg5, and Atg12 in the crosstalk between apoptosis and autophagy in the posterior silk gland of Bombyx mori
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Data from: Acute, delayed and chronic remote ischemic conditioning is associated with downregulation of mTOR and enhanced autophagy signaling
Background - Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our understanding of the cardioprotection and its underlying mediators and mechanisms remains incomplete. In this study we examine the effect of RIC on pro- autophagy signaling as a possible mechanism of benefit. Methods and Results - We examined the role of autophagy in the acute/first window (15 minutes after RIC), delayed/second window (24 hours after RIC) and chronic (24 hours after 9 days of repeated RIC) phases of cardioprotection. C57BL/6 mice (N=69) were allocated to each treatment phase and further stratified to receive RIC, induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion, or control treatment consisting solely of handling without transient ischemia. The groups included, group 1 (1W control), group 2 (1W RIC), group 3 (2W control), group 4 (2W RIC), group 5 (3W control) and group 6 (3W RIC). Hearts were isolated for assessment of cardiac function and infarct size after global ischemia using a Langendorff preparation. Infarct size was reduced in all three phases of cardioprotection, in association with improvements in post-ischemic left ventricular end diastolic pressure (LVEDP) and developed pressure (LVDP) (P<0.05). The pattern of autophagy signaling varied; 1W RIC increased AMPK levels and decreased the activation of mammalian target of rapamycin (mTOR), whereas chronic RIC was associated with persistent mTOR suppression and increased levels of autophagosome proteins, LC3II/I and Atg5. Conclusions - Cardioprotection following transient ischemia exists in both the acute and delayed/chronic phases of conditioning. RIC induces pro-autophagy signaling but the pattern of responses varies depending on the phase, with the most complete portfolio of responses observed when RIC is administered chronically.
Autophagy regulator ATG5 maintains cerebellar function by preventing its excessive glycolytic activity.
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Cross-species interactome analysis uncovers a conserved selective autophagy mechanism for protein quality control in plants
<p>This is all the source data associated with the manuscript which has the same title with this dataset.</p> <p>The abstract and the authors of the manuscripts are below:</p> <p><strong><span>Cross-species interactome analysis uncovers a conserved </span></strong></p> <p><strong><span>selective autophagy mechanism for protein quality control in plants</span></strong></p> <p><span> </span></p> <p><span>Víctor Sánchez de Medina Hernández<sup>1,2*</sup>, Marintia Mayola Nava García<sup>1,2*</sup>, Marion Clavel<sup>1,3</sup>, Ranjith K. Papareddy<sup>1</sup>, Veselin I. Andreev<sup>1</sup>, Varsha Mathur<sup>1</sup>, Azadeh Mohseni</span><sup><span>1,4</span></sup><span>, Marta García-León</span><sup><span>1</span></sup><span>, Peng Gao</span><sup><span>1</span></sup><span>, Juan Carlos de la Concepción</span><sup><span>1</span></sup><span>, </span><span>Lorenzo Picchianti<sup>1</sup><span>, Nenad Grujic<sup>1</sup>, Roksolana Kobylinska</span><sup>1</sup><span>, Alibek Abdrakhmanov</span><sup>1,2</sup><span>, Héloïse Duvergé</span><sup>1</sup><span>, Gaurav Anand</span><sup>5</sup><span>, Nils Leibrock</span><sup>1,4</sup><span>, Anita Bianchi</span><sup>1</sup><span>, Margot Raffeiner</span><sup>6</sup><span>, Timothy Scott Crawford<sup>7</sup>, Luca Argirò</span><sup>1</sup><span>, Mateusz Matuszkiewicz</span><sup>1,8</sup><span>, Cheuk-Ling Wun</span><sup>1</sup><span>, Jakob Valdbjørn Kanne</span><sup>9</sup><span>, Anton Meinhart</span><sup>10</sup><span>, Elisabeth Roitinger<sup>1</sup>, Isabel Bäurle<sup>7</sup>, Byung Ho Kang<sup>11</sup>, Morten Petersen</span><sup>9</sup><span>, Suayib Üstün</span><sup>6</sup><span>, Yogesh Kulathu</span><sup>5</sup><span>, Tim Clausen</span><sup>10</sup><span>, Silvia Ramundo<sup>1</sup>, Yasin Dagdas<sup>1</sup></span></span></p> <p><sup><span>1 </span></sup><span>Gregor Mendel Institute (GMI), Austrian Academy of Sciences, Vienna BioCenter (VBC), Vienna, Austria.</span></p> <p><sup><span>2 </span></sup><span>Vienna BioCenter PhD Program, Doctoral School of the University of Vienna and Medical University of Vienna, A-1030, Vienna, Austria.</span></p> <p><sup><span>3</span></sup><span> </span><span>Max-Planck-Institut für Molekulare Pflanzenphysiologie, Potsdam-Golm, Germany.</span></p> <p><sup><span>4</span></sup><span> Department of Applied Genetics and Cell Biology, Institute of Molecular Plant Biology, BOKU University, Vienna, Austria.</span></p> <p><sup><span>5</span></sup><span> MRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee, UK.</span></p> <p><sup><span>6 </span></sup><span>Faculty of Biology & Biotechnology, Ruhr-University of Bochum, 44780 Bochum, Germany.</span></p> <p><sup><span>7</span></sup><span> Institute for Biochemistry and Biology, University of Potsdam, Potsdam, Germany.</span></p> <p><sup><span>8 </span></sup><span>Department of Plant Genetics, Breeding and Biotechnology, Institute of Biology, Warsaw University of Life Sciences, Warsaw, Poland.</span></p> <p><sup><span>9 </span></sup><span>Functional Genomic Section, Department of Biology, University of Copenhagen, Copenhagen, Denmark.</span></p> <p><sup><span>10</span></sup><span> Research Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), Vienna, Austria.</span></p> <p><sup><span>11</span></sup><span> School of Life Sciences, Centre for Cell & Developmental Biology and State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.</span></p> <p><span> </span></p> <p><span>*These authors contributed equally to this work</span></p> <p><span> </span></p> <p><span>Correspondence: Yasin Dagdas, </span><span><a href="mailto:yasin.dagdas@gmi.oeaw.ac.at"><span>yasin.dagdas@gmi.oeaw.ac.at</span></a></span></p> <p><strong><span> </span></strong></p> <p><strong><span>Abstract</span></strong></p> <p><span>Selective autophagy is a fundamental protein quality control pathway that safeguards proteostasis by degrading damaged or surplus cellular components, particularly under stress. This process is orchestrated by selective autophagy receptors (SARs) that direct specific cargo for degradation. While significant strides have been made in understanding the molecular framework of selective autophagy, the diversity of SAR repertoires across species remain largely unexplored. Through a comparative interactome analysis across five model organisms, we identified a suite of conserved and lineage-specific SAR candidates. Among these, we validated CESAR as a conserved SAR critical for proteostasis under proteotoxic stress. CESAR specifically facilitates the degradation of hydrophobic, ubiquitinated protein aggregates and is indispensable for heat stress tolerance. Our study offers a rich resource for SAR discovery and positions CESAR as a pivotal regulator of proteostasis, with broad implications for improving stress resilience in plants.</span></p>
Figure S1. Autophagy inhibitors in the autophagy reporter THP1-Difluo hLC3 cell line
<p>Cells (5 ×10<sup>5</sup> cells/mL) were incubated with two concentrations of (<strong>a</strong>) mTOR activator MHY1485, (<strong>b</strong>) AMPK inhibitor dorsomorphin, (<strong>c</strong>) ULK1/2 inhibitor MRT68921, (<strong>d</strong>) PI3K class III inhibitor wortmannin, (<strong>e</strong>) autophagosome-lysosome fusion inhibitor chloroquine, and (<strong>f</strong>) late-stage autophagy inhibitor bafilomycin A1 for 24 h. Autophagic flux was determined by measuring the fluorescence of RFP and GFP. The ratio of median fluorescence intensity of RFP to GFP (MFI) was normalized (nMFI) to the vehicle control (CTRL DMSO). Data are means ±SEM of 4 independent experiments, each carried out in duplicate.</p>
Figure S2. Autophagy inhibitor bafilomycin A1 blocks proliferation of MEC-1 cells
<p>MEC-1 cells (3 ×10<sup>5</sup> cells/mL) were labeled with CFSE and treated with vehicle control (0.1% DMSO; CTRL DMSO) or 10 nM and 100 nM bafilomycin A1 or for 72 h. Retention of CFSE was determined using flow cytometry. Data are means ±SEM of 2 independent experiments.</p>
Dataset of: Macros to Quantify Exosome release and Autophagy at the Neuromuscular Junction of Drosophila Melanogaster
<p>Dataset of the future paper "Macros to Quantify Exosome release and Autophagy at the Neuromuscular Junction of Drosophila Melanogaster". If you have any doubts I can be found in this email: <a href="mailto:irene.sanchez-mirasierra@u-bordeaux.fr">irene.sanchez-mirasierra@u-bordeaux.fr</a></p>
Transcriptional profiling of the response to starvation and fattening reveals differential regulation of autophagy genes in mammals
<p>Nutrient deprivation (starvation) induced by fasting and hypercaloric regimens are stress factors that can influence cell and tissue homeostasis in mammals. One of the key cellular responses to changes in nutrient availability is the cell survival pathway, autophagy. While there has been much research into the protein networks regulating autophagy, less is known about the gene expression networks involved in this fundamental process. Here, we applied a network algorithm designed to analyze omics datasets, to identify sub-networks that are enriched for induced genes in response to starvation. This enabled us to identify two prominent active modules composed of key stress-induced transcription factors, including members of the Jun, Fos, and ATF families, and the other comprising autophagosome sub-network genes, including ULK1. The results were validated in the brain, liver, and muscle of fasting mice. Moreover, differential expression analysis of autophagy genes in the brain, liver, and muscle of high-fat diet-exposed mice, showed significant suppression of GABARAPL1 in the liver. Finally, our data provide a resource that may facilitate the future identification of regulators of autophagy.</p>
Fig. 5 in Unique guanidine-conjugated catechins from the leaves of Alchornea rugosa and their autophagy modulating activity
Fig. 5. (A) The level of autophagy marker protein expression in cells treated with compounds 4–7. LC3B was determined using the LC3B II/I ratio, which was then standardized against the control group (nontreated group). The p62 protein level was detected, and the expression level was normalized by dividing by the protein level in the control group. (CQ: chloroquine treatment group at 25 μM, Rapa: rapamycin treatment group at 0.25 μM). (B) GFP-mRFP-tagged LC3 puncta after treatment with the test compounds. HEK293 cells were treated with autophagy-regulating compounds 4–7, and LC3 puncta were detected by using confocal microscopy.
Fig. 4 in Unique guanidine-conjugated catechins from the leaves of Alchornea rugosa and their autophagy modulating activity
Fig. 4. Screening for autophagy regulation by compounds (1–9) isolated from A. rugosa in HEK293 cells. HEK293 cells stably expressing GFP-LC3 were treated with 20 μM compounds for 24 h, and confocal imaging was used to examine the production of LC3-GFP puncta.
Autophagy-Enhancers to Reduce Sleep Disturbances
ClinicalTrials.gov study NCT07383311. IPD Sharing: NO. Countries: 1. Publications: 4.
Autophagy and Pathological Aging
ClinicalTrials.gov study NCT03175874. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
An Exploratory Clinical Study on Autophagy and Multi-level Molecular Profiling During Spermidine Supplementation
ClinicalTrials.gov study NCT04823806. IPD Sharing: NO. Countries: 1. Publications: 5.
Inflammation and Metabolic Acidosis at Birth (AGAIN: AutophaGy AcIdosis Newborn)
ClinicalTrials.gov study NCT03897101. IPD Sharing: NO. Countries: 1. Publications: 9.
Study of Autophagy and the Effects of GALIG Gene Products in HIV-1 Infected Patients Who Are Under Antiretroviral Therapy Since Primary-infection, Chronic Phase, or Never Treated.
ClinicalTrials.gov study NCT04160455. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Fasting Mimicking Diet and Autophagy
ClinicalTrials.gov study NCT06115551. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Association of Autophagy-related Genes ,LncRNA and SNPs With Colorectal Cancer in Egyptian Population
ClinicalTrials.gov study NCT04729855. IPD Sharing: UNDECIDED. Countries: 1. Publications: 14.
Autophagy Markers in Endometrial Polyps
ClinicalTrials.gov study NCT04706000. IPD Sharing: UNDECIDED. Countries: 1. Publications: 5.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.