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https://www.readbyqxmd.com/read/27892768/tfeb-and-tfe3-the-art-of-multitasking-under-stress-conditions
#1
José A Martina, Rosa Puertollano
Cellular adaptation response to a myriad of stressors is key for survival. The lysosomal/autophagy pathway is inextricably connected to the stress response regulation. Two transcription factors, TFEB and TFE3, have recently emerged as master regulators of this degradative pathway. Their function modulating different cellular pathways will be discussed.
November 28, 2016: Transcription
https://www.readbyqxmd.com/read/27892481/autophagy-is-required-for-pdac-glutamine-metabolism
#2
Ju-Won Seo, Jungwon Choi, So-Yeon Lee, Suhyun Sung, Hyun Ju Yoo, Min-Ji Kang, Heesun Cheong, Jaekyoung Son
Macroautophagy (autophagy) is believed to maintain energy homeostasis by degrading unnecessary cellular components and molecules. Its implication in regulating cancer metabolism recently started to be uncovered. However, the precise roles of autophagy in cancer metabolism are still unclear. Here, we show that autophagy plays a critical role in glutamine metabolism, which is required for tumor survival. Pancreatic ductal adenocarcinoma (PDAC) cells require both autophagy and typical glutamine transporters to maintain intracellular glutamine levels...
November 28, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27884963/ectopic-fat-deposition-contributes-to-age-associated-pathology-in-caenorhabditis-elegans
#3
Konstantinos Palikaras, Meropi Mari, Barbara Petanidou, Angela Pasparaki, George Filippidis, Nektarios Tavernarakis
Age-dependent collapse of lipid homeostasis results in spillover of lipids and excessive fat deposition in non-adipose tissues. Ectopic fat contributes to lipotoxicity and has been implicated in the development of a metabolic syndrome that increases risk of age-associated diseases. However, the molecular mechanisms coupling ectopic fat accumulation with ageing remain obscure. Here, we use nonlinear imaging modalities to visualize and quantify age-dependent ectopic lipid accumulation in Caenorhabditis elegans...
November 24, 2016: Journal of Lipid Research
https://www.readbyqxmd.com/read/27875531/loss-of-c9orf72-enhances-autophagic-activity-via-deregulated-mtor-and-tfeb-signaling
#4
Janet Ugolino, Yon Ju Ji, Karen Conchina, Justin Chu, Raja Sekhar Nirujogi, Akhilesh Pandey, Nathan R Brady, Anne Hamacher-Brady, Jiou Wang
The most common cause of the neurodegenerative diseases amyotrophic lateral sclerosis and frontotemporal dementia is a hexanucleotide repeat expansion in C9orf72. Here we report a study of the C9orf72 protein by examining the consequences of loss of C9orf72 functions. Deletion of one or both alleles of the C9orf72 gene in mice causes age-dependent lethality phenotypes. We demonstrate that C9orf72 regulates nutrient sensing as the loss of C9orf72 decreases phosphorylation of the mTOR substrate S6K1. The transcription factor EB (TFEB), a master regulator of lysosomal and autophagy genes, which is negatively regulated by mTOR, is substantially up-regulated in C9orf72 loss-of-function animal and cellular models...
November 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27875098/hlh-30-tfeb-mediated-autophagy-functions-in-a-cell-autonomous-manner-for-epithelium-intrinsic-cellular-defense-against-bacterial-pore-forming-toxin-in-c-elegans
#5
Huan-Da Chen, Cheng-Yuan Kao, Bang-Yu Liu, Shin-Whei Huang, Cheng-Ju Kuo, Jhen-Wei Ruan, Yen-Hung Lin, Cheng-Rung Huang, Yu-Hung Chen, Horng-Dar Wang, Raffi V Aroian, Chang-Shi Chen
Autophagy is an evolutionarily conserved intracellular system that maintains cellular homeostasis by degrading and recycling damaged cellular components. The transcription factor HLH-30/TFEB-mediated autophagy has been reported to regulate tolerance to bacterial infection, but less is known about the bona fide bacterial effector that activates HLH-30 and autophagy. Here, we unveil that bacterial membrane pore-forming toxin (PFT) induces autophagy in an HLH-30-dependent manner in Caenorhabditis elegans. Moreover, autophagy controls the susceptibility of animals to PFT toxicity through xenophagic degradation of PFT and repair of membrane-pore cell-autonomously in the PFT-targeted intestinal cells in C...
November 22, 2016: Autophagy
https://www.readbyqxmd.com/read/27864122/sclerosing-tfeb-rearrangement-renal-cell-carcinoma-a-recurring-histologic-pattern
#6
Sean R Williamson, John N Eble, Nallasivam Palanisamy
Renal cell carcinoma with TFEB rearrangement [t(6;11)(p21;q13)] was initially recognized to be composed of dual populations of large cells with clear cytoplasm and small cells forming rosettes around hyaline material. With increasing awareness, however, the spectrum of described morphology has been found to be more heterogeneous. We report a 54 year-old woman who underwent partial nephrectomy for a 2.4 cm renal mass, composed of fibrosis, hyalinization, calcification and ossification, and a smaller component of epithelioid cells...
November 15, 2016: Human Pathology
https://www.readbyqxmd.com/read/27852774/a-drosophila-model-of-neuronopathic-gaucher-disease-demonstrates-lysosomal-autophagic-defects-and-altered-mtor-signalling-and-is-functionally-rescued-by-rapamycin
#7
Kerri J Kinghorn, Sebastian Grönke, Jorge Iván Castillo-Quan, Nathaniel S Woodling, Li Li, Ernestas Sirka, Matthew Gegg, Kevin Mills, John Hardy, Ivana Bjedov, Linda Partridge
Glucocerebrosidase (GBA1) mutations are associated with Gaucher disease (GD), an autosomal recessive disorder caused by functional deficiency of glucocerebrosidase (GBA), a lysosomal enzyme that hydrolyzes glucosylceramide to ceramide and glucose. Neuronopathic forms of GD can be associated with rapid neurological decline (Type II) or manifest as a chronic form (Type III) with a wide spectrum of neurological signs. Furthermore, there is now a well-established link between GBA1 mutations and Parkinson's disease (PD), with heterozygote mutations in GBA1 considered the commonest genetic defect in PD...
November 16, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27835930/master-autophagy-regulator-transcription-factor-eb-tfeb-regulates-cigarette-smoke-induced-autophagy-impairment-and-copd-emphysema-pathogenesis
#8
Manish Bodas, Neel Patel, David Silverberg, Kyla Walworth, Neeraj Vij
AIMS: Recent studies have shown that cigarette smoke (CS)-induced oxidative-stress impairs autophagy resulting in aggresome-formation that correlates with the severity of COPD-emphysema. Although, specific step in autophagy-pathway that is impaired is unknown. Hence, in this study we aimed to evaluate the role of master autophagy-regulator and transcription factor-EB (TFEB) in CS-induced COPD-emphysema pathogenesis. RESULTS: We first observed that TFEB-accumulates in the peri-nuclear spaces of the COPD lung tissues of tobacco-smokers and severe-emphysema subjects...
November 11, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27822418/inhibition-of-mtorc1-signaling-sensitizes-hepatocellular-carcinoma-cells-to-glycolytic-stress
#9
Xin Zhao, Peng Jiang, Xiang Deng, Zhonghu Li, Feng Tian, Fei Guo, Xiaowu Li, Shuguang Wang
Reprogrammed glucose metabolism, especially glycolysis, is profoundly implicated in tumor development or metastasis. As the interconnectedness and flexibility of metabolic signaling, targeting a metabolic signaling molecule may have limited anti-tumor effects. Here, Gene set enrichment analysis (GSEA) was used to explore the accompanied effectors of glycolysis in hepatocellular carcinoma (HCC). Based on the expression of lactate dehydrogenase A (LDHA), a key enzyme in catalyzing pyruvate into lactate, the glycolytic ability of HCC was defined as low group and high group...
2016: American Journal of Cancer Research
https://www.readbyqxmd.com/read/27813694/autophagy-flux-in-ca1-neurons-of-alzheimer-hippocampus-increased-induction-overburdens-failing-lysosomes-to-propel-neuritic-dystrophy
#10
Matteo Bordi, Martin J Berg, Panaiyur S Mohan, Corrinne M Peterhoff, Melissa J Alldred, Shaoli Che, Stephen D Ginsberg, Ralph A Nixon
Defective autophagy contributes to Alzheimer disease (AD) pathogenesis although evidence is conflicting on whether multiple stages are impaired. Here, for the first time, we have comprehensively evaluated the entire autophagic process specifically in CA1 pyramidal neurons of hippocampus from early and late-stage AD subjects and nondemented controls. CA1 neurons aspirated by laser capture microdissection were analyzed using a custom-designed microarray comprising 578 neuropathology- and neuroscience-associated genes...
December 2016: Autophagy
https://www.readbyqxmd.com/read/27786577/regulation-of-lysosomal-dynamics-and-autophagy-by-ctsb-cathepsin-b
#11
Si Ming Man, Thirumala-Devi Kanneganti
Cysteine cathepsins are responsible for driving proteolytic degradation within the lysosome and in the extralysosomal milieu. They also have an integral role in autophagy, antigen presentation, cellular stress signaling, metabolism and lysosome-dependent cell death. Here, we discuss our findings on the role of CTSB (cathepsin B), a member of the cysteine cathepsin family, in regulating the bioavailability of lysosomes and autophagosomes and consider how this regulatory response influences host susceptibility to infectious agents...
December 2016: Autophagy
https://www.readbyqxmd.com/read/27777789/foxo1-interacts-with-transcription-factor-eb-and-differentially-regulates-mitochondrial-uncoupling-proteins-via-autophagy-in-adipocytes
#12
Longhua Liu, Zhipeng Tao, Louise D Zheng, Joseph P Brooke, Cayleen M Smith, Dongmin Liu, Yun Chau Long, Zhiyong Cheng
Mitochondrial uncoupling proteins (UCPs) are inducible and play an important role in metabolic and redox homeostasis. Recent studies have suggested that FoxO1 controls mitochondrial biogenesis and morphology, but it remains largely unknown how FoxO1 may regulate mitochondrial UCPs. Here we show that FoxO1 interacted with transcription factor EB (Tfeb), a key regulator of autophagosome and lysosome, and mediated the expression of UCP1, UCP2 and UCP3 differentially via autophagy in adipocytes. UCP1 was down-regulated but UCP2 and UCP3 were upregulated during adipocyte differentiation, which was associated with increased Tfeb and autophagy activity...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27693506/trims-and-galectins-globally-cooperate-and-trim16-and-galectin-3-co-direct-autophagy-in-endomembrane-damage-homeostasis
#13
Santosh Chauhan, Suresh Kumar, Ashish Jain, Marisa Ponpuak, Michal H Mudd, Tomonori Kimura, Seong Won Choi, Ryan Peters, Michael Mandell, Jack-Ansgar Bruun, Terje Johansen, Vojo Deretic
Selective autophagy performs an array of tasks to maintain intracellular homeostasis, sterility, and organellar and cellular functionality. The fidelity of these processes depends on precise target recognition and limited activation of the autophagy apparatus in a localized fashion. Here we describe cooperation in such processes between the TRIM family and Galectin family of proteins. TRIMs, which are E3 ubiquitin ligases, displayed propensity to associate with Galectins. One specific TRIM, TRIM16, interacted with Galectin-3 in a ULK1-dependent manner...
October 10, 2016: Developmental Cell
https://www.readbyqxmd.com/read/27689619/autophagy-activation-by-transcription-factor-eb-tfeb-in-striatum-of-hdq175-q7-mice
#14
Petr Vodicka, Kathryn Chase, Maria Iuliano, Adelaide Tousley, Dana T Valentine, Ellen Sapp, Kimberly B Kegel-Gleason, Miguel Sena-Esteves, Neil Aronin, Marian DiFiglia
BACKGROUND: Mutant huntingtin (mHTT) is encoded by the Huntington's disease (HD) gene and its accumulation in the brain contributes to HD pathogenesis. Reducing mHTT levels through activation of the autophagosome-lysosomal pathway may have therapeutic benefit. Transcription factor EB (TFEB) regulates lysosome biogenesis and autophagy. OBJECTIVE: To examine if increasing TFEB protein levels in HD mouse striatum induces autophagy and influences mHTT levels. METHODS: We introduced cDNA encoding TFEB with an HA tag (TFEB-HA) under the control of neuron specific synapsin 1 promoter into the striatum of 3 month old HDQ175/Q7 mice using adeno-associated virus AAV2/9...
October 1, 2016: Journal of Huntington's Disease
https://www.readbyqxmd.com/read/27689333/curcumin-targets-the-tfeb-lysosome-pathway-for-induction-of-autophagy
#15
Jianbin Zhang, Jigang Wang, Jian Xu, Yuanqiang Lu, Jiukun Jiang, Liming Wang, Han-Ming Shen, Dajing Xia
Curcumin is a hydrophobic polyphenol derived from the herb Curcumalonga and its wide spectrum of pharmacological activities has been widely studied. It has been reported that Curcumin can induce autophagy through inhibition of the Akt-mTOR pathway. However, the effect of Curcumin on lysosome remains largely elusive. In this study, we first found that Curcumin treatment enhances autophagic flux in both human colon cancer HCT116 cells and mouse embryonic fibroblasts (MEFs). Moreover, Curcumin treatment promotes lysosomal function, evidenced by the increased lysosomal acidification and enzyme activity...
September 28, 2016: Oncotarget
https://www.readbyqxmd.com/read/27684505/turn-up-the-lysosome
#16
Paul Saftig, Albert Haas
Lysosomes are digestive organelles of the endocytic and autophagic pathways. Increasing lysosome enzyme activities could help to clear pathological cellular waste. A recent study shows that lysosomal digestive functions can be promoted in isolated cells and mice by pharmacologically stimulating the autophagy- and lysosome-regulating transcription factors TFEB and ZKSCAN3 through previously unrecognized mTORC1-independent pathways acting via PKC.
September 28, 2016: Nature Cell Biology
https://www.readbyqxmd.com/read/27677502/protein-coingestion-with-alcohol-following-strenuous-exercise-attenuates-alcohol-induced-intramyocellular-apoptosis-and-inhibition-of-autophagy
#17
William J Smiles, Evelyn B Parr, Vernon G Coffey, Orly Lacham-Kaplan, John A Hawley, Donny M Camera
Alcohol ingestion decreases post-exercise rates of muscle protein synthesis, but the mechanism(s) (e.g., increased protein breakdown) underlying this observation are unknown. Autophagy is an intracellular "recycling" system required for homeostatic substrate and organelle turnover; its dysregulation may provoke apoptosis and lead to muscle atrophy. We investigated the acute effects of alcohol ingestion on autophagic cell signaling responses to a bout of concurrent (combined resistance- and endurance-based) exercise...
September 27, 2016: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27668431/modelling-tfe-renal-cell-carcinoma-in-mice-reveals-a-critical-role-of-wnt-signaling
#18
Alessia Calcagnì, Lotte Kors, Eric Verschuren, Rossella De Cegli, Nicolina Zampelli, Edoardo Nusco, Stefano Confalonieri, Giovanni Bertalot, Salvatore Pece, Carmine Settembre, Gabriel G Malouf, Jaklien C Leemans, Emile de Heer, Marco Salvatore, Dorien Jm Peters, Pier Paolo Di Fiore, Andrea Ballabio
TFE-fusion renal cell carcinomas (TFE-fusion RCCs) are caused by chromosomal translocations that lead to overexpression of the TFEB and TFE3 genes (Kauffman et al., 2014). The mechanisms leading to kidney tumor development remain uncharacterized and effective therapies are yet to be identified. Hence, the need to model these diseases in an experimental animal system (Kauffman et al., 2014). Here, we show that kidney-specific TFEB overexpression in transgenic mice, resulted in renal clear cells, multi-layered basement membranes, severe cystic pathology, and ultimately papillary carcinomas with hepatic metastases...
September 26, 2016: ELife
https://www.readbyqxmd.com/read/27626694/novel-role-of-mir-29a-in-pancreatic-cancer-autophagy-and-its-therapeutic-potential
#19
Jason J Kwon, Jeffrey A Willy, Kayla A Quirin, Ronald C Wek, Murray Korc, Xiao-Ming Yin, Janaiah Kota
Pancreatic Ductal Adenocarcinoma (PDAC) is a highly lethal malignancy that responds poorly to current therapeutic modalities. In an effort to develop novel therapeutic strategies, we found downregulation of miR-29 in pancreatic cancer cells, and overexpression of miR-29a sensitized chemotherapeutic resistant pancreatic cancer cells to gemcitabine, reduced cancer cell viability, and increased cytotoxicity. Furthermore, miR-29a blocked autophagy flux, as evidenced by an accumulation of autophagosomes and autophagy markers, LC3B and p62, and a decrease in autophagosome-lysosome fusion...
September 10, 2016: Oncotarget
https://www.readbyqxmd.com/read/27620487/glucolipotoxicity-diminishes-cardiomyocyte-tfeb-and-inhibits-lysosomal-autophagy-during-obesity-and-diabetes
#20
Purvi C Trivedi, Jordan J Bartlett, Lester J Perez, Keith R Brunt, Jean Francois Legare, Ansar Hassan, Petra C Kienesberger, Thomas Pulinilkunnil
Impaired cardiac metabolism in the obese and diabetic heart leads to glucolipotoxicity and ensuing cardiomyopathy. Glucolipotoxicity causes cardiomyocyte injury by increasing energy insufficiency, impairing proteasomal-mediated protein degradation and inducing apoptosis. Proteasome-evading proteins are degraded by autophagy in the lysosome, whose metabolism and function are regulated by master regulator transcription factor EB (TFEB). Limited studies have examined the impact of glucolipotoxicity on intra-lysosomal signaling proteins and their regulators...
December 2016: Biochimica et Biophysica Acta
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