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https://www.readbyqxmd.com/read/28516065/mir-142-5p-disrupts-neuronal-morphogenesis-underlying-porcine-hemagglutinating-encephalomyelitis-virus-infection-by-targeting-ulk1
#1
Zi Li, Yungang Lan, Kui Zhao, Xiaoling Lv, Ning Ding, Huijun Lu, Jing Zhang, Huiqing Yue, Junchao Shi, Deguang Song, Feng Gao, Wenqi He
Porcine hemagglutinating encephalomyelitis virus (PHEV) invades the central nervous system (CNS) and causes neurodegenerative disease in suckling piglets, but the understanding of its neuropathogenicity for neurological dysfunction remains limited. Here, we report that miR-142-5p is localized to neurons and negatively regulates neuronal morphogenesis in porcine hemagglutinating encephalomyelitis (PHE). This phenotype was mediated by miR-142-5p inhibition of an mRNA encoding unc-51-like-kinase1 (Ulk1), which controls axon outgrowth and dendrite formation...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28510306/a-polymorphism-in-mir-1262-regulatory-region-confers-the-risk-of-lung-cancer-in-chinese-population
#2
Kaipeng Xie, Mengxi Chen, Meng Zhu, Cheng Wang, Na Qin, Cheng Liang, Ci Song, Juncheng Dai, Guangfu Jin, Hongbing Shen, Dongxing Lin, Hongxia Ma, Zhibin Hu
It has been proposed that the majority of disease-associated loci identified by genome-wide association studies (GWAS) are enriched in non-coding regions, such as the promoter, enhancer or non-coding RNA genes. Thus, we performed a two-stage case-control study to systematically evaluate the association of genetic variants in miRNA regulatory regions (promoter and enhancer) with lung cancer risk in 7,763 subjects (discovery stage: 2,331 cases and 3,077 controls; validation stage: 1,065 cases and 1,290 controls)...
May 16, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28498429/sbi0206965-a-novel-inhibitor-of-ulk1-suppresses-non-small-cell-lung-cancer-cell-growth-by-modulating-both-autophagy-and-apoptosis-pathways
#3
Fang Tang, Pengchao Hu, Zetian Yang, Chao Xue, Jun Gong, Shaoxing Sun, Liu Shi, Shimin Zhang, Zhenzhen Li, Chunxu Yang, Junhong Zhang, Conghua Xie
Lung cancer is a major public health problem worldwide. Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer cases. Autophagy has recently sparked great interest, and it is thought to participate in a variety of diseases, including lung cancer. Uncoordinated (Unc) 51-like kinase 1 (Ulk1), a serine/threonine kinase, plays a central role in the autophagy pathway. However, the role of Ulk1 in NSCLC remains unclear. We report that NSCLC cell lines exhibited high expression of Ulk1 and that Ulk1 was negatively correlated with prognosis in lung cancer patients...
May 10, 2017: Oncology Reports
https://www.readbyqxmd.com/read/28492544/halofuginone-dually-regulates-autophagic-flux-through-nutrient-sensing-pathways-in-colorectal-cancer
#4
Guo-Qing Chen, Rui-Hong Gong, Da-Jian Yang, Ge Zhang, Ai-Ping Lu, Siu-Cheong Yan, Shu-Hai Lin, Zhao-Xiang Bian
Autophagy has a key role in metabolism and impacts on tumorigenesis. Our previous study found that halofuginone (HF) exerts anticancer activity in colorectal cancer (CRC) by downregulating Akt/mTORC1 (mechanistic target of rapamycin complex 1) signaling pathway. But whether and how HF regulates autophagy and metabolism to inhibit cancer growth remains an open question. Here, we unveil that HF activates ULK1 by downregulation of its phosphorylation site at Ser757 through Akt/mTORC1 signaling pathway, resulting in induction of autophagic flux under nutrient-rich condition...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28486929/ulk1-phosphorylates-sec23a-and-mediates-autophagy-induced-inhibition-of-er-to-golgi-traffic
#5
Wenjia Gan, Caiyun Zhang, Ka Yu Siu, Ayano Satoh, Julian A Tanner, Sidney Yu
BACKGROUND: Autophagy is an inducible autodigestive process that allows cells to recycle proteins and other materials for survival during stress and nutrient deprived conditions. The kinase ULK1 is required to activate this process. ULK1 phosphorylates a number of target proteins and regulates many cellular processes including the early secretory pathway. Recently, ULK1 has been demonstrated to phosphorylate Sec16 and affects the transport of serotonin transporter at the ER exit sites (ERES), but whether ULK1 may affect the transport of other cargo proteins and general secretion has not been fully addressed...
May 10, 2017: BMC Cell Biology
https://www.readbyqxmd.com/read/28484969/autophagy-activation-alleviates-amyloid-%C3%AE-induced-oxidative-stress-apoptosis-and-neurotoxicity-in-human-neuroblastoma-sh-sy5y-cells
#6
Abhishek Kumar Singh, Akalabya Bissoyi, Mahendra Pratap Kashyap, Pradeep Kumar Patra, Syed Ibrahim Rizvi
Autophagy is an evolutionary conserved catabolic process that ensures continuous removal of damaged cell organelles and long-lived protein aggregates to maintain cellular homeostasis. Although autophagy has been implicated in amyloid-β (Aβ) production and deposition, its role in pathogenesis of Alzheimer's disease remains elusive. Thus, the present study was undertaken to assess the cytoprotective and neuroprotective potential of autophagy on Aβ-induced oxidative stress, apoptosis and neurotoxicity in human neuroblastoma SH-SY5Y cells...
May 8, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28482233/activated-akt-mtor-autophagy-in-local-t-cells-of-oral-lichen-planus
#7
Na Zhang, Jing Zhang, Ya-Qin Tan, Ge-Fei Du, Rui Lu, Gang Zhou
Oral lichen planus (OLP) is a chronic inflammatory disease regulated by T cell-mediated immune response. Autophagy and its major inhibitory pathway Akt/mTOR participate in T cell metabolism and homeostasis, which has been implicated in autoimmune diseases. In this study, the potential involvement of autophagy and its regulatory Akt/mTOR pathway were investigated in local T cells of OLP. The expression of Akt/mTOR pathway and autophagy-related proteins in OLP local lesions, as well as in T cells, were measured by immunohistochemistry and double-labeling immunofluorescence, respectively...
May 5, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28430962/ulk1-prevents-cardiac-dysfunction-in-obesity-through-autophagy-meditated-regulation-of-lipid-metabolism
#8
Minae An, Dong-Ryeol Ryu, Jang Won Park, Ji Ha Choi, Eun-Mi Park, Kyung Eun Lee, Minna Woo, Minsuk Kim
Aims: Autophagy is essential to maintain tissue homeostasis, particularly in long-lived cells such as cardiomyocytes. Whereas many studies support the importance of autophagy in the mechanisms underlying obesity-related cardiac dysfunction, the role of autophagy in cardiac lipid metabolism remains unclear. In the heart, lipotoxicity is exacerbated by cardiac lipoprotein lipase (LPL), which mediates accumulation of fatty acids to the heart through intravascular triglyceride (TG) hydrolysis...
April 17, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28421673/endothelial-erbb4-deficit-induces-alterations-in-exploratory-behavior-and-brain-energy-metabolism-in-mice
#9
Gang Wu, Xiu-Xiu Liu, Nan-Nan Lu, Qi-Bing Liu, Yun Tian, Wei-Feng Ye, Guo-Jun Jiang, Rong-Rong Tao, Feng Han, Ying-Mei Lu
AIMS: The receptor tyrosine kinase ErbB4 is present throughout the primate brain and has a distinct functional profile. In this study, we investigate the potential role of endothelial ErbB4 receptor signaling in the brain. RESULTS: Here, we show that the endothelial cell-specific deletion of ErbB4 induces decreased exploratory behavior in adult mice. However, the water maze task for spatial memory and the memory reconsolidation test reveal no changes; additionally, we observe no impairment in CaMKII phosphorylation in Cdh5Cre;ErbB4(f/f) mice, which indicates that the endothelial ErbB4 deficit leads to decreased exploratory activity rather than direct memory deficits...
April 18, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28421304/increased-autophagic-degradation-contributes-to-the-neuroprotection-of-hydrogen-sulfide-against-cerebral-ischemia-reperfusion-injury
#10
Yuanjun Zhu, Mengyang Shui, Xiaoyan Liu, Wenhui Hu, Yinye Wang
Hydrogen sulfide (H2S), an endogenous gaseous signal molecule, exhibits protective effect against ischemic injury. However, its underlying mechanism is not fully understood. We have recently reported that exogenous H2S decreases the accumulation of autophagic vacuoles in mouse brain with ischemia/reperfusion (I/R) injury. To further investigate whether this H2S-induced reduction of autophagic vacuoles is caused by the decreased autophagosome synthesis and/or the increased autophagic degradation inautophagic flux, we performed in vitro and in vivo studies using SH-SY5Y cells for the oxygen and glucose deprivation/reoxygenation (OGD/R) and mice for the cerebral I/R, respectively...
April 18, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28420820/high-insulin-impaired-ovarian-function-in-early-pregnant-mice-and-the-role-of-autophagy-in-this-process
#11
Yan Su, Juan Wu, Junlin He, Xueqing Liu, Xuemei Chen, Yubin Ding, Chen Zhang, Wenqi Chen, Yingxiong Wang, Rufei Gao
Metabolic disorders, such as PCOS (polycystic ovarian syndrome) and T2DM (type 2 diabetes mellitus), are associated with menstrual dysfunction, anovulation, infertility, and early pregnancy loss. Ovarian dysfunction is not only related to low pregnancy rates but also to the increased risk of miscarriage. Women with PCOS or T2DM, characterized by hyperinsulinemia, commonly experience ovarian dysfunction. In this study, we first explored whether high insulin levels directly affected ovarian functioning during embryo implantation...
April 18, 2017: Endocrine Journal
https://www.readbyqxmd.com/read/28420621/association-between-polymorphisms-of-autophagy-pathway-and-responses-in-non-small-cell-lung-cancer-patients-treated-with-platinum-based-chemotherapy
#12
Wang Shiming, Song Xiao, Zhao Xueying, Chen Hongyan, Wang Jiucun, Wu Junjie, Gao Zhiqiang, Qian Ji, Bai Chunxue, Li Qiang, Han Baohui, Lu Daru
Platinum-based chemotherapy is an important treatment for non-small cell lung cancer. However, the effectiveness of the treatment varies among the patients. We investigated the association between DNA polymorphisms of the autophagy pathway and responses of such treatment among 1004 Chinese patients. Ninety-nine SNPs located on 13 genes of the autophagy pathway were genotyped and assessed for their association with clinical benefit, progression-free survival (PFS) and overall survival (OS). The results showed that rs7953348 (G>A) (P=0...
March 20, 2017: Yi Chuan, Hereditas
https://www.readbyqxmd.com/read/28410240/ulk1-over-expression-in-human-gastric-cancer-is-correlated-with-patients-t-classification-and-cancer-relapse
#13
Min-Bin Chen, Xiao-Zhi Ji, Yuan-Yuan Liu, Ping Zeng, Xin-Yu Xu, Rong Ma, Zheng-Dong Guo, Jian-Wei Lu, Ji-Feng Feng
Ulk1 is a key autophagy protein. Here, we tested expression and potential function of Ulk1 in human gastric cancer. Ulk1 mRNA and protein were significantly elevated in multiple fresh human gastric cancer tissues. Its level was relatively low in surrounding normal epithelial tissues. Ulk1 over-expression was also observed in several gastric cancer cell lines (AGS, HGC-27, and SNU601). Remarkably, Ulk1 knockdown by targeted-shRNA inhibited AGS gastric cancer cell survival and proliferation. On the other hand, exogenous Ulk1 over-expression could further promote AGS cell survival and proliferation...
May 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28401013/resistin-confers-resistance-to-doxorubicin-induced-apoptosis-in-human-breast-cancer-cells-through-autophagy-induction
#14
Zhenyu Liu, Aiping Shi, Dong Song, Bing Han, Zhiru Zhang, Le Ma, Dongxu Liu, Zhimin Fan
Clear evidence has linked obesity to a high risk of incidence as well as poor clinical outcome of breast cancer. It has been proven that changes in the levels of adipokines caused by obesity are associated with the initiation and progression of breast cancer. Resistin is a novel adipokine that is upregulated in breast cancer patients and promotes breast cancer cell growth, invasion, and migration. The aim of the study was to investigate whether resistin affected the efficacy of doxorubicin (Dox), one of the most effective anthracycline chemotherapeutic agents in the treatment of breast cancer...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/28401008/autophagy-inhibits-cell-death-induced-by-the-anti-cancer-drug-morusin
#15
Sang Woo Cho, Wooju Na, Minji Choi, Shin Jung Kang, Seok-Geun Lee, Cheol Yong Choi
Autophagy is a cellular process by which damaged organelles and dysfunctional proteins are degraded. Morusin is an anti-cancer drug isolated from the root bark of Morus alba. Morusin induces apoptosis in human prostate cancer cells by reducing STAT3 activity. In this study, we examined whether morusin induces autophagy and also examined the effects of autophagy on the morusin-induced apoptosis. Morusin induces LC3-II accumulation and ULK1 activation in HeLa cells. In addition, we found that induction of ULK1 Ser317 phosphorylation and reduction of ULK1 Ser757 phosphorylation occurred simultaneously during morusin-induced autophagy...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/28389629/inhibition-of-p70-s6-kinase-s6k1-activity-by-a77-1726-the-active-metabolite-of-leflunomide-induces-autophagy-through-tak1-mediated-ampk-and-jnk-activation
#16
Xiulong Xu, Jing Sun, Ruilong Song, Michelle E Doscas, Ashley J Williamson, Jingsong Zhou, Jun Sun, Xinan Jiao, Xiufan Liu, Yi Li
mTOR activation suppresses autophagy by phosphorylating ULK1 at S757 and suppressing its enzymatic activity. Here we report that feedback activation of mTOR in the PI-3 kinase pathway by two p70 S6 kinase (S6K1) inhibitors (PF-4708671 and A77 1726, the active metabolite of an immunosuppressive drug leflunomide) or by S6K1 knockdown did not suppress but rather induced autophagy. Suppression of S6K1 activity led to the phosphorylation and activation of AMPK, which then phosphorylated ULK1 at S555. While mTOR feedback activation led to increased phosphorylation of ULK1 at S757, this modification did not the disrupt ULK1-AMPK interaction nor dampen ULK1 S555 phosphorylation and the induction of autophagy...
May 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28389568/hepatitis-c-virus-triggers-golgi-fragmentation-and-autophagy-through-the-immunity-related-gtpase-m
#17
Marianne D Hansen, Ingvild B Johnsen, Kim A Stiberg, Tatyana Sherstova, Takaji Wakita, Gabriel Mary Richard, Richard K Kandasamy, Eliane F Meurs, Marit W Anthonsen
Positive-stranded RNA viruses, such as hepatitis C virus (HCV), assemble their viral replication complexes by remodeling host intracellular membranes to a membranous web. The precise composition of these replication complexes and the detailed mechanisms by which they are formed are incompletely understood. Here we show that the human immunity-related GTPase M (IRGM), known to contribute to autophagy, plays a previously unrecognized role in this process. We show that IRGM is localized at the Golgi apparatus and regulates the fragmentation of Golgi membranes in response to HCV infection, leading to colocalization of Golgi vesicles with replicating HCV...
April 25, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28381396/caspase-3-controls-aml1-eto-driven-leukemogenesis-via-autophagy-modulation-in-a-ulk1-dependent-manner
#18
Na Man, Yurong Tan, Xiao-Jian Sun, Fan Liu, Guoyan Cheng, Sarah Greenblatt, Camilo Martinez, Daniel L Karl, Koji Ando, Ming Sun, Dan Hou, Bingyi Chen, Mingjiang Xu, Feng-Chun Yang, Zhu Chen, Saijuan Chen, Stephen D Nimer, Lan Wang
AML1-ETO (AE), a fusion oncoprotein, generated by the t(8;21), can trigger acute myeloid leukemia (AML) in collaboration with mutations including c-Kit, ASXL1/2, FLT3, N-RAS, and K-RAS. Caspase-3, a key executor among its family, plays multiple roles in cellular processes, including hematopoietic development and leukemia progression. Caspase-3 was revealed to directly cleave AE in vitro, suggesting that AE may accumulate in a Caspase-3 compromised background and thereby accelerate leukemogenesis. Therefore, we developed a Caspase-3 knockout genetic mouse model of AML and found that loss of Caspase-3 actually delayed AML1-ETO9a (AE9a)-driven leukemogenesis, indicating that Caspase-3 may play distinct roles in the initiation and/or progression of AML...
April 5, 2017: Blood
https://www.readbyqxmd.com/read/28381171/identification-and-validation-of-a-novel-autophagy-gene-expression-signature-for-human-bladder-cancer-patients
#19
Sanaa Eissa, Marwa Matboli, Nahla Awad, Yousif Kotb
We sought to identify and validate a novel urinary autophagy transcript signature in patients with bladder cancer and evaluate its clinical utility. We performed an initial screening for seven autophagy transcript-based panel (autophagy-related protein 12 (ATG12); WD repeat domain, phosphoinositide interacting 2 (WIPI2); FYVE and coiled-coil domain-containing protein 1 (FYCO1); microtubule-associated protein light chain (MAPLC3); RB1-inducible coiled-coil 1 (RB1CC1); tachylectin-II-like beta-propeller domain 1 (TECPR1); and Unc-51-like kinase (ULK1)) that was identified based on bioinformatics analysis followed by SYBR Green-based polymerase chain reaction array validation in paired tissue and urine samples...
April 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28379541/resistance-to-apoptosis-and-autophagy-leads-to-enhanced-survival-in-sertoli-cells
#20
Ferial Aslani, Tim Sebastian, Miguel Keidel, Suada Fröhlich, Hans-Peter Elsässer, Hans-Christian Schuppe, Jörg Klug, Poornima Mahavadi, Monika Fijak, Martin Bergmann, Andreas Meinhardt, Sudhanshu Bhushan
STUDY QUESTION: What is the underlying mechanism of Sertoli cell (SC) resistance to cell death? SUMMARY ANSWER: High expression of pro-survival B cell lymphoma-2 (BCL2) proteins and inhibition of apoptosis and autophagy prolongs SC survival upon exposure to stress stimuli. WHAT IS KNOWN ALREADY: In human and in experimental models of orchitis, tolerogenic SC survive stress conditions, while germ cells undergo massive apoptosis. In general, non-dividing highly differentiated cells tend to resist stress conditions for a longer time by favoring activation of pro-survival mechanisms and inhibition of cell death pathways...
April 3, 2017: Molecular Human Reproduction
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