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junying yuan

Yi Ding, Chang Gong, De Huang, Rui Chen, Pinpin Sui, Kevin H Lin, Gehao Liang, Lifeng Yuan, Handan Xiang, Junying Chen, Tao Yin, Peter B Alexander, Qian-Fei Wang, Er-Wei Song, Qi-Jing Li, Kris C Wood, Xiao-Fan Wang
Intrinsic resistance to anti-HER2 therapy in breast cancer remains an obstacle in the clinic, limiting its efficacy. However, the biological basis for intrinsic resistance is poorly understood. Here we performed a CRISPR/Cas9-mediated loss-of-function genetic profiling and identified TALDO1, which encodes the rate-limiting transaldolase (TA) enzyme in the non-oxidative pentose phosphate pathway, as essential for cellular survival following pharmacological HER2 blockade. Suppression of TA increases cell susceptibility to HER2 inhibition in two intrinsically resistant breast cancer cell lines with HER2 amplification...
October 15, 2018: Nature Communications
Junying Yuan, Jun Wang, Jieqiong Ma, Dengna Zhu, Zhenhuan Zhang, Jianan Li
OBJECTIVE: To evaluate the prevalence of, and risk factors for, cerebral palsy in Henan province, China. METHODS: The prevalence of cerebral palsy in children aged 0-6 years between September 2011 and September 2012 was investigated using a stratified-clustered-random sampling method. An age-, sex- , and residence-matched control group of typically developing children was recruited. Univariate analysis and multinomial logistic regression analysis were used to identify risk factors associated with cerebral palsy...
October 9, 2018: Journal of Rehabilitation Medicine
Jinhua Zhang, Shasha Hou, Jianchun Gu, Tian Tian, Qi Yuan, Junying Jia, Zhihai Qin, Zhinan Chen
S100A4 plays important roles in tumor development and metastasis, but its role in regulating inflammation and colitis-associated tumorigenesis has not been well characterized. Here, we report that S100A4 expression was increased in azoxymethane (AOM) and dextran sulfate sodium (DSS) induced colorectal cancer (CRC) in mice. After AOM/DSS treatment, both S100A4-TK mice with the selective depletion of S100A4-expressing cells and S100A4-deficient (S100A4-/- ) mice developed fewer and smaller tumors than wild-type (WT) control littermates...
2018: Oncoimmunology
Haoyan Li, Yanjia Fang, Chunyi Niu, Hengyi Cao, Ting Mi, Hong Zhu, Junying Yuan, Jidong Zhu
Protooncogene c-MYC , a master transcription factor, is a major driver of human tumorigenesis. Development of pharmacological agents for inhibiting c-MYC as an anticancer therapy has been a longstanding but elusive goal in the cancer field. E3 ubiquitin ligase cIAP1 has been shown to mediate the activation of c-MYC by destabilizing MAD1, a key antagonist of c-MYC. Here we developed a high-throughput assay for cIAP1 ubiquitination and identified D19, a small-molecule inhibitor of E3 ligase activity of cIAP1...
October 2, 2018: Proceedings of the National Academy of Sciences of the United States of America
Daichao Xu, Taijie Jin, Hong Zhu, Hongbo Chen, Dimitry Ofengeim, Chengyu Zou, Lauren Mifflin, Lifeng Pan, Palak Amin, Wanjin Li, Bing Shan, Masanori Gomi Naito, Huyan Meng, Ying Li, Heling Pan, Liviu Aron, Xian Adiconis, Joshua Z Levin, Bruce A Yankner, Junying Yuan
Aging is a major risk factor for both genetic and sporadic neurodegenerative disorders. However, it is unclear how aging interacts with genetic predispositions to promote neurodegeneration. Here, we investigate how partial loss of function of TBK1, a major genetic cause for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) comorbidity, leads to age-dependent neurodegeneration. We show that TBK1 is an endogenous inhibitor of RIPK1 and the embryonic lethality of Tbk1-/- mice is dependent on RIPK1 kinase activity...
September 6, 2018: Cell
Junying Fu, Zhiyuan Wang, Wen Luo, Shiyou Xing, Pengmei Lv, Zhongming Wang, Zhenhong Yuan
Sanger's reaction, which was originally developed for amino acid detection, was utilized for enzyme immobilization. The newly synthesized polymer support, which was called polymer NO2 -4-fluorostyrene-divinylbenzene (pNFD), was embedded with a Sanger's reagent-like functional group for immobilizing enzymes covalently under mild reaction conditions. Using Burkholderia cepacia lipase (BCL) as the target enzyme, the immobilization efficiency and activity of pNFD-BCL reached as high as 1.2 mg·g-1 and 33.21 U·g-1 (a specific activity of 27 675 U·g-1 ), respectively, realizing 90% activity recovery...
September 19, 2018: ACS Applied Materials & Interfaces
Yuze Yuan, Nan Ran, Lingxin Xiong, Guoqiang Wang, Xuewa Guan, Ziyan Wang, Yingqiao Guo, Zhiqiang Pang, Keyong Fang, Junying Lu, Chao Zhang, Ruipeng Zheng, Jingtong Zheng, Jie Ma, Fang Wang
Obesity, one of the most severe public health problems of the 21st century, is a common metabolic syndrome due to excess body fat. The incidence and severity of obesity-related asthma have undergone a dramatic increase. Because obesity-related asthma is poorly controlled using conventional therapies, alternative and complementary therapies are urgently needed. Lipid metabolism may be abnormal in obesity-related asthma, and immune modulation therapies need to be investigated. Herein, we describe the immune regulators of lipid metabolism in obesity as well as the interplay of obesity and asthma...
2018: Journal of Immunology Research
Yu Wang, Bing Shan, Yaosi Liang, Huiting Wei, Junying Yuan
Parkin (Park2), a RING-between-RING-type E3 ubiquitin ligase, has been implicated in regulating NF-κB. Mutations in Parkin are associated with Parkinson's disease. Here we investigated the interaction of Parkin with Receptor-interacting protein kinase 1 (RIPK1) kinase, a key mediator of multiple signaling pathways activated by TNFR1 including NF-κB pathway. We report that Parkin interacts with RIPK1 and mediates K63 ubiquitination of RIPK1 on K376 in TNFR1-signaling pathway. The expression of Parkin promotes the recruitment of transforming growth factor β (TGF-β)-activated kinase 1 (TAK1), nuclear factor-κB (NF-κB) essential molecule (NEMO), Sharpin and A20 in complex I associated with TNFR1 upon TNFα stimulation...
June 28, 2018: Cell Death & Disease
Palak Amin, Marcus Florez, Ayaz Najafov, Heling Pan, Jiefei Geng, Dimitry Ofengeim, Slawomir A Dziedzic, Huibing Wang, Vica Jean Barrett, Yasushi Ito, Matthew J LaVoie, Junying Yuan
Stimulation of cells with TNFα can promote distinct cell death pathways, including RIPK1-independent apoptosis, necroptosis, and RIPK1-dependent apoptosis (RDA)-the latter of which we still know little about. Here we show that RDA involves the rapid formation of a distinct detergent-insoluble, highly ubiquitinated, and activated RIPK1 pool, termed "iuRIPK1." iuRIPK1 forms after RIPK1 activation in TNF-receptor-associated complex I, and before cytosolic complex II formation and caspase activation...
June 26, 2018: Proceedings of the National Academy of Sciences of the United States of America
Xuewa Guan, Yanjiao Lu, Guoqiang Wang, Peter Gibson, Fang Chen, Keyong Fang, Ziyan Wang, Zhiqiang Pang, Yingqiao Guo, Junying Lu, Yuze Yuan, Nan Ran, Fang Wang
Chronic obstructive pulmonary disease (COPD) is associated with irreversible persistent airflow limitation and enhanced inflammation. The episodes of acute exacerbation (AECOPD) largely depend on the colonized pathogens such as nontypeable Haemophilus influenzae (NTHi), one of the most commonly isolated bacteria. Regulatory T cells (Tregs) are critical in controlling inflammatory immune responses and maintaining tolerance; however, their role in AECOPD is poorly understood. In this study, we hypothesized a regulatory role of Tregs, as NTHi participated in the progress of COPD...
2018: Mediators of Inflammation
Kezhou Zhu, Wei Liang, Zaijun Ma, Daichao Xu, Shuangyi Cao, Xiaojuan Lu, Nan Liu, Bing Shan, Lihui Qian, Junying Yuan
Necroptosis, a form of regulated necrotic cell death, is mediated by receptor interacting protein 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL). However, the mechanism by which necroptosis promotes inflammation is still unclear. Here we report that the expression of cytokines is robustly upregulated in a cell-autonomous manner during necroptosis induced by tumor necrosis factor alpha (TNFα). We demonstrate that TNFα-induced necroptosis leads to two waves of cytokine production. The first wave, more transient and weaker than the second, is in response to TNFα alone; whereas the second wave depends upon the necroptotic signaling...
May 1, 2018: Cell Death & Disease
Yuan Luo, Xiaodong Cao, Junfeng Chen, Jianwei Gu, Jitong Zhao, Junying Sun
Osteoblast differentiation was found to be regulated by a variety of cell signaling and intracellular regulatory factors. In this study, we aimed at investigating the regulatory effect of microRNA-224 on osteoblast differentiation and its molecular mechanism. Expression of miR-224 in the osteoblasts, adipose-derived mesenchymal stem cells (MSC-A), bone marrow-derived mesenchymal stem cells (MSC-B) and mbilical cord-derived mesenchymal stem cells (MSC-U) were detected using RT-PCR. Expression of miR-224 was lower in osteoblast than in the three mesenchymal stem cells and it revealed a decreasing time-dependent trend from 0 day to 28 days during osteoblast differentiation...
October 2018: Journal of Cellular Physiology
Shouheng Tuo, Junying Zhang, Xiguo Yuan, Zongzhen He, Yajun Liu, Zhaowen Liu
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.
April 17, 2018: Scientific Reports
Bing Shan, Heling Pan, Ayaz Najafov, Junying Yuan
Necroptosis, a form of regulated necrotic cell death mediated by RIPK1 (receptor-interacting protein kinase 1) kinase activity, RIPK3, and MLKL (mixed-lineage kinase domain-like pseudokinase), can be activated under apoptosis-deficient conditions. Modulating the activation of RIPK1 by ubiquitination and phosphorylation is critical to control both necroptosis and apoptosis. Mutant mice with kinase-dead RIPK1 or RIPK3 and MLKL deficiency show no detrimental phenotype in regard to development and adult homeostasis...
March 1, 2018: Genes & Development
Xiguo Yuan, Junying Zhang, Liying Yang, Jun Bai, Peizhen Fan
Analyzing copy number variations (CNVs) from next-generation sequencing (NGS) data has become a common approach to detect disease susceptibility genes. The main challenge is how to utilize the NGS data with limited coverage depth to detect significant CNVs. Here, we introduce a new statistical method, the derivative of correlation coefficient (DCC), to detect significant CNVs that recurrently occur in multiple samples using read depth signals. We use a sliding window to calculate a correlation coefficient for each genome bin, and compute corresponding derivatives by fitting curves to the correlation coefficient...
March 2018: IEEE Transactions on Nanobioscience
Dan Liu, Daguo Mi, Tuanjie Zhang, Yanping Zhang, Junying Yan, Yaxian Wang, Xuefeng Tan, Ying Yuan, Yumin Yang, Xiaosong Gu, Wen Hu
The repair of peripheral nerve laceration injury to obtain optimal function recovery remains a big challenge in the clinic. Misdirection of regenerating axons to inappropriate target, as a result of forced mismatch of endoneurial sheaths in the case of end-to-end nerve anastomosis or nerve autografting, represents one major drawback that limits nerve function recovery. Here we tested whether tubulation repair of a nerve defect could be beneficial in terms of nerve regeneration accuracy and nerve function. We employed sequential retrograde neuronal tracing to assess the accuracy of motor axon regeneration into the tibial nerve after sciatic nerve laceration and entubulation in adult Sprague-Dawley rats...
February 21, 2018: Scientific Reports
Huyan Meng, Zhen Liu, Xingyan Li, Huibing Wang, Taijie Jin, Guowei Wu, Bing Shan, Dana E Christofferson, Chunting Qi, Qiang Yu, Ying Li, Junying Yuan
RIPK1 is a critical mediator of cell death and inflammation downstream of TNFR1 upon stimulation by TNFα, a potent proinflammatory cytokine involved in a multitude of human inflammatory and degenerative diseases. RIPK1 contains an N-terminal kinase domain, an intermediate domain, and a C-terminal death domain (DD). The kinase activity of RIPK1 promotes cell death and inflammation. Here, we investigated the involvement of RIPK1-DD in the regulation of RIPK1 kinase activity. We show that a charge-conserved mutation of a lysine located on the surface of DD (K599R in human RIPK1 or K584R in murine RIPK1) blocks RIPK1 activation in necroptosis and RIPK1-dependent apoptosis and the formation of complex II...
February 27, 2018: Proceedings of the National Academy of Sciences of the United States of America
Faxiang Li, Daichao Xu, Yingli Wang, Zixuan Zhou, Jianping Liu, Shichen Hu, Yukang Gong, Junying Yuan, Lifeng Pan
OPTN (optineurin), a ubiquitin-binding scaffold protein, functions as an important macroautophagy/autophagy receptor in selective autophagy processes. Mutations in OPTN have been linked with human neurodegenerative diseases including ALS and glaucoma. However, the mechanistic basis underlying the recognition of ubiquitin by OPTN and its regulation by TBK1-mediated phosphorylation are still elusive. Here, we demonstrate that the UBAN domain of OPTN preferentially recognizes linear ubiquitin chain and forms an asymmetric 2:1 stoichiometry complex with the linear diubiquitin...
2018: Autophagy
Amanda Tomie Ouchida, Yingbo Li, Jiefei Geng, Ayaz Najafov, Dimitry Ofengeim, Xiaoxiao Sun, Qiang Yu, Junying Yuan
Drug combinations have been increasingly applied in chemotherapy as a strategy to enhance the efficacy of anti-cancer treatment. The appropriate drug combinations may achieve synergistic effects beyond monotherapies alone. AC220 (Quizartinib), an FLT3 receptor tyrosine kinase inhibitor, developed for the treatment of AML, has been tested in phase II human clinical trials. However, AC220 as a monotherapy is not efficacious enough. In this study, we performed a small-molecule screening of 12 640 compounds in order to find a compound that increase the AC220 efficacy in chemotherapy...
January 26, 2018: Cell Death & Disease
Lorenzo Galluzzi, Ilio Vitale, Stuart A Aaronson, John M Abrams, Dieter Adam, Patrizia Agostinis, Emad S Alnemri, Lucia Altucci, Ivano Amelio, David W Andrews, Margherita Annicchiarico-Petruzzelli, Alexey V Antonov, Eli Arama, Eric H Baehrecke, Nickolai A Barlev, Nicolas G Bazan, Francesca Bernassola, Mathieu J M Bertrand, Katiuscia Bianchi, Mikhail V Blagosklonny, Klas Blomgren, Christoph Borner, Patricia Boya, Catherine Brenner, Michelangelo Campanella, Eleonora Candi, Didac Carmona-Gutierrez, Francesco Cecconi, Francis K-M Chan, Navdeep S Chandel, Emily H Cheng, Jerry E Chipuk, John A Cidlowski, Aaron Ciechanover, Gerald M Cohen, Marcus Conrad, Juan R Cubillos-Ruiz, Peter E Czabotar, Vincenzo D'Angiolella, Ted M Dawson, Valina L Dawson, Vincenzo De Laurenzi, Ruggero De Maria, Klaus-Michael Debatin, Ralph J DeBerardinis, Mohanish Deshmukh, Nicola Di Daniele, Francesco Di Virgilio, Vishva M Dixit, Scott J Dixon, Colin S Duckett, Brian D Dynlacht, Wafik S El-Deiry, John W Elrod, Gian Maria Fimia, Simone Fulda, Ana J García-Sáez, Abhishek D Garg, Carmen Garrido, Evripidis Gavathiotis, Pierre Golstein, Eyal Gottlieb, Douglas R Green, Lloyd A Greene, Hinrich Gronemeyer, Atan Gross, Gyorgy Hajnoczky, J Marie Hardwick, Isaac S Harris, Michael O Hengartner, Claudio Hetz, Hidenori Ichijo, Marja Jäättelä, Bertrand Joseph, Philipp J Jost, Philippe P Juin, William J Kaiser, Michael Karin, Thomas Kaufmann, Oliver Kepp, Adi Kimchi, Richard N Kitsis, Daniel J Klionsky, Richard A Knight, Sharad Kumar, Sam W Lee, John J Lemasters, Beth Levine, Andreas Linkermann, Stuart A Lipton, Richard A Lockshin, Carlos López-Otín, Scott W Lowe, Tom Luedde, Enrico Lugli, Marion MacFarlane, Frank Madeo, Michal Malewicz, Walter Malorni, Gwenola Manic, Jean-Christophe Marine, Seamus J Martin, Jean-Claude Martinou, Jan Paul Medema, Patrick Mehlen, Pascal Meier, Sonia Melino, Edward A Miao, Jeffery D Molkentin, Ute M Moll, Cristina Muñoz-Pinedo, Shigekazu Nagata, Gabriel Nuñez, Andrew Oberst, Moshe Oren, Michael Overholtzer, Michele Pagano, Theocharis Panaretakis, Manolis Pasparakis, Josef M Penninger, David M Pereira, Shazib Pervaiz, Marcus E Peter, Mauro Piacentini, Paolo Pinton, Jochen H M Prehn, Hamsa Puthalakath, Gabriel A Rabinovich, Markus Rehm, Rosario Rizzuto, Cecilia M P Rodrigues, David C Rubinsztein, Thomas Rudel, Kevin M Ryan, Emre Sayan, Luca Scorrano, Feng Shao, Yufang Shi, John Silke, Hans-Uwe Simon, Antonella Sistigu, Brent R Stockwell, Andreas Strasser, Gyorgy Szabadkai, Stephen W G Tait, Daolin Tang, Nektarios Tavernarakis, Andrew Thorburn, Yoshihide Tsujimoto, Boris Turk, Tom Vanden Berghe, Peter Vandenabeele, Matthew G Vander Heiden, Andreas Villunger, Herbert W Virgin, Karen H Vousden, Domagoj Vucic, Erwin F Wagner, Henning Walczak, David Wallach, Ying Wang, James A Wells, Will Wood, Junying Yuan, Zahra Zakeri, Boris Zhivotovsky, Laurence Zitvogel, Gerry Melino, Guido Kroemer
Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes...
March 2018: Cell Death and Differentiation
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