3,016 results match your criteria Autophagy[Journal]


MTORC1 coordinates the autophagy and apoptosis signaling in articular chondrocytes in osteoarthritic temporomandibular joint.

Autophagy 2019 Apr 21:1-18. Epub 2019 Apr 21.

a State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD , School of Stomatology, the Fourth Military Medical University , Xi'an , China.

A switch from autophagy to apoptosis is implicated in chondrocytes during the osteoarthritis (OA) progression with currently unknown mechanism(s). In this study we utilized a flow fluid shear stress (FFSS) model in cultured chondrocytes and a unilateral anterior crossbite (UAC) animal model. We found that both FFSS and UAC actively induced endoplasmic reticulum stress (ERS) in the temporomandibular joints (TMJ) chondrocytes, as demonstrated by dramatic increases in expression of HSPA5, p-EIF2AK3, p-ERN1 and ATF6. Read More

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http://dx.doi.org/10.1080/15548627.2019.1606647DOI Listing

The autophagic degradation of cytosolic pools of peroxisomal proteins by a new selective pathway.

Autophagy 2019 Apr 21:1-13. Epub 2019 Apr 21.

a College of Life Sciences , Shandong Normal University , Jinan , Shandong , China.

Damaged or redundant peroxisomes and their luminal cargoes are removed by pexophagy, a selective autophagy pathway. In yeasts, pexophagy depends mostly on the pexophagy receptors, such as Atg30 for Pichia pastoris and Atg36 for Saccharomyces cerevisiae, the autophagy scaffold proteins, Atg11 and Atg17, and the core autophagy machinery. In P. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1603546DOI Listing
April 2019
1 Read

Vault RNA emerges as a regulator of selective autophagy.

Autophagy 2019 Apr 21. Epub 2019 Apr 21.

a European Molecular Biology Laboratory , Meyerhofstrasse 1, 69117 Heidelberg , Germany.

The selective autophagic receptor SQSTM1/p62 ushers cargo to phagophores, the precursors of autophagosomes, and serves as a platform for autophagy initiation. We discovered that SQSTM1 is an RNA-binding protein that interacts with vault RNAs. Vault RNAs are small non-coding RNAs found in many eukaryotes and transcribed by POLR3 (RNA polymerase III). Read More

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http://dx.doi.org/10.1080/15548627.2019.1609861DOI Listing

Proteasome dysfunction induces excessive proteome instability and loss of mitostasis that can be mitigated by enhancing mitochondrial fusion or autophagy.

Autophagy 2019 Apr 19:1-17. Epub 2019 Apr 19.

a Department of Cell Biology and Biophysics, Faculty of Biology , National and Kapodistrian University of Athens , Athens , Greece.

The ubiquitin-proteasome pathway (UPP) is central to proteostasis network (PN) functionality and proteome quality control. Yet, the functional implication of the UPP in tissue homeodynamics at the whole organism level and its potential cross-talk with other proteostatic or mitostatic modules are not well understood. We show here that knock down (KD) of proteasome subunits in Drosophila flies, induced, for most subunits, developmental lethality. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596477DOI Listing

Mitigation of cocaine-mediated mitochondrial damage, defective mitophagy and microglial activation by superoxide dismutase mimetics.

Autophagy 2019 Apr 16. Epub 2019 Apr 16.

a Department of Pharmacology and Experimental Neuroscience , University of Nebraska Medical Center , Omaha , NE 68198-5880 , USA .

Although cocaine exposure has been shown to potentiate neuroinflammation by upregulating glial activation in the brain, the role of mitophagy in this process remains an enigma. In the present study, we sought to examine the role of impaired mitophagy in cocaine-mediated activation of microglia and to determine the ameliorative potential of superoxide dismutase mimetics in this context. Our findings demonstrated that exposure of mouse primary microglial cells (mPMs) to cocaine resulted in decreased mitochondrial membrane potential, that was accompanied by increased expression of mitophagy markers, PINK1 and PRKN. Read More

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http://dx.doi.org/10.1080/15548627.2019.1607686DOI Listing
April 2019
11.753 Impact Factor

Cell quality control mechanisms maintain stemness and differentiation potential of P19 embryonic carcinoma cells.

Autophagy 2019 Apr 16. Epub 2019 Apr 16.

a CNC-Center for Neuroscience and Cell Biology, University of Coimbra , UC Biotech, Biocant Park, 3060-197 Cantanhede , Portugal .

Given the relatively long life of stem cells (SCs), efficient mechanisms of quality control to balance cell survival and resistance to external and internal stress are required. Our objective was to test the relevance of cell quality control mechanisms for SCs maintenance, differentiation and resistance to cell death. We compared cell quality control in P19 stem cells (P19SCs) before and after differentiation (P19dCs). Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1607694DOI Listing
April 2019
1 Read

An atypical LIR motif within UBA5 (ubiquitin like modifier activating enzyme 5) interacts with GABARAP proteins and mediates membrane localization of UBA5.

Autophagy 2019 Apr 16. Epub 2019 Apr 16.

a Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University , Max-von-Laue Str. 9, 60438 Frankfurt am Main , Germany.

Short linear motifs, known as LC3-interacting regions (LIRs), interact with mactoautophagy/autophagy modifiers (Atg8/LC3/GABARAP proteins) via a conserved universal mechanism. Typically, this includes the occupancy of 2 hydrophobic pockets on the surface of Atg8-family proteins by 2 specific aromatic and hydrophobic residues within the LIR motifs. Here, we describe an alternative mechanism of Atg8-family protein interaction with the non-canonical UBA5 LIR, an E1-like enzyme of the ufmylation pathway that preferentially interacts with GABARAP but not LC3 proteins. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1606637DOI Listing
April 2019
1 Read

Age-dependent accumulation of oligomeric SNCA/α-synuclein from impaired degradation in mutant LRRK2 knockin mouse model of Parkinson disease: role for therapeutic activation of chaperone-mediated autophagy (CMA).

Autophagy 2019 Apr 14:1-24. Epub 2019 Apr 14.

a Division of Neurology, Department of Medicine , University of Hong Kong, Queen Mary Hospital , Hong Kong S.A.R. , China.

Parkinson disease (PD) is an age-related neurodegenerative disorder associated with misfolded SNCA/α-synuclein accumulation in brain. Impaired catabolism of SNCA potentiates formation of its toxic oligomers. LRRK2 (leucine-rich repeat kinase-2) mutations predispose to familial and sporadic PD. Read More

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http://dx.doi.org/10.1080/15548627.2019.1603545DOI Listing
April 2019
2 Reads

HIF1A and NFAT5 coordinate Na-boosted antibacterial defense via enhanced autophagy and autolysosomal targeting.

Autophagy 2019 04 14:1-18. Epub 2019 Apr 14.

a Institute of Clinical Microbiology and Hygiene , University Hospital of Regensburg and University of Regensburg , Regensburg , Germany.

Abstract: Infection and inflammation are able to induce diet-independent Na-accumulation without commensurate water retention in afflicted tissues, which favors the pro-inflammatory activation of mouse macrophages and augments their antibacterial and antiparasitic activity. While Na-boosted host defense against the protozoan parasite Leishmania major is mediated by increased expression of the leishmanicidal NOS2 (nitric oxide synthase 2, inducible), the molecular mechanisms underpinning this enhanced antibacterial defense of mouse macrophages with high Na (HS) exposure are unknown. Here, we provide evidence that HS-increased antibacterial activity against E. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1596483DOI Listing
April 2019
1 Read

Human LC3 and GABARAP subfamily members achieve functional specificity via specific structural modulations.

Autophagy 2019 Apr 14. Epub 2019 Apr 14.

a CSIR-Institute of Genomics and Integrative Biology , Mathura Road, New Delhi 110025 , India.

Autophagy is a conserved adaptive cellular pathway essential to maintain a variety of physiological functions. Core components of this machinery are the six human Atg8 orthologs that initiate formation of appropriate protein complexes. While these proteins are routinely used as indicators of autophagic flux, it is presently not possible to discern their individual biological functions due to our inability to predict specific binding partners. Read More

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http://dx.doi.org/10.1080/15548627.2019.1606636DOI Listing

The negative effect of lipid challenge on autophagy inhibits T cell responses.

Autophagy 2019 Apr 14. Epub 2019 Apr 14.

a Department of Pathology , Albert Einstein College of Medicine , Bronx , NY USA.

Obesity is associated with changes in the immune system that significantly hinder its ability to mount efficient immune responses. Previous studies have reported a dysregulation of immune responses caused by lipid challenge; however, the mechanisms underlying that dysregulation are still not completely understood. Autophagy is an essential catabolic process through which cellular components are degraded by the lysosomal machinery. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1606635DOI Listing
April 2019
1 Read

Autophagy and Cancer Research in Iran.

Autophagy 2019 Apr 14. Epub 2019 Apr 14.

b Autophagy Research Center, Health Policy Research Center, Institute of Health , Shiraz University of Medical Sciences ; Shiraz , Iran.

In August 2018, three events were held in Iran on clinical biochemistry, molecular biology, cancer/autophagy, laboratory management, and proteomics. On August 25-28 at the Isfahan University of Medical Sciences, the 15 National Biochemistry Congress and the 6 International Congress on Biochemistry and Molecular Biology were held, gathering together international professors from Canada, the USA, Germany, Australia, Italy, France, and Sweden, as well as Iran to discuss mainly the roles of autophagy in cancer therapy. On August 29, a one-day "Autophagy" symposium was held at the Shiraz University of Medical Sciences. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1606638DOI Listing
April 2019
2 Reads

Autophagy in Xenopus laevis rod photoreceptors is independently regulated by phototransduction and misfolded RHO.

Autophagy 2019 Apr 12:1-20. Epub 2019 Apr 12.

a Department of Ophthalmology and Visual Sciences , University of British Columbia , Vancouver , British Columbia , Canada.

We previously reported autophagic structures in rod photoreceptors expressing a misfolding RHO (rhodopsin) mutant (RHO), suggesting that autophagy may play a role in degrading the mutant RHO and/or be involved in photoreceptor cell death. To further examine autophagy in normal and diseased rods, we generated transgenic Xenopus laevis tadpoles expressing the dually fluorescent autophagy marker mRFP-eGFP-LC3 in rods, which changes from green to yellow and finally red as autophagic structures develop and mature. Using transgenic lines with constitutive and inducible expression, we determined the time-course of autophagy in rod photoreceptors: autophagosomes last for 6 to 8 hours before fusing with lysosomes, and acidified autolysosomes last for about 28 hours before being degraded. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596487DOI Listing

Small molecule-driven NLRP3 inflammation inhibition via interplay between ubiquitination and autophagy: implications for Parkinson disease.

Autophagy 2019 Apr 9:1-22. Epub 2019 Apr 9.

a Department of Pharmacology, School of Medicine and Life Sciences , Nanjing University of Chinese Medicine , Nanjing , Jiangsu , China.

Aging-related, nonresolving inflammation in both the central nervous system (CNS) and periphery predisposes individuals to the development of neurodegenerative disorders (NDDs). Inflammasomes are thought to be especially relevant to immune homeostasis, and their dysregulation contributes to inflammation and NDDs. However, few agents have been clinically shown to reduce NDD incidence by targeting inflammasomes. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596481DOI Listing
April 2019
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Long noncoding RNA CA7-4 promotes autophagy and apoptosis via sponging MIR877-3P and MIR5680 in high glucose-induced vascular endothelial cells.

Autophagy 2019 Apr 7:1-16. Epub 2019 Apr 7.

a Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science , Shandong University , Jinan , P. R. China.

Vascular endothelial cells (VECs) that form the inner wall of blood vessels can be injured by high glucose-induced autophagy and apoptosis. Although the role of long noncoding RNA in regulating cell fate has received widespread attention, long noncoding RNAs (lncRNAs) that can both regulate autophagy and apoptosis need to be discovered. In this study, we identified that a small chemical molecule, 3-benzyl-5-([2-nitrophenoxy] methyl)-dihydrofuran-2(3H)-one (3BDO), synthesized by us, could inhibit VEC autophagy and apoptosis induced by a high concentration of glucose. Read More

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http://dx.doi.org/10.1080/15548627.2019.1598750DOI Listing

The PARK10 gene USP24 is a negative regulator of autophagy and ULK1 protein stability.

Autophagy 2019 Apr 7:1-14. Epub 2019 Apr 7.

a Department of Anesthesiology & Shock , Trauma and Anesthesiology Research Center, University of Maryland School of Medicine , Baltimore , MD , USA.

Recent studies indicate a causative relationship between defects in autophagy and dopaminergic neuron degeneration in Parkinson disease (PD). However, it is not fully understood how autophagy is regulated in the context of PD. Here we identify USP24 (ubiquitin specific peptidase 24), a gene located in the PARK10 (Parkinson disease 10 [susceptibility]) locus associated with late onset PD, as a novel negative regulator of autophagy. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1598754DOI Listing
April 2019
3 Reads

RAB2 regulates the formation of autophagosome and autolysosome in mammalian cells.

Autophagy 2019 Apr 6:1-13. Epub 2019 Apr 6.

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

Multiple sources contribute membrane and protein machineries to construct functional macroautophagic/autophagic structures. However, the underlying molecular mechanisms remain elusive. Here, we show that RAB2 connects the Golgi network to autophagy pathway by delivering membrane and by sequentially engaging distinct autophagy machineries. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596478DOI Listing
April 2019
1 Read

Emerging views of mitophagy in immunity and autoimmune diseases.

Autophagy 2019 Apr 5:1-15. Epub 2019 Apr 5.

a Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health , Inflammatory Bowel Disease Research Center , Shanghai , China.

Mitophagy is a vital form of autophagy for selective removal of dysfunctional or redundant mitochondria. Accumulating evidence implicates elimination of dysfunctional mitochondria as a powerful means employed by autophagy to keep the immune system in check. The process of mitophagy may restrict inflammatory cytokine secretion and directly regulate mitochondrial antigen presentation and immune cell homeostasis. Read More

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http://dx.doi.org/10.1080/15548627.2019.1603547DOI Listing
April 2019
1 Read

LRRK2 mutations impair depolarization-induced mitophagy through inhibition of mitochondrial accumulation of RAB10.

Autophagy 2019 Apr 4:1-20. Epub 2019 Apr 4.

a Department of Neurosciences , Laboratory for Parkinson Research , Leuven , Belgium.

Parkinson disease (PD) is a disabling, incurable disorder with increasing prevalence in the western world. In rare cases PD is caused by mutations in the genes for PINK1 (PTEN induced kinase 1) or PRKN (parkin RBR E3 ubiquitin protein ligase), which impair the selective autophagic elimination of damaged mitochondria (mitophagy). Mutations in the gene encoding LRRK2 (leucine rich repeat kinase 2) are the most common monogenic cause of PD. Read More

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http://dx.doi.org/10.1080/15548627.2019.1603548DOI Listing
April 2019
2 Reads

A study of autophagy in hemocytes of the Pacific oyster, Crassostrea gigas.

Autophagy 2019 Apr 2:1-9. Epub 2019 Apr 2.

a SG2M-LGPMM, Laboratoire de Génétique et Pathologie des Mollusques Marins , Ifremer , La Tremblade , France.

Macroautophagy is a mechanism that is involved in various cellular processes, including cellular homeostasis and innate immunity. This pathway has been described in organisms ranging in complexity from yeasts to mammals, and recent results indicate that it occurs in the mantle of the Pacific oyster, Crassostrea gigas. However, the autophagy pathway has never been explored in the hemocytes of C. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596490DOI Listing
April 2019
2 Reads

Retinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulation.

Autophagy 2019 Apr 2:1-19. Epub 2019 Apr 2.

a Institute of Anatomy and Cell Biology , Ulm University , Ulm , DE , Germany.

Mutations in the TBK1 (TANK binding kinase 1) gene are causally linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). TBK1 phosphorylates the cargo receptors OPTN and SQSTM1 regulating a critical step in macroautophagy/autophagy. Disruption of the autophagic flux leads to accumulation of cytosolic protein aggregates, which are a hallmark of ALS. Read More

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http://dx.doi.org/10.1080/15548627.2019.1589257DOI Listing
April 2019
3 Reads
11.753 Impact Factor

GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia.

Autophagy 2019 Mar 30:1-15. Epub 2019 Mar 30.

c Leukemia Research Institute , The Catholic University of Korea , Seoul , Republic of Korea.

Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity. However, recent clinical evidence indicates that a substantial proportion of CML patients exhibit BCR-ABL-dependent or independent resistance to imatinib. Despite the importance of imatinib resistance in CML, the underlying molecular mechanisms of this resistance are largely unknown. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596492DOI Listing
March 2019
3 Reads
11.753 Impact Factor

Mitophagy and NAD inhibit Alzheimer disease.

Authors:
Evandro F Fang

Autophagy 2019 Mar 28:1-3. Epub 2019 Mar 28.

a Department of Clinical Molecular Biology , University of Oslo and Akershus University Hospital , Lørenskog , Norway.

Our latest publication on the inhibition of Alzheimer disease (AD) through mitophagy consolidates the 'defective mitophagy hypothesis of AD etiology'. Dementia (majorly AD) affects over 50 million people worldwide, and for AD there is no cure. AD leads to progressive loss of cognition, and pathological hallmarks of AD include aggregates of amyloid-β peptides extracellularly and MAPT (microtubule associated protein tau) intracellularly. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596497DOI Listing

Correction.

Authors:

Autophagy 2019 Mar 28:1-3. Epub 2019 Mar 28.

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http://dx.doi.org/10.1080/15548627.2019.1599190DOI Listing

Mitochondrial respiratory chain deficiency inhibits lysosomal hydrolysis.

Autophagy 2019 Mar 27:1-20. Epub 2019 Mar 27.

a Institute of Cellular Biochemistry , University Medical Center Goettingen , Goettingen , Germany.

Mitochondria are key organelles for cellular metabolism, and regulate several processes including cell death and macroautophagy/autophagy. Here, we show that mitochondrial respiratory chain (RC) deficiency deactivates AMP-activated protein kinase (AMPK, a key regulator of energy homeostasis) signaling in tissue and in cultured cells. The deactivation of AMPK in RC-deficiency is due to increased expression of the AMPK-inhibiting protein FLCN (folliculin). Read More

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http://dx.doi.org/10.1080/15548627.2019.1586256DOI Listing
March 2019
2 Reads
11.753 Impact Factor

Targeted interplay between bacterial pathogens and host autophagy.

Autophagy 2019 Mar 25:1-14. Epub 2019 Mar 25.

d School of Life Sciences , University of Warwick , Coventry , UK.

Due to the critical role played by autophagy in pathogen clearance, pathogens have developed diverse strategies to subvert it. Despite previous key findings of bacteria-autophagy interplay, asystems-level insight into selective targeting by the host and autophagy modulation by the pathogens is lacking. We predicted potential interactions between human autophagy proteins and effector proteins from 56 pathogenic bacterial species by identifying bacterial proteins predicted to have recognition motifs for selective autophagy receptors SQSTM1/p62, CALCOCO2/NDP52 and MAP1LC3/LC3. Read More

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http://dx.doi.org/10.1080/15548627.2019.1590519DOI Listing

Regorafenib induces lethal autophagy arrest by stabilizing PSAT1 in glioblastoma.

Autophagy 2019 Mar 25:1-17. Epub 2019 Mar 25.

a State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and West China School of Basic Medical Sciences & Forensic Medicine , Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , P.R. China.

GBM (glioblastoma multiforme) is the most common and aggressive brain tumor with no curative options available. Therefore, it is imperative to develop novel potent therapeutic drugs for GBM treatment. Here, we show that regorafenib, an oral multi-kinase inhibitor, exhibits superior therapeutic efficacy over temozolomide, the first-line chemotherapeutic agent for GBM treatment both in vitro and in vivo. Read More

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http://dx.doi.org/10.1080/15548627.2019.1598752DOI Listing
March 2019
11.753 Impact Factor

Identification of transcription factors that regulate ATG8 expression and autophagy in Arabidopsis.

Autophagy 2019 Mar 25:1-17. Epub 2019 Mar 25.

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

Autophagy is a conserved catabolic process in eukaryotes that contributes to cell survival in response to multiple stresses and is important for organism fitness. In Arabidopsis thaliana, the core machinery of autophagy is well defined, but its transcriptional regulation is largely unknown. The ATG8 (autophagy-related 8) protein plays central roles in decorating autophagosomes and binding to specific cargo receptors to recruit cargo to autophagosomes. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1598753DOI Listing
March 2019
28 Reads

Dual roles of ULK1 (unc-51 like autophagy activating kinase 1) in cytoprotection against lipotoxicity.

Autophagy 2019 Mar 25:1-20. Epub 2019 Mar 25.

a Severance Biomedical Science Institute, Yonsei Biomedical Research Institute , Yonsei University College of Medicine , Seoul , Republic of Korea.

Saturated fatty acid (SFA)-induced lipotoxicity is caused by the accumulation of reactive oxygen species (ROS), which is associated with damaged mitochondria. Moreover, lipotoxicity is crucial for the progression of nonalcoholic steatohepatitis (NASH). Autophagy is required for the clearance of protein aggregates or damaged mitochondria to maintain cellular metabolic homeostasis. Read More

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http://dx.doi.org/10.1080/15548627.2019.1598751DOI Listing
March 2019
2 Reads
11.753 Impact Factor

Actin filaments are dispensable for bulk autophagy in plants.

Autophagy 2019 Mar 23:1-16. Epub 2019 Mar 23.

a MOE Key Laboratory of Bioinformatics, Tsinghua-Peking Joint Center for Life Sciences, School of Life Sciences , Tsinghua University , Beijing , China.

Actin filament, also known as microfilament, is one of two major cytoskeletal elements in plants and plays important roles in various biological processes. Like in animal cells, actin filaments have been thought to participate in autophagy in plants. However, surprisingly, in this study we found that actin filaments are dispensable for the occurrence of autophagy in plants. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1596496DOI Listing
March 2019
5 Reads

Autophagy protein ATG5 regulates CD36 expression and anti-tumor MHC class II antigen presentation in dendritic cells.

Autophagy 2019 Mar 22:1-16. Epub 2019 Mar 22.

a Graduate School of Medical Science and Engineering , Korea Advanced Institute of Science and Technology (KAIST) , Daejeon , Republic of Korea.

Macroautophagy/autophagy has been implicated in cytoplasmic and viral antigen presentation on major histocompatibility complex (MHC) class II molecules. However, the role of autophagy in the presentation of phagocytized tumor-associated antigens in vivo remains unclear. Following the administration of apoptotic tumor cells and in vivo chemotherapy, mice with a dendritic cell-specific deletion of Atg5, a key autophagy gene, exhibit reduced CD4 T-cell priming but not CD8 cytotoxic T-cell priming. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596493DOI Listing
March 2019
2 Reads

Activation of PPARA-mediated autophagy reduces Alzheimer disease-like pathology and cognitive decline in a murine model.

Autophagy 2019 Mar 22:1-18. Epub 2019 Mar 22.

a Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province , Kunming Institute of Zoology , Kunming , Yunnan , China.

Alzheimer disease (AD) is the most common neurodegenerative disease. An imbalance between the production and clearance of Aβ (amyloid beta) is considered to be actively involved in AD pathogenesis. Macroautophagy/autophagy is a major cellular pathway leading to the removal of aggregated proteins, and upregulation of autophagy represents a plausible therapeutic strategy to combat overproduction of neurotoxic Aβ. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596488DOI Listing
March 2019
1 Read
11.753 Impact Factor

Suppression of autophagy during mitosis via CUL4-RING ubiquitin ligases-mediated WIPI2 polyubiquitination and proteasomal degradation.

Autophagy 2019 Mar 22:1-18. Epub 2019 Mar 22.

a Department of Physiology, Yong Loo Lin School of Medicine , National University of Singapore , Singapore , Singapore.

Macroautophagy/autophagy is a cellular process in which cytosolic contents are degraded by lysosome in response to various stress conditions. Apart from its role in the maintenance of cellular homeostasis, autophagy also involves in regulation of cell cycle progression under nutrient-deprivation conditions. However, whether and how autophagy is regulated by the cell cycle especially during mitosis remains largely undefined. Read More

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https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1
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http://dx.doi.org/10.1080/15548627.2019.1596484DOI Listing
March 2019
4 Reads
11.753 Impact Factor

Deficiency of mitophagy receptor FUNDC1 impairs mitochondrial quality and aggravates dietary-induced obesity and metabolic syndrome.

Autophagy 2019 Mar 22:1-17. Epub 2019 Mar 22.

a State Key Laboratory of Membrane Biology, Institute of Zoology , Chinese Academy of Sciences , Beijing , China.

There is overwhelming evidence for an association between impaired mitochondrial function and metabolic syndrome. Mitophagy, a process that selectively removes damaged mitochondria via a specialized form of autophagy, is essential for mitochondrial quality control (mitochondrial QC) and metabolic homeostasis. We thus addressed the potential role of defective mitophagy in the pathogenesis of metabolic disorders. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596482DOI Listing
March 2019
4 Reads
11.753 Impact Factor

Reduced autophagy efficiency induces innate immune activation leading to neurodegeneration.

Autophagy 2019 Mar 22:1-3. Epub 2019 Mar 22.

a National Institute of Neurological Disorders and Stroke , National Institutes of Health , Bethesda , Maryland , USA.

Macroautophagy/autophagy and innate immunity are central processes in neurodegeneration, but it has been unclear whether they work independently or in combination to assault the neuron. We recently demonstrated that reduced efficiency of autophagy causes hyperactivation of innate immunity, which in turn is necessary and sufficient for loss of dopaminergic neurons in a Cdk5-mediated model of degeneration in Drosophila. Genetically restoring autophagy, or reducing innate immune activation, rescues the dopaminergic neuron loss that occurs due to altered Cdk5 activity. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596499DOI Listing
March 2019
11.753 Impact Factor

RUBCNL/Pacer and RUBCN/Rubicon in regulation of autolysosome formation and lipid metabolism.

Autophagy 2019 Mar 20:1-2. Epub 2019 Mar 20.

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

Recently, we identified a vertebrate-specific macroautophagy/autophagy regulator, RUBCNL/Pacer, which promotes autolysosome formation by engaging the class III phosphatidylinositol 3-kinase (PtdIns3K) and HOPS complexes. Hepatocyte-specific rubcnl knockout in mice results in impaired autophagy flux, glycogen and lipid accumulation, and liver fibrosis. We further showed that under nutrient-rich conditions RUBCNL is inactivated by MTORC1-mediated phosphorylation. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596500DOI Listing
March 2019
2 Reads

The BARA necessities of PtdIns 3-kinase activation in autophagy.

Autophagy 2019 Mar 20:1-2. Epub 2019 Mar 20.

a Department of Molecular and Cell Biology , University of California , Berkeley , CA , USA.

Macroautophagy/autophagy is an evolutionarily conserved degradation system with fundamental biological functions. The activation of the class III phosphatidylinositol 3-kinase (PtdIns3K) complexes and the subsequent production of phosphatidylinositol 3-phosphate (PtdIns3P) are pivotal to autophagy. Using a combination of structural biology, biochemistry, and biophysics, we revealed how the non-catalytic subunit BECN1 serves as a membrane-binding switch in the regulation of PtdIns3K complexes and autophagy. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596501DOI Listing
March 2019
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Loss of MIEF1/MiD51 confers susceptibility to BAX-mediated cell death and PINK1-PRKN-dependent mitophagy.

Autophagy 2019 Mar 20:1-19. Epub 2019 Mar 20.

a Department of Biological Sciences, Faculty of Science , National University of Singapore , Singapore , Singapore.

Mitochondrial dynamics is highly implicated in a plethora of cellular processes including apoptosis and mitophagy. However, little is known about the scope and precise functions of mitochondrial dynamics proteins for mitochondrial quality control and cellular homeostasis. Whether mitochondrial dynamics proteins serve in cellular processes reliant on mitochondrial fission-fusion is still not fully explored. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596494DOI Listing

Impaired TFEB-mediated lysosomal biogenesis promotes the development of pancreatitis in mice and is associated with human pancreatitis.

Autophagy 2019 Mar 20:1-16. Epub 2019 Mar 20.

a Department of Pharmacology, Toxicology and Therapeutics , University of Kansas Medical Center , Kansas City , USA.

Impaired macroautophagy/autophagy has been implicated in experimental and human pancreatitis. However, the transcriptional control governing the autophagy-lysosomal process in pancreatitis is largely unknown. We investigated the role and mechanisms of TFEB (transcription factor EB), a master regulator of lysosomal biogenesis, in the pathogenesis of experimental pancreatitis. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596486DOI Listing
March 2019
4 Reads
11.753 Impact Factor

KLF2 (kruppel like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.

Autophagy 2019 Mar 20:1-13. Epub 2019 Mar 20.

a Department of Pharmaceutical Sciences, School of Pharmacy , Texas Tech University Health Sciences Center , Amarillo , TX , USA.

Macroautophagy/autophagy is involved in myeloid cellular repair, destruction, and osteoclast differentiation; conversely, KLF2 (kruppel-like factor 2 [lung]) regulates myeloid cell activation and differentiation. To investigate the specific role of KLF2 in autophagy, osteoclastic differentiation was induced in monocytes in presence or absence of the autophagy inhibitor 3-methyladenine (3-MA), KLF2 inducer geranylgeranyl transferase inhibitor (GGTI298), and adenoviral overexpression of KLF2. We found that the number of autophagic cells and multinucleated osteoclasts were significantly decreased in presence of 3-MA, GGTI298, and KLF2 overexpressed cells indicating involvement of KLF2 in these processes. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596491DOI Listing

Adventures in spacetime: circadian rhythms and the dynamics of protein catabolism.

Autophagy 2019 Mar 20:1-2. Epub 2019 Mar 20.

a Division of Pulmonary and Critical Care Medicine , Washington University School of Medicine , St. Louis , MO , USA.

Circadian rhythms help cells to organize complex processes, but how they shape the kinetics of protein catabolism is unclear. In a recent paper, we employed proteomics to map daily biological rhythms in autophagic flux in mouse liver, and correlated these rhythms with proteasome activity. We also explored the effect of inflammation caused by endotoxin on autophagy dynamics. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596498DOI Listing

Autophagy-dependent secretion: mechanism, factors secreted, and disease implications.

Autophagy 2019 Mar 20:1-12. Epub 2019 Mar 20.

a Departments of Otolaryngology , University of Kansas Medical Center , Kansas City , KS , USA.

Although best understood as a degradative pathway, recent evidence demonstrates pronounced involvement of the macroautophagic/autophagic molecular machinery in cellular secretion. With either overexpression or inhibition of autophagy mediators, dramatic alterations in the cellular secretory profile occur. This affects secretion of a plethora of factors ranging from cytokines, to granule contents, and even viral particles. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596479DOI Listing

Intestinal epithelial HMGB1 inhibits bacterial infection via STAT3 regulation of autophagy.

Autophagy 2019 Mar 20:1-19. Epub 2019 Mar 20.

a Department of Medicine , University of Illinois at Chicago , Chicago , IL , USA.

Extracellular HMGB1 (high mobility group box 1) is considered as a damage-associated molecular pattern protein. However, little is known about its intracellular role. We studied the mechanism whereby intestinal epithelial HMGB1 contributes to host defense, using cell culture, colonoids, conditional intestinal epithelial HMGB1-knockout mice with Salmonella-colitis, il10 mice, and human samples. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596485DOI Listing
March 2019
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GORASP2/GRASP55 collaborates with the PtdIns3K UVRAG complex to facilitate autophagosome-lysosome fusion.

Autophagy 2019 Mar 20:1-14. Epub 2019 Mar 20.

a Department of Molecular, Cellular and Developmental Biology , University of Michigan , Ann Arbor , MI , USA.

It has been indicated that the Golgi apparatus contributes to autophagy, but how it is involved in autophagosome formation and maturation is not well understood. Here we show that amino acid starvation causes trans-Golgi derived membrane fragments to colocalize with autophagosomes. Depletion of the Golgi stacking protein GORASP2/GRASP55, but not GORASP1/GRASP65, increases both MAP1LC3 (LC3)-II and SQSTM1/p62 levels. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596480DOI Listing
March 2019
11.753 Impact Factor

Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway.

Autophagy 2019 Mar 20:1-19. Epub 2019 Mar 20.

a Division of PK-PD-Toxicology and Formulation , CSIR-Indian Institute of Integrative Medicine , Jammu , India.

Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease. Macroautophagy/autophagy is one of the important mechanisms for clearance of both intracellular and extracellular Aβ. Here, through screening, we identified alborixin, an ionophore, as a potent inducer of autophagy. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596476DOI Listing
March 2019
1 Read
11.753 Impact Factor

Atg14 protects the intestinal epithelium from TNF-triggered villus atrophy.

Autophagy 2019 Mar 20:1-12. Epub 2019 Mar 20.

a Department of Pathology and Immunology , Washington University in St. Louis , St. Louis , MO , USA.

Regulation of intestinal epithelial turnover is a key component of villus maintenance in the intestine. The balance of cell turnover can be perturbed by various extrinsic factors including the cytokine TNF, a cell signaling protein that mediates both proliferative and cytotoxic outcomes. Under conditions of infection and damage, defects in autophagy are associated with TNF-mediated cell death and tissue damage in the intestinal epithelium. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596495DOI Listing

Cross-regulation of defective endolysosome trafficking and enhanced autophagy through TFEB in UNC13D deficiency.

Autophagy 2019 Mar 20:1-19. Epub 2019 Mar 20.

a Department of Molecular Medicine , The Scripps Research Institute , La Jolla , CA , USA.

Several lines of evidence support the occurrence of cross-regulation between the endocytic pathway and autophagy, but the molecular mechanisms regulating this process are not well-understood. Here, we show that the calcium sensor UNC13D regulates the molecular mechanism of late endosomal trafficking and endosomal maturation, and defects in UNC13D lead to macroautophagy upregulation. unc13d-null cells showed impaired endosomal trafficking and defective endocytic flux. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596475DOI Listing
March 2019
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PSEN2 (presenilin 2) mutants linked to familial Alzheimer disease impair autophagy by altering Ca homeostasis.

Autophagy 2019 Mar 20:1-19. Epub 2019 Mar 20.

a Department of Biomedical Sciences , University of Padua , Padua , Italy.

PSEN2 (presenilin 2) is one of the 3 proteins that, when mutated, causes early onset familial Alzheimer disease (FAD) cases. In addition to its well-known role within the γ-secretase complex (the enzyme ultimately responsible for Aβ peptides formation), PSEN2 is endowed with some γ-secretase-independent functions in distinct cell signaling pathways, such as the modulation of intracellular Ca homeostasis. Here, by using different FAD-PSEN2 cell models, we demonstrate that mutated PSEN2 impairs autophagy by causing a block in the degradative flux at the level of the autophagosome-lysosome fusion step. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596489DOI Listing
March 2019
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The Pat1-Lsm complex prevents 3' to 5' degradation of a specific subset of ATG mRNAs during nitrogen starvation-induced autophagy.

Autophagy 2019 Apr 18;15(4):750-751. Epub 2019 Mar 18.

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

Deregulation of macroautophagy/autophagy, a conserved catabolic recycling pathway, has been implicated in the onset and development of several diseases. While post-translational regulation of auto-phagy-related (Atg) proteins has been an important research focus leading to significant breakthroughs in understanding autophagy regulation, less is known about the post-transcriptional regulation of ATG transcripts. In a recent study we showed that, during nitrogen starvation, the RNA-binding complex Pat1-Lsm is involved in binding and preventing the 3' to 5' exosome-mediated degradation of a specific subset of ATG mRNAs. Read More

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http://dx.doi.org/10.1080/15548627.2019.1587262DOI Listing

Correction.

Authors:

Autophagy 2019 Mar 11. Epub 2019 Mar 11.

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http://dx.doi.org/10.1080/15548627.2019.1589725DOI Listing