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https://www.readbyqxmd.com/read/27904666/ad-hgf-improves-the-cardiac-remodeling-of-rat-following-myocardial-infarction-by-upregulating-autophagy-and-necroptosis-and-inhibiting-apoptosis
#1
Jiabao Liu, Peng Wu, Yunle Wang, Yingqiang Du, Nan A, Shuiyuan Liu, Yiming Zhang, Ningtian Zhou, Zhihui Xu, Zhijian Yang
Cell death in MI is the most critical determinant of subsequent left ventricular remodeling and heart failure. Besides apoptosis, autophagy and necroptosis have been recently found to be another two regulated cell death styles. HGF has been reported to have a protective role in MI, but its impact on the three death styles remains unclear. Thus, our study was performed to investigate the distribution of autophagy, apoptosis and necroptosis in cardiac tissues after MI and explore the role and mechanism of Ad-HGF on cardiac remodeling by regulating the three death styles...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27882921/a-mutation-in-vps15-pik3r4-causes-a-ciliopathy-and-affects-ift20-release-from-the-cis-golgi
#2
Corinne Stoetzel, Séverine Bär, Johan-Owen De Craene, Sophie Scheidecker, Christelle Etard, Johana Chicher, Jennifer R Reck, Isabelle Perrault, Véronique Geoffroy, Kirsley Chennen, Uwe Strähle, Philippe Hammann, Sylvie Friant, Hélène Dollfus
Ciliopathies are a group of diseases that affect kidney and retina among other organs. Here, we identify a missense mutation in PIK3R4 (phosphoinositide 3-kinase regulatory subunit 4, named VPS15) in a family with a ciliopathy phenotype. Besides being required for trafficking and autophagy, we show that VPS15 regulates primary cilium length in human fibroblasts, as well as ciliary processes in zebrafish. Furthermore, we demonstrate its interaction with the golgin GM130 and its localization to the Golgi. The VPS15-R998Q patient mutation impairs Golgi trafficking functions in humanized yeast cells...
November 24, 2016: Nature Communications
https://www.readbyqxmd.com/read/27821547/endosomal-phosphatidylinositol-3-kinase-is-essential-for-canonical-gpcr-signaling
#3
Yasunori Uchida, Florentine U Rutaganira, Damien Jullie, Kevan M Shokat, Mark von Zastrow
G protein-coupled receptors (GPCRs), the largest family of signaling receptors, are critically regulated by endosomal trafficking, suggesting that endosomes might provide new strategies for manipulating GPCR signaling. Here we test this hypothesis by focusing on class III phosphatidylinositol (PI) 3-kinase or Vps34, an essential regulator of endosomal trafficking. We verify that Vps34 is required for recycling of the β2-adrenoceptor (β2AR), a prototypical GPCR, and then investigate the effects of Vps34 inhibition on the canonical cAMP response elicited by β2AR activation...
November 7, 2016: Molecular Pharmacology
https://www.readbyqxmd.com/read/27812735/hygromycin-b-hypersensitive-hhy-mutants-implicate-an-intact-trans-golgi-and-late-endosome-interface-in-efficient-tor1-vacuolar-localization-and-torc1-function
#4
Daniele E Ejzykowicz, Kristopher M Locken, Fiona J Ruiz, Surya P Manandhar, Daniel K Olson, Editte Gharakhanian
Saccharomyces cerevisiae vacuoles are functionally analogous to mammalian lysosomes. Both also serve as physical platforms for Tor Complex 1 (TORC1) signal transduction, the master regulator of cellular growth and proliferation. Hygromycin B is a eukaryotic translation inhibitor. We recently reported on hygromycin B hypersensitive (hhy) mutants that fail to grow at subtranslation inhibitory concentrations of the drug and exhibit vacuolar defects (Banuelos et al. in Curr Genet 56:121-137, 2010). Here, we show that hhy phenotype is not due to increased sensitivity to translation inhibition and establish a super HHY (s-HHY) subgroup of genes comprised of ARF1, CHC1, DRS2, SAC1, VPS1, VPS34, VPS45, VPS52, and VPS54 that function exclusively or inclusively at trans-Golgi and late endosome interface...
November 3, 2016: Current Genetics
https://www.readbyqxmd.com/read/27793976/vps34-regulates-rab7-and-late-endocytic-trafficking-through-recruitment-of-the-gtpase-activating-protein-armus
#5
Nadia Jaber, Noor Mohd-Naim, Ziqing Wang, Jennifer L DeLeon, Seong Kim, Hua Zhong, Namratha Sheshadri, Zhixun Dou, Aimee L Edinger, Guangwei Du, Vania M M Braga, Wei-Xing Zong
The class III phosphoinositide 3-kinase (PI3K) Vps34 (also known as PIK3C3 in mammals) produces phosphatidylinositol 3-phosphate [PI(3)P] on both early and late endosome membranes to control membrane dynamics. We used Vps34-deficient cells to delineate whether Vps34 has additional roles in endocytic trafficking. In Vps34(-/-) mouse embryonic fibroblasts (MEFs), transferrin recycling and EEA1 membrane localization were unaffected despite elevated Rab5-GTP levels. Strikingly, a large increase in Rab7-GTP levels, an accumulation of enlarged late endosomes, and decreased EGFR degradation were observed in Vps34-deficient cells...
December 1, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27784791/an-affinity-directed-protein-missile-system-for-targeted-proteolysis
#6
Luke J Fulcher, Thomas Macartney, Polyxeni Bozatzi, Annika Hornberger, Alejandro Rojas-Fernandez, Gopal P Sapkota
The von Hippel-Lindau (VHL) protein serves to recruit the hypoxia-inducible factor alpha (HIF1α) protein under normoxia to the CUL2 E3 ubiquitin ligase for its ubiquitylation and degradation through the proteasome. In this report, we modify VHL to engineer an affinity-directed protein missile (AdPROM) system to direct specific endogenous target proteins for proteolysis in mammalian cells. The proteolytic AdPROM construct harbours a cameloid anti-green fluorescence protein (aGFP) nanobody that is fused to VHL for either constitutive or tetracycline-inducible expression...
October 2016: Open Biology
https://www.readbyqxmd.com/read/27630019/characterization-of-atg38-and-nrbf2-a-fifth-subunit-of-the-autophagic-vps34-pik3c3-complex
#7
Yohei Ohashi, Nicolas Soler, Miguel García Ortegón, Lufei Zhang, Marie L Kirsten, Olga Perisic, Glenn R Masson, John E Burke, Arjen J Jakobi, Apostolos A Apostolakis, Christopher M Johnson, Maki Ohashi, Nicholas T Ktistakis, Carsten Sachse, Roger L Williams
The phosphatidylinositol 3-kinase Vps34 is part of several protein complexes. The structural organization of heterotetrameric complexes is starting to emerge, but little is known about organization of additional accessory subunits that interact with these assemblies. Combining hydrogen-deuterium exchange mass spectrometry (HDX-MS), X-ray crystallography and electron microscopy (EM), we have characterized Atg38 and its human ortholog NRBF2, accessory components of complex I consisting of Vps15-Vps34-Vps30/Atg6-Atg14 (yeast) and PIK3R4/VPS15-PIK3C3/VPS34-BECN1/Beclin 1-ATG14 (human)...
November 2016: Autophagy
https://www.readbyqxmd.com/read/27621469/ptdins-4-5-p2-signaling-regulates-atg14-and-autophagy
#8
Xiaojun Tan, Narendra Thapa, Yihan Liao, Suyong Choi, Richard A Anderson
Autophagy is a regulated self-digestion pathway with fundamental roles in cell homeostasis and diseases. Autophagy is regulated by coordinated actions of a series of autophagy-related (ATG) proteins. The Barkor/ATG14(L)-VPS34 (a class III phosphatidylinositol 3-kinase) complex and its product phosphatidylinositol 3-phosphate [PtdIns(3)P] play key roles in autophagy initiation. ATG14 contains a C-terminal Barkor/ATG14(L) autophagosome-targeting sequence (BATS) domain that senses the curvature of PtdIns(3)P-containing membrane...
September 27, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27607605/role-of-class-iii-phosphoinositide-3-kinase-in-the-brain-development-possible-involvement-in-specific-learning-disorders
#9
Yutaka Inaguma, Ayumi Matsumoto, Mariko Noda, Hidenori Tabata, Akihiko Maeda, Masahide Goto, Daisuke Usui, Eriko F Jimbo, Kiyoshi Kikkawa, Mamitaro Ohtsuki, Mariko Y Momoi, Hitoshi Osaka, Takanori Yamagata, Koh-Ichi Nagata
Class III phosphoinositide 3-kinase (PIK3C3 or mammalian vacuolar protein sorting 34 homolog, Vps34) regulates vesicular trafficking, autophagy, and nutrient sensing. Recently, we reported that PIK3C3 is expressed in mouse cerebral cortex throughout the developmental process, especially at early embryonic stage. We thus examined the role of PIK3C3 in the development of the mouse cerebral cortex. Acute silencing of PIK3C3 with in utero electroporation method caused positional defects of excitatory neurons during corticogenesis...
October 2016: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27603757/the-phosphatidylinositol-3-kinase-class-iii-complex-containing%C3%A2-tcvps15-and-tcvps34-participates-in-autophagy-in-trypanosoma-cruzi
#10
Alejandra C Schoijet, Tamara Sternlieb, Guillermo D Alonso
Autophagy is a degradative process by which eukaryotic cells digest their own components to provide aminoacids that may function as energy source under nutritional stress conditions. There is experimental evidence for autophagy in parasitic protists belonging to the family Trypanosomatidae. However, few proteins implicated in this process have been characterized so far in these parasites. Moreover, it has been shown that autophagy is involved in Trypanosoma cruzi differentiation and thus might have a role in pathogenicity...
September 7, 2016: Journal of Eukaryotic Microbiology
https://www.readbyqxmd.com/read/27559127/the-ccz1-mon1-rab7-module-and-rab5-control-distinct-steps-of-autophagy
#11
Krisztina Hegedűs, Szabolcs Takáts, Attila Boda, András Jipa, Péter Nagy, Kata Varga, Attila L Kovács, Gábor Juhász
The small GTPase Rab5 promotes recruitment of the Ccz1-Mon1 guanosine exchange complex to endosomes to activate Rab7, which facilitates endosome maturation and fusion with lysosomes. How these factors function during autophagy is incompletely understood. Here we show that autophagosomes accumulate due to impaired fusion with lysosomes upon loss of the Ccz1-Mon1-Rab7 module in starved Drosophila fat cells. In contrast, autophagosomes generated in Rab5-null mutant cells normally fuse with lysosomes during the starvation response...
October 15, 2016: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/27541856/ehrlichia-secretes-etf-1-to-induce-autophagy-and-capture-nutrients-for-its-growth-through-rab5-and-class-iii-phosphatidylinositol-3-kinase
#12
Mingqun Lin, Hongyan Liu, Qingming Xiong, Hua Niu, Zhihui Cheng, Akitsugu Yamamoto, Yasuko Rikihisa
Ehrlichia chaffeensis is an obligatory intracellular bacterium that causes a potentially fatal emerging zoonosis, human monocytic ehrlichiosis. E. chaffeensis has a limited capacity for biosynthesis and metabolism and thus depends mostly on host-synthesized nutrients for growth. Although the host cell cytoplasm is rich with these nutrients, as E. chaffeensis is confined within the early endosome-like membrane-bound compartment, only host nutrients that enter the compartment can be used by this bacterium. How this occurs is unknown...
November 2016: Autophagy
https://www.readbyqxmd.com/read/27534530/the-role-of-amino-acid-induced-mammalian-target-of-rapamycin-complex-1-mtorc1-signaling-in-insulin-resistance
#13
REVIEW
Mee-Sup Yoon, Cheol Soo Choi
Mammalian target of rapamycin (mTOR) controls cell growth and metabolism in response to nutrients, energy, and growth factors. Recent findings have placed the lysosome at the core of mTOR complex 1 (mTORC1) regulation by amino acids. Two parallel pathways, Rag GTPase-Ragulator and Vps34-phospholipase D1 (PLD1), regulate mTOR activation on the lysosome. This review describes the recent advances in understanding amino acid-induced mTOR signaling with a particular focus on the role of mTOR in insulin resistance...
2016: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/27513923/angiogenic-factor-aggf1-activates-autophagy-with-an-essential-role-in-therapeutic-angiogenesis-for-heart-disease
#14
Qiulun Lu, Yufeng Yao, Zhenkun Hu, Changqing Hu, Qixue Song, Jian Ye, Chengqi Xu, Annabel Z Wang, Qiuyun Chen, Qing Kenneth Wang
AGGF1 is an angiogenic factor with therapeutic potential to treat coronary artery disease (CAD) and myocardial infarction (MI). However, the underlying mechanism for AGGF1-mediated therapeutic angiogenesis is unknown. Here, we show for the first time that AGGF1 activates autophagy, a housekeeping catabolic cellular process, in endothelial cells (ECs), HL1, H9C2, and vascular smooth muscle cells. Studies with Atg5 small interfering RNA (siRNA) and the autophagy inhibitors bafilomycin A1 (Baf) and chloroquine demonstrate that autophagy is required for AGGF1-mediated EC proliferation, migration, capillary tube formation, and aortic ring-based angiogenesis...
August 2016: PLoS Biology
https://www.readbyqxmd.com/read/27488670/new-pieces-in-the-complex-puzzle-of-aberrant-vacuolation-focus-on-active-vacuolar-h-atpase-and-functional-cycle-of-rab5-are-required-for-the-vacuolation-defect-triggered-by-ptdins-3-5-p2-loss-under-pikfyve-or-vps34-deficiency
#15
EDITORIAL
Loredana Saveanu, Sophie Lotersztajn
No abstract text is available yet for this article.
September 1, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27477288/leucyl-trna-synthetase-activates-vps34-in-amino-acid-sensing-mtorc1-signaling
#16
Mee-Sup Yoon, Kook Son, Edwin Arauz, Jung Min Han, Sunghoon Kim, Jie Chen
Amino acid availability activates signaling by the mammalian target of rapamycin (mTOR) complex 1, mTORC1, a master regulator of cell growth. The class III PI-3-kinase Vps34 mediates amino acid signaling to mTORC1 by regulating lysosomal translocation and activation of the phospholipase PLD1. Here, we identify leucyl-tRNA synthetase (LRS) as a leucine sensor for the activation of Vps34-PLD1 upstream of mTORC1. LRS is necessary for amino acid-induced Vps34 activation, cellular PI(3)P level increase, PLD1 activation, and PLD1 lysosomal translocation...
August 9, 2016: Cell Reports
https://www.readbyqxmd.com/read/27470591/the-intricate-regulation-and-complex-functions-of-the-class-iii-phosphoinositide-3-kinase-vps34
#17
REVIEW
Jonathan M Backer
The Class III phosphoinositide 3-kinase Vps34 (vacuolar protein sorting 34) plays important roles in endocytic trafficking, macroautophagy, phagocytosis, cytokinesis and nutrient sensing. Recent studies have provided exciting new insights into the structure and regulation of this lipid kinase, and new cellular functions for Vps34 have emerged. This review critically examines the wealth of new data on this important enzyme, and attempts to integrate these findings with current models of Vps34 signalling.
August 1, 2016: Biochemical Journal
https://www.readbyqxmd.com/read/27460191/acetylation-modification-regulates-grp78-secretion-in-colon-cancer-cells
#18
Zongwei Li, Ming Zhuang, Lichao Zhang, Xingnan Zheng, Peng Yang, Zhuoyu Li
High glucose-regulated protein 78 (GRP78) expression contributes to the acquisition of a wide range of phenotypic cancer hallmarks, and the pleiotropic oncogenic functions of GRP78 may result from its diverse subcellular distribution. Interestingly, GRP78 has been reported to be secreted from solid tumour cells, participating in cell-cell communication in the tumour microenvironment. However, the mechanism underlying this secretion remains elusive. Here, we report that GRP78 is secreted from colon cancer cells via exosomes...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27459239/role-for-dusp1-dual-specificity-protein-phosphatase-1-in-the-regulation-of-autophagy
#19
Juan Wang, Jun-Ying Zhou, Dhonghyo Kho, John J Reiners, Gen Sheng Wu
Accumulating evidence suggests that mitogen-activated protein kinases (MAPKs) regulate macroautophagy/autophagy. However, the involvement of dual-specificity protein phosphatases (DUSPs), endogenous inhibitors for MAPKs, in autophagy remains to be determined. Here we report that DUSP1/MKP-1, the founding member of the DUSP family, plays a critical role in regulating autophagy. Specifically, we demonstrate that DUSP1 knockdown by shRNA in human ovarian cancer CAOV3 cells and knockout in murine embryonic fibroblasts, increases both basal and rapamycin-increased autophagic flux...
October 2, 2016: Autophagy
https://www.readbyqxmd.com/read/27447747/simultaneous-inhibition-of-vps34-kinase-would-enhance-pi3k%C3%AE-inhibitor-cytotoxicity-in-the-b-cell-malignancies
#20
Xiaochuan Liu, Aoli Wang, Xiaofei Liang, Juanjuan Liu, Fengming Zou, Cheng Chen, Zheng Zhao, Yuanxin Deng, Hong Wu, Ziping Qi, Beilei Wang, Li Wang, Feiyang Liu, Yunhe Xu, Wenchao Wang, Stacey M Fernandes, Richard M Stone, Ilene A Galinsky, Jennifer R Brown, Teckpeng Loh, James D Griffin, Shanchun Zhang, Ellen L Weisberg, Xin Zhang, Jing Liu, Qingsong Liu
PI3Kδ has been found to be over-expressed in B-Cell-related malignancies. Despite the clinical success of the first selective PI3Kδ inhibitor, CAL-101, inhibition of PI3Kδ itself did not show too much cytotoxic efficacy against cancer cells. One possible reason is that PI3Kδ inhibition induced autophagy that protects the cells from death. Since class III PI3K isoform PIK3C3/Vps34 participates in autophagy initiation and progression, we predicted that a PI3Kδ and Vps34 dual inhibitor might improve the anti-proliferative activity observed for PI3Kδ-targeted inhibitors...
July 18, 2016: Oncotarget
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