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autophagy and heat shock protein

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https://www.readbyqxmd.com/read/28301987/properties-of-epithelial-cells-and-vaginal-secretions-in-pregnant-women-when-lactobacillus-crispatus-or-lactobacillus-iners-dominate-the-vaginal-microbiome
#1
Julie Leizer, Dimitrios Nasioudis, Larry J Forney, G Maria Schneider, Karol Gliniewicz, Allison Boester, Steven S Witkin
OBJECTIVE: Our objective was to determine differences in properties of vaginal epithelial cells and the composition of vaginal secretions when Lactobacillus crispatus or Lactobacillus iners are numerically dominant in the vaginal microenvironment of pregnant women. METHODS: The vaginal microbiomes of 157 first-trimester pregnant women were identified by classifying partial 16S gene sequences amplified from the V1 to V3 region of bacterial ribosomal 16S RNA genes...
January 1, 2017: Reproductive Sciences
https://www.readbyqxmd.com/read/28293421/protein-misfolding-in-neurodegenerative-diseases-implications-and-strategies
#2
REVIEW
Patrick Sweeney, Hyunsun Park, Marc Baumann, John Dunlop, Judith Frydman, Ron Kopito, Alexander McCampbell, Gabrielle Leblanc, Anjli Venkateswaran, Antti Nurmi, Robert Hodgson
A hallmark of neurodegenerative proteinopathies is the formation of misfolded protein aggregates that cause cellular toxicity and contribute to cellular proteostatic collapse. Therapeutic options are currently being explored that target different steps in the production and processing of proteins implicated in neurodegenerative disease, including synthesis, chaperone-assisted folding and trafficking, and degradation via the proteasome and autophagy pathways. Other therapies, like mTOR inhibitors and activators of the heat shock response, can rebalance the entire proteostatic network...
2017: Translational Neurodegeneration
https://www.readbyqxmd.com/read/28275944/fine-tuning-of-actin-dynamics-by-the-hspb8-bag3-chaperone-complex-facilitates-cytokinesis-and-contributes-to-its-impact-on-cell-division
#3
Alice Anaïs Varlet, Margit Fuchs, Carole Luthold, Herman Lambert, Jacques Landry, Josée N Lavoie
The small heat shock protein HSPB8 and its co-chaperone BAG3 are proposed to regulate cytoskeletal proteostasis in response to mechanical signaling in muscle cells. Here, we show that in dividing cells, the HSPB8-BAG3 complex is instrumental to the accurate disassembly of the actin-based contractile ring during cytokinesis, a process required to allow abscission of daughter cells. Silencing of HSPB8 markedly decreased the mitotic levels of BAG3 in HeLa cells, supporting its crucial role in BAG3 mitotic functions...
March 8, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28206988/inhibition-of-autophagy-blocks-cathepsins-tbid-mitochondrial-apoptotic-signaling-pathway-via-stabilization-of-lysosomal-membrane-in-ischemic-astrocytes
#4
Xian-Yong Zhou, Yu Luo, Yong-Ming Zhu, Zhi-He Liu, Thomas A Kent, Jia-Guo Rong, Wei Li, Shi-Gang Qiao, Min Li, Yong Ni, Kazumi Ishidoh, Hui-Ling Zhang
Our previous study and others have demonstrated that autophagy is activated in ischemic astrocytes and contributes to astrocytic cell death. However, the mechanisms of ischemia-induced autophagy remain largely unknown. In this study, we established a rat's model of permanent middle cerebral artery occlusion (pMCAO) and an in vitro oxygen and glucose deprivation (OGD) model. Autophagy was inhibited by either pharmacological treatment with 3-methyladenine (3-MA) and wortmannin (Wort) or genetic treatment with knockdown of Atg5 in primary cultured astrocytes and knockout of Atg5 in mouse embryonic fibroblast (MEF) cells, respectively...
February 16, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28188022/interplay-between-hsp90-and-nrf2-pathways-in-diabetes-associated-atherosclerosis
#5
Iolanda Lazaro, Ainhoa Oguiza, Carlota Recio, Laura Lopez-Sanz, Susana Bernal, Jesus Egido, Carmen Gomez-Guerrero
INTRODUCTION: Oxidative stress and inflammation are determinant processes in the development of diabetic vascular complications. Heat shock protein 90 (HSP90) overexpression in atherosclerotic plaques plays a role in sustaining inflammatory mechanisms, and its specific inhibition prevents atherosclerosis. The present work investigates, in a mouse model of diabetes-driven atherosclerosis, whether atheroprotection by pharmacological HSP90 inhibition is accomplished by bolstering antioxidant defense mechanisms headed by nuclear factor erythroid-derived 2-like 2 (Nrf2)...
February 7, 2017: Clínica e Investigación en Arteriosclerosis
https://www.readbyqxmd.com/read/28157209/autophagy-induced-by-damps-facilitates-the-inflammation-response-in-lungs-undergoing-ischemia-reperfusion-injury-through-promoting-traf6-ubiquitination
#6
Xingguang Liu, Hao Cao, Jian Li, Bo Wang, Peng Zhang, Xu Dong Zhang, Zhongmin Liu, Hongbin Yuan, Zhenzhen Zhan
Lung ischemia-reperfusion (I/R) injury remains one of the most common complications after various cardiopulmonary surgeries. The inflammation response triggered by the released damage-associated molecular patterns (DAMPs) aggravates lung tissue damage. However, little is known about the role of autophagy in the pathogenesis of lung I/R injury. Here, we report that a variety of inflammation-related and autophagy-associated genes are rapidly upregulated, which facilitate the inflammation response in a minipig lung I/R injury model...
February 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28131906/a-novel-hdac6-inhibitor-tubastatin-a-controls-hdac6-p97-vcp-mediated-ubiquitination-autophagy-turnover-and-reverses-temozolomide-induced-er-stress-tolerance-in-gbm-cells
#7
Zong-Yang Li, Ce Zhang, Yuan Zhang, Lei Chen, Bao-Dong Chen, Qing-Zhong Li, Xie-Jun Zhang, Wei-Ping Li
Temozolomide (TMZ) is the cornerstone of therapy for glioblastoma multiforme (GBM). However, its efficacy is limited due to the development of multidrug resistance (MDR). In this study, we first identified the occurrence of ER stress-tolerance (ERST) in glioma cells and confirmed that ERST was positively correlated with TMZ resistance. We further showed that the seesaw-effect of HDAC6-p97/VCP (increased HDAC6 and decreased p97/VCP) in glioma cells was crucial to ERST-associated TMZ resistance. Moreover, the combination treatment of Tubastatin A (TUB, a selective inhibitor of HDAC6) and TMZ synergistically overcame ERST, reduced cell viability and induced apoptosis in TMZ-resistant glioma cells...
January 26, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28120291/role-of-shsps-in-organizing-cytosolic-protein-aggregation-and-disaggregation
#8
REVIEW
Axel Mogk, Bernd Bukau
Small heat shock proteins (sHsps) exhibit an ATP-independent chaperone activity to prevent the aggregation of misfolded proteins in vitro. The seemingly conflicting presence of sHsps in insoluble protein aggregates in cells obstructs a precise definition of sHsp function in proteostasis networks. Recent findings specify sHsp activities in protein quality control systems. The sHsps of yeast, Hsp42 and Hsp26, interact with early unfolding intermediates of substrates, keeping them in a ready-to-refold conformation close to the native state...
January 24, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28116619/hdac6-regulates-sensitivity-to-cell-death-in-response-to-stress-and-post-stress-recovery
#9
Hyun-Wook Ryu, Hye-Rim Won, Dong Hoon Lee, So Hee Kwon
Histone deacetylase 6 (HDAC6) plays an important role in stress responses such as misfolded protein-induced aggresomes, autophagy, and stress granules. However, precisely how HDAC6 manages response during and after cellular stress remains largely unknown. This study aimed to investigate the effect of HDAC6 on various stress and post-stress recovery responses. We showed that HIF-1α protein levels were reduced in HDAC6 knockout (KO) MEFs compared to wild-type (WT) MEFs in hypoxia. Furthermore, under hypoxia, HIF-1α levels were also reduced following rescue with either a catalytically inactive or a ubiqiutin-binding mutant HDAC6...
January 23, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28110670/galnt6-stabilizes-grp78-protein-by-o-glycosylation-and-enhances-its-activity-to-suppress-apoptosis-under-stress-condition
#10
Jiaying Lin, Suyoun Chung, Koji Ueda, Koichi Matsuda, Yusuke Nakamura, Jae-Hyun Park
We previously reported that overexpression of an O-type glycosyltransferase, GALNT6 (polypeptide N-acetylgalactosaminyltransferase 6) played critical roles in mammary carcinogenesis. To further investigate the biological function of GALNT6, we screened a substrate protein(s) of GALNT6 using a VVA (Vicia villosa agglutinin) lectin (specific to GalNAc-Ser/Thr) pull-down method followed by mass spectrometry analysis. Here we report GRP78 (glucose-regulated protein 78, also known as HSPA5, heat shock 70 kDa protein 5), which is highly expressed in cancer cells and indicated to play important roles in various cellular processes including ER (endoplasmic reticulum) stress and autophagy, as a novel substrate of GALNT6...
January 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/28108519/bone-marrow-adipocytes-facilitate-fatty-acid-oxidation-activating-ampk-and-a-transcriptional-network-supporting-survival-of-acute-monocytic-leukemia-cells
#11
Yoko Tabe, Shinichi Yamamoto, Kaori Saitoh, Kazumasa Sekihara, Norikazu Monma, Kazuho Ikeo, Kaoru Mogushi, Masato Shikami, Vivian Ruvolo, Jo Ishizawa, Numsen Hail, Saiko Kazuno, Mamoru Igarashi, Hiromichi Matsushita, Yasunari Yamanaka, Hajime Arai, Isao Nagaoka, Takashi Miida, Yoshihide Hayashizaki, Marina Konopleva, Michael Andreeff
Leukemia cells in the bone marrow must meet the biochemical demands of increased cell proliferation and also survive by continually adapting to fluctuations in nutrient and oxygen availability. Thus, targeting metabolic abnormalities in leukemia cells located in the bone marrow is a novel therapeutic approach. In this study, we investigated the metabolic role of bone marrow adipocytes in supporting the growth of leukemic blasts. Prevention of nutrient starvation-induced apoptosis of leukemic cells by bone marrow adipocytes, as well as the metabolic and molecular mechanisms involved in this process, was investigated using various analytic techniques...
March 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28073914/serine-threonine-kinase-unc-51-like-kinase-1-ulk1-phosphorylates-the-co-chaperone-cell-division-cycle-protein-37-cdc37-and-thereby-disrupts-the-stability-of-cdc37-client-proteins
#12
Ran Li, Fengjie Yuan, Wan Fu, Luyao Zhang, Nan Zhang, Yanan Wang, Ke Ma, Xue Li, Lina Wang, Wei-Guo Zhu, Ying Zhao
The serine/threonine kinase Unc-51-like kinase-1 (Ulk1) is thought to be essential for induction of autophagy, an intracellular bulk degradation process that is activated by various stresses. Although several proteins have been suggested as Ulk1 substrates during autophagic process, it still remains largely unknown about Ulk1's physiological substrates. Here, by performing in vitro and in vivo phosphorylation assay, we report that the co-chaperone cell division cycle protein 37 (Cdc37) is a Ulk1 substrate. Ulk1-mediated phosphorylation of Ser-339 in Cdc37 compromised the recruitment of client kinases to a complex comprising Cdc37 and heat shock protein 90 (Hsp90) but only modestly affected Cdc37 binding to Hsp90...
February 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28060751/the-small-heat-shock-protein-b8-hspb8-modulates-proliferation-and-migration-of-breast-cancer-cells
#13
Margherita Piccolella, Valeria Crippa, Riccardo Cristofani, Paola Rusmini, Mariarita Galbiati, Maria Elena Cicardi, Marco Meroni, Nicola Ferri, Federica F Morelli, Serena Carra, Elio Messi, Angelo Poletti
Breast cancer (BC) is one of the major causes of cancer death in women and is closely related to hormonal dysregulation. Estrogen receptor (ER)-positive BCs are generally treated with anti hormone therapy using antiestrogens or aromatase inhibitors. However, BC cells may become resistant to endocrine therapy, a process facilitated by autophagy, which may either promote or suppress tumor expansion. The autophagy facilitator HSPB8 has been found overexpressed in some BC. Here we found that HSPB8 is highly expressed and differentially modulated by natural or synthetic selective ER modulators (SERMs), in the triple-positive hormone-sensitive BC (MCF-7) cells, but not in triple-negative MDA-MB-231 BC cells...
February 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/28011268/nip-snap-1-and-2-mitochondrial-proteins-are-maintained-by-heat-shock-protein-60
#14
Soh Yamamoto, Tomoya Okamoto, Noriko Ogasawara, Shin Hashimoto, Tsukasa Shiraishi, Toyotaka Sato, Keisuke Yamamoto, Hiroyuki Tsutsumi, Kenichi Takano, Testuo Himi, Hideaki Itoh, Shin-Ichi Yokota
NIP-SNAP-1 and -2 are ubiquitous proteins thought to be associated with maintenance of mitochondrial function, neuronal transmission, and autophagy. However, their physiological functions remain largely unknown. To elucidate their functional importance, we screened for proteins that interact with NIP-SNAP-1 and -2, resulting in identification of HSP60 and P62/SQSTM1 as binding proteins. NIP-SNAP-1 and -2 localized in the mitochondrial inner membrane space, whereas HSP60 localized in the matrix. Native gel electrophoresis and filter trap assays revealed that human HSP60 prevented aggregation of newly synthesized NIP-SNAP-2 in an in vitro translation system...
December 21, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27959772/cellular-defense-or-viral-assist-the-dilemma-of-hdac6
#15
Kai Zheng, Yingchun Jiang, Zhendan He, Kaio Kitazato, Yifei Wang
AbstractHistone deacetylase 6 (HDAC6) is an unique cytoplasmic deacetylase that regulates various important biological processes via preventing protein aggregation and deacetylating different non-histone substrates including tubulin, heat shock protein 90 (Hsp90), cortactin, retinoic acid inducible gene I (RIG-1) and β-catenin. Growing evidences have indicated a dual role for HDAC6 in viral infection and pathogenesis: HDAC6 may represent a host defense mechanism against viral infection through modulating microtubule, triggering antiviral immune response and stimulating protective autophagy, or it may be hijacked by the virus to enhance proinflammatory response...
December 12, 2016: Journal of General Virology
https://www.readbyqxmd.com/read/27939888/chaperone-mediated-autophagy-promotes-lung-cancer-cell-survival-through-selective-stabilization-of-the-pro-survival-protein-mcl1
#16
Junya Suzuki, Wataru Nakajima, Hidenori Suzuki, Yumi Asano, Nobuyuki Tanaka
Autophagy is a dynamic recycling system using lysosomal proteolysis that produces new proteins and energy for cellular renovation and homeostasis. Although macroautophagy is known to serve as a survival pathway in many cancer cells, the role of chaperone-mediated autophagy (CMA), a selective protein degradation system, in cancer is not fully understood. Here, we demonstrated that lysosomal proteolysis, but not macroautophagy, attenuated apoptosis induced by the tyrosine kinase inhibitor, crizotinib, in the non-small-cell lung cancer (NSCLC) cell line, EBC1...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27936516/neuroprotection-of-hypoxic-postconditioning-against-global-cerebral-ischemia-through-influencing-posttranslational-regulations-of-heat-shock-protein-27-in-adult-rats
#17
Lixuan Zhan, Liu Liu, Kongping Li, Baoxing Wu, Dandan Liu, Donghai Liang, Haixia Wen, Yanmei Wang, Weiwen Sun, Weiping Liao, En Xu
We previously reported that hypoxic postconditioning (HPC) ameliorated hippocampal neuronal death induced by transient global cerebral ischemia (tGCI) in adult rats. However, the mechanism of HPC-induced neuroprotection is still elusive. Notably, heat shock protein 27 (Hsp27) has recently emerged as a potent neuroprotectant in cerebral ischemia. Although its robust protective effect on stroke has been recognized, the mechanism of Hsp27-mediated neuroprotection is largely unknown. Here, we investigated the potential molecular mechanism by which HPC modulates the posttranslational regulations of Hsp27 after tGCI...
December 9, 2016: Brain Pathology
https://www.readbyqxmd.com/read/27928720/cardioprotection-of-exercise-preconditioning-involving-heat-shock-protein-70-and-concurrent-autophagy-a-potential-chaperone-assisted-selective-macroautophagy-effect
#18
Yang Yuan, Shan-Shan Pan, Yu-Jun Shen
It has been confirmed that exercise preconditioning (EP) has a protective effect on acute cardiovascular stress. However, how Hsp70 participates in EP-induced cardioprotection is unknown. EP may involve Hsp70 to repair unfolded proteins or may also stabilize the function of the endoplasmic reticulum via Hsp70-related autophagy to work on a protective formation. Our EP protocol involves four periods of 10 min running with 10 min recovery intervals. We added a period of exhaustive running to test this protective effect, using histology and molecular biotechnology methods to detect related markers...
December 7, 2016: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/27896217/adapt-recycle-and-move-on-proteostasis-and-trafficking-mechanisms-in-melanoma
#19
REVIEW
Seyma Demirsoy, Shaun Martin, Hannelore Maes, Patrizia Agostinis
Melanoma has emerged as a paradigm of a highly aggressive and plastic cancer, capable to co-opt the tumor stroma in order to adapt to the hostile microenvironment, suppress immunosurveillance mechanisms, and disseminate. In particular, oncogene- and aneuploidy-driven dysregulations of proteostasis in melanoma cells impose a rewiring of central proteostatic processes, such as the heat shock and unfolded protein responses, autophagy, and the endo-lysosomal system, to avoid proteotoxicity. Research over the past decade has indicated that alterations in key nodes of these proteostasis pathways act in conjunction with crucial oncogenic drivers to increase intrinsic adaptations of melanoma cells against proteotoxic stress, modulate the high metabolic demand of these cancer cells and the interface with other stromal cells, through the heightened release of soluble factors or exosomes...
2016: Frontiers in Oncology
https://www.readbyqxmd.com/read/27874054/combinational-immunotherapy-with-allo-dribble-vaccines-and-anti-ox40-co-stimulation-leads-to-generation-of-cross-reactive-effector-t-cells-and-tumor-regression
#20
Guangjie Yu, Yuhuan Li, Zhihua Cui, Nicholas P Morris, Andrew D Weinberg, Bernard A Fox, Walter J Urba, Lixin Wang, Hong-Ming Hu
It is well-known that vaccines comprising of irradiated whole tumor cells or tumor-derived heat shock proteins can generate tumor-specific immune responses. In contrast, we showed recently that vaccines composed of autophagosomes (DRibbles) derived from syngeneic sarcomas could induce cross-reactive T-cell responses and cross-protection against the tumor. This unusual property of DRibbles was related to the selective recruitment of defective ribosomal products (DRiPs) and other short-lived proteins (SLiPs) into autophagosomes via sequestosome (SQSTM1, p62) mediated association of ubiquitinated SLiPs to the autophagy gene product LC3...
November 22, 2016: Scientific Reports
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