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  • Cell Research
    Department of Medical Microbiology Immunology and Cell Biology Southern Illinois University School of Medicine Springfield IL 62794 9621 USA 2 Cancer Biology Research Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China 3 Department of Endocrinology PLA General Hospital Beijing 100853 China 4 Department of Pulmonary Medicine Zhongshan Hospital Fudan University Shanghai 200032 China 5 Cancer Institute University of Mississippi Medical Center Cancer Institute 2500 N State St Guyton 2 Suite G651 Jackson MS 39216 4505 USA Correspondence Yin Yuan Tel 1 601 815 6849 E mail ymo umc edu It is well known that upon stress the level of the tumor suppressor p53 is remarkably elevated However despite extensive studies the underlying mechanism involving important inter players for stress induced p53 regulation is still not fully understood We present evidence that the human lincRNA RoR RoR is a strong negative regulator of p53 Unlike MDM2 that causes p53 degradation through the ubiquitin proteasome pathway RoR suppresses p53 translation through direct interaction with the heterogeneous nuclear ribonucleoprotein I hnRNP I Importantly a 28 base RoR sequence carrying hnRNP I binding motifs is essential and sufficient for p53 repression We further show that RoR

    Original URL path: http://www.cell-research.com/arts.asp?id=1626 (2016-02-14)
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  • Cell Research
    amyloid β pathology Xiaosong Liu 1 Xiaohui Zhao 1 Xianglu Zeng 1 Koen Bossers 3 Dick F Swaab 3 Jian Zhao 1 2 and Gang Pei 1 2 4 Correspondence Gang Pei Jian Zhao E mail gpei sibs ac cn jzhao sibs ac cn Alzheimer s disease AD is a progressive and complex neurodegenerative disease in which the γ secretase mediated amyloid β Aβ pathology plays an important role We found that a multifunctional protein β arrestin1 facilitated the formation of NCT APH 1 anterior pharynx defective phenotype 1 precomplex and mature γ secretase complex through its functional interaction with APH 1 Deficiency of β arrestin1 or inhibition of binding of β arrestin1 with APH 1 by small peptides reduced Aβ production without affecting Notch processing Genetic ablation of β arrestin1 diminished Aβ pathology and behavioral deficits in transgenic AD mice Moreover in brains of sporadic AD patients and transgenic AD mice the expression of β arrestin1 was upregulated and correlated well with neuropathological severity and senile Aβ plaques Thus our study identifies a regulatory mechanism underlying both γ secretase assembly and AD pathogenesis and indicates that specific reduction of Aβ pathology can be achieved by regulation of the γ

    Original URL path: http://www.cell-research.com/arts.asp?id=1627 (2016-02-14)
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  • Cell Research
    1 and Peter ten Dijke 1 1 Department of Molecular Cell Biology Cancer Genomics Centre Netherlands and Centre for Biomedical Genetics Leiden University Medical Center Postbus 9600 2300 RC Leiden The Netherlands Correspondence Peter ten Dijke Tel 31 71 526 9269 E mail p ten dijke lumc nl Tumor necrosis factor TNF receptor associated factor 6 TRAF6 is a key regulator of the activation of transcription factor NF κB by the interleukin 1 receptor IL 1R Toll like receptor TLR superfamily Recruitment of TRAF6 to the receptor associated IRAK1 IRAK4 MyD88 adaptor protein complex induces lysine 63 K63 autopolyubiquitination of TRAF6 which leads to further recruitment of downstream regulators such as TAB2 3 and TAK1 and subsequently triggers NF κB activation Here we identified the putative E2 ubiquitin conjugating UBC enzyme UBE2O as a novel negative regulator of TRAF6 dependent NF κB signaling We found that UBE2O binds to TRAF6 to inhibit its K63 polyubiquitination and to prevent the activation of NF κB by IL 1β and lipopolysaccharides LPS We further show that the inhibitory effect of UBE2O is independent of its carboxy terminal UBC domain In contrast we found that UBE2O acts to disrupt the IL 1β induced association

    Original URL path: http://www.cell-research.com/arts.asp?id=1628 (2016-02-14)
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  • Cell Research
    Correspondence Xue Jun Li Tel 1 860 679 3026 E mail xjli uchc edu Establishing human cell models of spinal muscular atrophy SMA to mimic motor neuron specific phenotypes holds the key to understanding the pathogenesis of this devastating disease Here we developed a closely representative cell model of SMA by knocking down the disease determining gene survival motor neuron SMN in human embryonic stem cells hESCs Our study with this cell model demonstrated that knocking down of SMN does not interfere with neural induction or the initial specification of spinal motor neurons Notably the axonal outgrowth of spinal motor neurons was significantly impaired and these disease mimicking neurons subsequently degenerated Furthermore these disease phenotypes were caused by SMN full length SMN FL but not SMN Δ7 lacking exon 7 knockdown and were specific to spinal motor neurons Restoring the expression of SMN FL completely ameliorated all of the disease phenotypes including specific axonal defects and motor neuron loss Finally knockdown of SMN FL led to excessive mitochondrial oxidative stress in human motor neuron progenitors The involvement of oxidative stress in the degeneration of spinal motor neurons in the SMA cell model was further confirmed by the administration of N

    Original URL path: http://www.cell-research.com/arts.asp?id=1629 (2016-02-14)
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  • Cell Research
    York NY 10065 USA 2 School of Life Science and Biotechnology Shanghai Jiao Tong University Shanghai 200240 China 3 Department of Biology Lafayette College Easton PA 18042 USA 4 Lester and Sue Smith Breast Center Department of Molecular and Cell Biology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA 5 Department of Pediatrics Weill Cornell Medical College 1300 York Avenue New York NY 10065 USA 6 Graduate Program in Immunology and Microbial Pathogenesis Weill Graduate School of Medical Sciences Cornell University 1300 York Avenue New York NY 10065 USA Correspondence Xiaojing Ma E mail xim2002 sjtu edu cn xim2002 med cornell edu CCL5 is a member of the CC chemokine family expressed in a wide array of immune and non immune cells in response to stress signals CCL5 expression correlates with advanced human breast cancer However its functional significance and mode of action have not been established Here we show that CCL5 deficient mice are resistant to highly aggressive triple negative mammary tumor growth Hematopoietic CCL5 is dominant in this phenotype The absence of hematopoietic CCL5 causes aberrant generation of CD11b Gr 1 myeloid derived suppressor cells MDSCs in the bone marrow in response to tumor growth by accumulating Ly6Chi and Ly6G MDSCs with impaired capacity to suppress cytotoxicity of CD8 T cells These properties of CCL5 are observed in both orthotopic and spontaneous mammary tumors Antibody mediated systemic blockade of CCL5 inhibits tumor progression and enhances the efficacy of therapeutic vaccination against non immunogenic tumors CCL5 also helps maintain the immunosuppressive capacity of human MDSCs Our study uncovers a novel chemokine independent activity of the hematopoietically derived CCL5 that promotes mammary tumor progression via generating MDSCs in the bone marrow in cooperation with tumor derived colony stimulating factors The study sheds considerable light on the interplay

    Original URL path: http://www.cell-research.com/arts.asp?id=1630 (2016-02-14)
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  • Cell Research
    Membrane Biotechnology Tsinghua University Beijing 100084 China 2 Center for Structural Biology School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China 3 Tsinghua Peking Center for Life Sciences Tsinghua University Beijing 100084 China 4 MOE Key Laboratory of Bioinformatics Tsinghua University Beijing 100084 China 5 Howard Hughes Medical Institute Department of Cardiology Children s Hospital Boston Department of Neurobiology Harvard Medical School Boston MA 02115 USA 6 Shanghai Institute of Applied Physics Chinese Academy of Sciences 239 Zhangheng Road Shanghai 201204 China Correspondence Haipeng Gong E mail hgong tsinghua edu cn NaChBac is a bacterial voltage gated sodium Nav channel that shows sequence similarity to voltage gated calcium channels To understand the ion permeation mechanism of Nav channels we combined molecular dynamics simulation structural biology and electrophysiological approaches to investigate the recently determined structure of NavRh a marine bacterial NaChBac ortholog Two Na binding sites are identified in the selectivity filter SF in our simulations The extracellular Na ion first approaches site 1 constituted by the side groups of Ser181 and Glu183 and then spontaneously arrives at the energetically more favorable site 2 formed by the carbonyl oxygens of Leu179 and Thr178 In contrast Ca2 ions

    Original URL path: http://www.cell-research.com/arts.asp?id=1631 (2016-02-14)
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  • Cell Research
    1 Ruhua Zhang 1 Sheng Ping Li 2 Yi Xin Zeng 1 Yuxin Yin 3 and Tiebang Kang 1 1 State Key Laboratory of Oncology in South China Department of Experimental Research Sun Yat Sen University Cancer Center Guangzhou 510060 Guangdong China 2 Department of Liver Cancer Sun Yat Sen University Cancer Center Guangzhou 510060 Guangdong China 3 Institute of System Biomedicine School of Basic Medical Sciences Peking University Beijing 100191 China Correspondence Tiebang Kang Tel 86 20 87343183 E mail kangtb mail sysu edu cn The tumor suppressor p53 is essential for several cellular processes that are involved in the response to diverse genotoxic stress including cell cycle arrest DNA repair apoptosis and senescence Studies of the regulation of p53 have mostly focused on its stability and transactivation however new regulatory molecules for p53 have also been frequently identified Here we report that human ssDNA binding protein SSB1 hSSB1 a novel DNA damage associated protein can interact with p53 and protect p53 from ubiquitin mediated degradation Furthermore hSSB1 also associates with the acetyltransferase p300 and is required for efficient transcriptional activation of the p53 target gene p21 by affecting the acetylation of p53 at lysine382 Functionally the hSSB1 knockdown

    Original URL path: http://www.cell-research.com/arts.asp?id=1632 (2016-02-14)
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  • Cell Research
    Hua Zhao 1 X Edward Zhou 2 Zhong Shan Wu 1 3 Wei Yi 1 Yong Xu 1 4 Suling Li 1 Ting Hai Xu 1 Yue Liu 1 Run Ze Chen 1 Amanda Kovach 2 Yangyong Kang 2 Li Hou 1 2 Yuanzheng He 2 Cen Xie 5 Wanling Song 5 Dafang Zhong 5 Yechun Xu 5 Yonghong Wang 6 Jiayang Li 6 Chenghai Zhang 1 Karsten Melcher 2 and H Eric Xu 1 2 1 VARI SIMM Center Center for Structure and Function of Drug Targets CAS Key Laboratory of Receptor Research Shanghai Institute of Materia Medica Chinese Academy of Sciences Shanghai 201203 China 2 Laboratory of Structural Sciences Center for Structural Biology and Drug Discovery Van Andel Research Institute MI 49503 USA 3 Wuhan National Laboratory for Optoelectronics Britton Chance Center for Biomedical Photonics Huazhong University of Science and Technology Wuhan Hubei 430074 China 4 Institute of Chemical Biology Guangzhou Institutes of Biomedicine and Health Chinese Academy of Sciences Guangzhou Guangdong 510530 China 5 Shanghai Institute of Materia Medica Chinese Academy of Sciences Shanghai 201203 China 6 State Key Laboratory of Plant Genomics and National Center for Plant Gene Research Beijing Institute of Genetics and Developmental Biology

    Original URL path: http://www.cell-research.com/arts.asp?id=1633 (2016-02-14)
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