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  • Cell Research
    X Institutes Ministry of Education Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders Institute of Social Cognitive and Behavioral Sciences Shanghai Jiao Tong University Shanghai 200030 China 3 Shanghai Key Laboratory of Psychotic Disorders Shanghai Mental Health Center Shanghai Jiao Tong University School of Medicine Shanghai 200030 China 4 Department of Endocrinology Huashan Hospital Shanghai Medical College Fudan University Shanghai 200040 China 5 State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 6 Department of Neuropathology Huashan Hospital Shanghai Medical College Fudan University Shanghai 200040 China 7 Department of Radiology Huashan Hospital Shanghai Medical College Fudan University Shanghai 200040 China 8 Department of Epidemiology School of Public Health Fudan University Shanghai 200032 China 9 Department of Neurosurgery Shanghai 5th People s Hospital Shanghai 200240 China 10 Department of Neurosurgery Provincial hospital Shandong University Jinan Shandong 250021 China 11 Shanghai Institute of Immunology Department of Immunobiology and Microbiology Shanghai Jiao Tong University School of Medicine Shanghai 200025 China 12 Shandong Provincial Key Laboratory of Metabolic Disease the Affiliated Hospital of Qingdao University Qingdao Shandong 266003 China Correspondence Yong Yong Shi Tel Fax 86 21 62932151 E mail shiyongyong gmail com Yao Zhao Tel Fax 86 21 52888728 E mail zhaoyaohs vip sina com Chuan Xin Huang Tel Fax 86 21 52888683 E mail huangcx shsmu edu cn Cushing s disease also known as adrenocorticotropic hormone ACTH secreting pituitary adenomas PAs that cause excess cortisol production accounts for up to 85 of corticotrophin dependent Cushing s syndrome cases However the genetic alterations in this disease are unclear Here we performed whole exome sequencing of DNA derived from 12 ACTH secreting PAs and matched blood samples which revealed three types of somatic mutations in a candidate

    Original URL path: http://www.cell-research.com/arts.asp?id=2080 (2016-02-14)
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  • Cell Research
    Xu Zhang 1 4 1 Institute of Neuroscience and State Key Laboratory of Neuroscience CAS Center for Excellence in Brain Science Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 2 State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 3 Shanghai Clinical Center Chinese Academy of Sciences XuHui Central Hospital Shanghai China 4 School of Life Science and Technology ShanghaiTech University Shanghai 200031 China Correspondence Xu Zhang Tel 86 21 54921726 Fax 86 21 54921762 E mail xu zhang ion ac cn Na K ATPase NKA is required to generate the resting membrane potential in neurons Nociceptive afferent neurons express not only the α and β subunits of NKA but also the γ subunit FXYD2 However the neural function of FXYD2 is unknown The present study shows that FXYD2 in nociceptive neurons is necessary for maintaining the mechanical allodynia induced by peripheral inflammation FXYD2 interacted with α1NKA and negatively regulated the NKA activity depolarizing the membrane potential of nociceptive neurons Mechanical allodynia initiated in FXYD2 deficient mice was abolished 4 days after inflammation whereas it persisted for at least 3 weeks

    Original URL path: http://www.cell-research.com/arts.asp?id=2073 (2016-02-14)
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  • Cell Research
    1 Department of Orthopaedics and Traumatology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China 2 Department of Obstetrics and Gynaecology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China 3 Laboratory of Chromatin and Human Disease Key Laboratory of Regenerative Biology South China Institute for Stem Cell Biology and Regenerative Medicine Guangzhou Institutes of Biomedicine and Health Chinese Academy of Sciences Guangzhou China 4 Department of Chemical Pathology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China 5 Genome Regulation Laboratory Guangzhou Institutes of Biomedicine and Health Chinese Academy of Sciences Guangzhou China Correspondence Huating Wang Tel 852 3763 6047 Fax 852 2636 0008 E mail huating wang cuhk edu hk Hao Sun E mail haosun cuhk edu hk Emerging studies document the roles of long non coding RNAs LncRNAs in regulating gene expression at chromatin level but relatively less is known how they regulate DNA methylation Here we identify an lncRNA Dum developmental pluripotency associated 2 Dppa2 Upstream binding Muscle lncRNA in skeletal myoblast cells The expression of Dum is dynamically regulated during myogenesis in vitro and

    Original URL path: http://www.cell-research.com/arts.asp?id=2074 (2016-02-14)
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  • Cell Research
    Key laboratory for Molecular Animal Nutrition Ministry of Education Innovation Center for Signaling Network College of Life Sciences 2 College of Animal Sciences Zhejiang University 866 Yu Hang Tang Road Hangzhou Zhenjiang 310058 China 3 College of Natural Resources and Environment South China Agricultural University Guangzhou Guangdong 510650 China 4 National Key Laboratory of Organ Failure Research National Clinical Research Center for Kidney Disease and Division of Nephrology Nanfang Hospital Southern Medical University Guangzhou Guangdong 510515 China 5 Developmental and Stem Cell Institute West China Second University Hospital Sichuan University Chengdu Sichuan 610041 China 6 Biomedical Research Council Agency for Science and Technology Research Singapore Correspondence Jun Chen E mail chenjun2009 zju edu cn Jinrong Peng E mail pengjr zju edu cn The inhibitory role of p53 in DNA double strand break DSB repair seems contradictory to its tumor suppressing property The p53 isoform Δ113p53 Δ133p53 is a p53 target gene that antagonizes p53 apoptotic activity However information on its functions in DNA damage repair is lacking Here we report that Δ113p53 expression is strongly induced by γ irradiation but not by UV irradiation or heat shock treatment Strikingly Δ113p53 promotes DNA DSB repair pathways including homologous recombination non homologous end joining and single strand annealing To study the biological significance of Δ113p53 in promoting DNA DSB repair we generated a zebrafish Δ113p53M M mutant via the transcription activator like effector nuclease technique and found that the mutant is more sensitive to γ irradiation The human ortholog Δ133p53 is also only induced by γ irradiation and functions to promote DNA DSB repair Δ133p53 knockdown cells were arrested at the G2 phase at the later stage in response to γ irradiation due to a high level of unrepaired DNA DSBs which finally led to cell senescence Furthermore Δ113p53 Δ133p53 promotes DNA

    Original URL path: http://www.cell-research.com/arts.asp?id=2075 (2016-02-14)
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  • Cell Research
    3410 Fax 44 617 632 2662 E mail martin hemler dfci harvard edu In normal melanocytes TGF β signaling has a cytostatic effect However in primary melanoma cells TGF β induced cytostasis is diminished thus allowing melanoma growth Later a second phase of TGF β signaling supports melanoma EMT like changes invasion and metastasis In parallel with these present absent present TGF β signaling phases cell surface protein EWI motif containing protein 2 EWI 2 or IgSF8 is absent present absent in melanocytes primary melanoma and metastatic melanoma respectively suggesting that EWI 2 may serve as a negative regulator of TGF β signaling Using melanoma cell lines and melanoma short term cultures we performed RNAi and overexpression experiments and found that EWI 2 negatively regulates TGF β signaling and its downstream events including cytostasis in vitro and in vivo EMT like changes cell migration CD271 dependent invasion and lung metastasis in vivo When EWI 2 is present it associates with cell surface tetraspanin proteins CD9 and CD81 molecules not previously linked to TGF β signaling Indeed when associated with EWI 2 CD9 and CD81 are sequestered and have no impact on TβR2 TβR1 association or TGF β signaling However when

    Original URL path: http://www.cell-research.com/arts.asp?id=2076 (2016-02-14)
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  • Cell Research
    Chuan He 1 1 Department of Chemistry and Institute for Biophysical Dynamics Howard Hughes Medical Institute The University of Chicago 929 E 57th Street Chicago IL 60637 USA Correspondence Chuan He E mail chuanhe uchicago edu The TET family of dioxygenases can oxidize 5 methylcytosine 5mC to 5 hydroxymethylcytosine 5hmC 5 formylcytosine 5fC and 5 carboxylcytosine 5caC in mammalian genomic DNA via a stepwise manner1 2 3 4 5 5fC

    Original URL path: http://www.cell-research.com/arts.asp?id=2077 (2016-02-14)
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  • Cell Research
    Stewart 1 and James A Thomson 1 2 3 1 Morgridge Institute for Research Madison WI USA 2 Department of Cell and Regenerative Biology University of Wisconsin Madison Madison WI USA 3 Department of Molecular Cellular and Developmental Biology University of California Santa Barbara Santa Barbara CA USA 4 Current address Department of Molecular and Cellular Biology Baylor College of Medicine Houston TX USA 5 Current address Division of Biomedical Statistics and Informatics Department of Health Sciences Research Mayo Clinic College of Medicine Rochester MN USA Correspondence James A Thomson E mail JThomson morgridge org Aptamers are short stretches of nucleotides or amino acid residues that are engineered to bind to various targets from small chemicals to large proteins and live cells1 2 3 4 5 Aptamers are normally selected through a process called systematic evolution of ligands by exponential enrichment SELEX in which aptamers are selected from a random library of oligonucleotides or peptides against a target through repeated rounds of selection and amplification2 As a versatile affinity reagent aptamers can be used to modulate the behavior of cells6 7 to detect chemical substances in solution8 9 as alternatives to antibodies5 10 and as therapeutic reagents for human diseases11

    Original URL path: http://www.cell-research.com/arts.asp?id=2078 (2016-02-14)
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  • Cell Research
    Schuyler Lee 1 Yinghua Peng 1 Eric Bunker 1 Chong Shen 2 Emilie Giaime 3 Jie Shen 3 Jingshi Shen 2 Zongyao Zhou 1 and Xuedong Liu 1 1 Department of Chemistry and Biochemistry Jennie Smoly Caruthers Biotechnology Building JSCBB University of Colorado Boulder Boulder 3415 Colorado Ave CO 80303 USA 2 Department of MCD Biology University of Colorado Boulder Boulder 3415 Colorado Ave CO 80303 USA 3 Center for Neurologic Diseases Brigham and Women s Hospital Program in Neuroscience Harvard Medical School New Research Building Rm 636E 77 Avenue Louis Pasteur Boston MA 02115 USA Correspondence Xuedong Liu Tel 001 303 735 6161 Fax 001 303 735 6161 E mail Xuedong Liu colorado edu PINK1 and Parkin have been implicated in mitochondrial quality control mitochondrial fusion fission dynamics and axonal mitochondrial mobility in neurons1 2 The PINK1 Parkin pathway is very dynamic and the biological responses mediated by the PINK1 Parkin pathway differ spatially and kinetically in different cell types2 Therefore tools to dynamically probe the function of the PINK1 Parkin pathway are highly desirable Here we report a chemical genetic approach to probe the function of PINK1 in mitophagy and mitochondrial mobility Our results validate the roles of

    Original URL path: http://www.cell-research.com/arts.asp?id=2079 (2016-02-14)
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