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  • Cell Research
    for active DNA demethylation and genomic imprinting in Arabidopsis Yan Li 1 2 Cheng Guo Duan 3 Xiaohong Zhu 1 3 Weiqiang Qian 2 and Jian Kang Zhu 1 3 1 Shanghai Center for Plant Stress Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200032 China 2 State Key Laboratory of Protein and Plant Gene Research School of Life Sciences and Peking Tsinghua Center for Life Science

    Original URL path: http://www.cell-research.com/arts.asp?id=2120 (2016-02-14)
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  • Cell Research
    Activation of complement leads to robust and efficient proteolytic cascades which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory molecules More recently however the role of complement in the immune response has been expanded due to observations that link complement activation to adaptive immune responses It is now appreciated that complement is a functional bridge between innate and adaptive immune responses that allows an integrated host defense to pathogenic challenges As such a study of its functions allows insight into the molecular underpinnings of host pathogen interactions as well as the organization and orchestration of the host immune response This review attempts to summarize the roles that complement plays in both innate and adaptive immune responses and the consequences of these interactions on host defense H5N1 influenza viruses outbreaks and biological properties Gabriele Neumann 1 Hualan Chen 2 George F Gao 3 Yuelong Shu 4 and Yoshihiro Kawaoka 1 5 Cell Research 2010 20 51 61 doi 10 1038 cr 2009 124 published online 3 November 2009 Full Text PDF All known subtypes of influenza A viruses are maintained in wild waterfowl the natural reservoir of these viruses Influenza A viruses are isolated from a variety of animal species with varying morbidity and mortality rates More importantly influenza A viruses cause respiratory disease in humans with potentially fatal outcome Local or global outbreaks in humans are typically characterized by excess hospitalizations and deaths In 1997 highly pathogenic avian influenza viruses of the H5N1 subtype emerged in Hong Kong that transmitted to humans resulting in the first documented cases of human death by avian influenza virus infection A new outbreak started in July 2003 in poultry in Vietnam Indonesia and Thailand and highly pathogenic avian H5N1 influenza viruses have since spread throughout Asia and into Europe and Africa These viruses continue to infect humans with a high mortality rate and cause worldwide concern of a looming pandemic Moreover H5N1 virus outbreaks have had devastating effects on the poultry industries throughout Asia Since H5N1 virus outbreaks appear to originate from Southern China we here examine H5N1 influenza viruses in China with an emphasis on their biological properties ORIGINAL ARTICLES IL 23 signaling enhances Th2 polarization and regulates allergic airway inflammation Juan Peng 1 2 3 Xuexian O Yang 1 Seon Hee Chang 1 Jiong Yang 2 3 and Chen Dong 1 Cell Research 2010 20 62 71 doi 10 1038 cr 2009 128 published online 24 November 2009 Full Text PDF IL 23 IL 17 axis is an important regulator in various inflammatory diseases However the role of IL 23 in allergic airway inflammation is not well understood In this study we show that in an allergen induced asthma model mice with transgenic overexpression of IL 23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production whereas those deficient in IL 23 displayed reduced airway inflammation In vitro IL 23 IL 23R signaling promoted

    Original URL path: http://www.cell-research.com/artsmore.asp?id=42 (2016-02-14)
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  • Cell Research
    histone H3 lysine 9 H3K9me2 1 but not for H3K9me3 Our analyses also reveal how human PHF8 discriminates between methylation states and achieves sequence specificity for methylated H3K9 The in vitro demethylation assay also showed that the F279S mutant observed in clinical patients possesses no demethylation activity suggesting that loss of enzymatic activity is crucial for pathogenesis of PHF8 patients Taken together these results will shed light on the molecular mechanism underlying PHF8 associated developmental and neurological diseases ATF4 regulates lipid metabolism and thermogenesis Chunxia Wang Zhiying Huang Ying Du Ying Cheng Shanghai Chen and Feifan Guo Cell Research 2010 20 174 184 doi 10 1038 cr 2010 4 published online 12 January 2010 Full Text PDF Activating transcription factor 4 ATF4 has been shown to play key roles in many physiological processes There are no reports however demonstrating a direct link between ATF4 and lipid metabolism We noticed that Atf4 deficient mice are lean suggesting a possible role for ATF4 in regulating lipid metabolism The goal of our current study is to investigate the involvement of ATF4 in lipid metabolism and elucidate the underlying mechanisms Studies using Atf4 deficient mice revealed increased energy expenditure as measured by oxygen consumption These mice also showed increases in lipolysis expression of uncoupling protein 2 UCP2 and β oxidation genes and decreases in expression of lipogenic genes in white adipose tissue WAT suggesting increased utilization and decreased synthesis of fatty acids respectively Expression of UCP1 2 and 3 was also increased in brown adipose tissue BAT suggesting increased thermogenesis The effect of ATF4 deletion on expression of UCPs in BAT suggests that increased thermogenesis may underlie increased energy expenditure Thus our study identifies a possible new function for ATF4 in regulating lipid metabolism and thermogenesis Small ubiquitin related modifier paralogs are indispensable but functionally redundant during early development of zebrafish Hao Yuan 1 2 Jun Zhou 2 Min Deng 3 Xi Liu 2 Morgane Le Bras 4 Hugues de The 2 4 Sai Juan Chen 1 2 Zhu Chen 1 2 Ting Xi Liu 3 and Jun Zhu 2 Cell Research 2010 20 185 196 doi 10 1038 cr 2009 101 published online 25 August 2009 Full Text PDF The Small ubiquitin related modifier SUMO conjugation to a variety of proteins regulates diverse cellular processes including transcription cell cycle regulation and maintenance of genome integrity To investigate in vivo biological function of SUMO paralogs we inactivated them in the early development of zebrafish While zebrafish embryos deficient for all three SUMO paralogs as Ubc9 deficient ones displayed severe defects loss of individual SUMO paralog was compatible with a normal development SUMO deficient embryos can be rescued by a single human or zebrafish SUMO While key structural basic lysine residues and N terminal unstructured stretch of SUMO are critical for in vivo rescue the consensus K11 sumoylation site of SUMO2 is dispensable implying that chain formation on this potential site is unessential for normal development Inactivation of all three SUMOs triggered p53 dependent apoptosis

    Original URL path: http://www.cell-research.com/artsmore.asp?id=41 (2016-02-14)
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  • Cell Research
    Our finding therefore suggests that the ancient OsMADS6 gene is able to specify floral state by determining floral organ and meristem identities in monocot crop rice together with OsMADS1 S100A8 A9 induces autophagy and apoptosis via ROS mediated cross talk between mitochondria and lysosomes that involves BNIP3 Saeid Ghavami 1 2 3 Mehdi Eshragi 1 Sudharsana R Ande 1 Walter J Chazin 4 Thomas Klonisch 5 Andrew J Halayko 2 3 Karol D Mcneill 3 Mohammad Hashemi 6 Claus Kerkhoff 7 and Marek Los 8 Cell Research 2010 20 314 331 doi 10 1038 cr 2009 129 published online 24 November 2009 Full Text PDF The complex formed by two members of the S100 calcium binding protein family S100A8 A9 exerts apoptosis inducing activity in various cells of different origins Here we present evidence that the underlying molecular mechanisms involve both programmed cell death I PCD I apoptosis and PCD II autophagy like death Treatment of cells with S100A8 A9 caused the increase of Beclin 1 expression as well as Atg12 Atg5 formation S100A8 A9 induced cell death was partially inhibited by the specific PI3 kinase class III inhibitor 3 methyladenine 3 MA and by the vacuole H ATPase inhibitor bafilomycin A1 Baf A1 S100A8 A9 provoked the translocation of BNIP3 a BH3 only pro apoptotic Bcl2 family member to mitochondria Consistent with this finding ΔTM BNIP3 overexpression partially inhibited S100A8 A9 induced cell death decreased reactive oxygen species ROS generation and partially protected against the decrease in mitochondrial transmembrane potential in S100A8 A9 treated cells In addition either ΔTM BNIP3 overexpression or N acetyl L cysteine co treatment decreased lysosomal activation in cells treated with S100A8 A9 Our data indicate that S100A8 A9 promoted cell death occurs through the cross talk of mitochondria and lysosomes via ROS and the process involves BNIP3 Wwp2 mediates Oct4 ubiquitination and its own auto ubiquitination in a dosage dependent manner Bing Liao 1 2 4 and Ying Jin 1 2 3 Cell Research 2010 20 332 344 doi 10 1038 cr 2009 136 published online 8 December 2009 Full Text PDF Transcription factor Oct4 plays critical roles in maintaining pluripotency and controlling lineage commitment of embryonic stem cells ESCs Our previous study indicates that Wwp2 a mouse HECT type E3 ubiquitin ligase ubiquitinates Oct4 and promotes its degradation in a heterologous system However roles of Wwp2 in regulating endogenous Oct4 protein levels as well as molecular characteristics of the function of Wwp2 have not been determined Here we report that Wwp2 plays an important role in Oct4 ubiquitination and degradation during differentiation of embryonal carcinoma cells ECCs although it does not appear to affect Oct4 protein levels in the undifferentiated ECCs and ESCs Importantly inhibition of Wwp2 expression by specific RNA interference elevates the Oct4 protein level leading to attenuation in retinoid acid induced activation of differentiation related marker genes Mechanistically Wwp2 catalyzes Oct4 poly ubiquitination via the lysine 63 linkage in a dosage dependent manner Interestingly Wwp2 also regulates its own ligase

    Original URL path: http://www.cell-research.com/artsmore.asp?id=40 (2016-02-14)
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  • Cell Research
    and Malcolm G Parker 1 Cell Research 2010 20 434 444 doi 10 1038 cr 2010 11 published online 26 January 2010 Full Text PDF We investigated the ability of fetal mesenchymal stem cells fMSCs to differentiate into brown and white adipocytes and compared the expression of a number of marker genes and key regulatory factors We showed that the expression of key adipocyte regulators and markers during differentiation is similar to that in other human and murine adipocyte models including induction of PPARγ2 and FABP4 Notably we found that the preadipocyte marker Pref 1 is induced early in differentiation and then declines markedly as the process continues suggesting that fMSCs first acquire preadipocyte characteristics as they commit to the adipogenic lineage prior to their differentiation into mature adipocytes After adipogenic induction some stem cell isolates differentiated into cells resembling brown adipocytes and others into white adipocytes Detailed investigation of one isolate showed that the novel brown fat determining factor PRDM16 is expressed both before and after differentiation Importantly these cells exhibited elevated basal UCP 1 expression which was dependent on the activity of the orphan nuclear receptor ERRa highlighting a novel role for ERRa in human brown fat Thus fMSCs represent a useful in vitro model for human adipogenesis and provide opportunities to study the stages prior to commitment to the adipocyte lineage They also offer invaluable insights into the characteristics of human brown fat Length of the ORF position of the first AUG and the Kozak motif are important factors in potential dual coding transcripts Heng Xu 1 Ping Wang 1 Yujie Fu 1 Yufang Zheng 3 Quan Tang 1 Lizhen Si 1 Jin You 1 Zhenguo Zhang 1 Yufei Zhu 1 Li Zhou 1 Zejun Wei 1 Bin Lin 1 Landian Hu 1 2 and Xiangyin Kong 1 2 Cell Research 2010 20 445 457 doi 10 1038 cr 2010 25 published online 16 February 2010 Full Text PDF A single mammalian transcript normally encodes one protein but the transcript of GNAS G protein α subunit contains two reading frames and produces two structurally unrelated proteins XLαs and ALEX No other confirmed GNAS like dual coding transcripts have been reported to date even though many such candidate genes have been predicted by bioinformatics analysis In this study we constructed a series of vectors to test how two protein products were translated from a single transcript in vitro The length of the ORF open reading frame position of the first AUG and the Kozak motif were found to be important factors These factors as well as 55 bp NMD nonsense mediated mRNA decay rule were used in a bioinformatics search for candidate dual coding transcripts A total of 1307 750 and 474 two ORF containing transcripts were found in human mouse and rat respectively of which 170 89 and 70 respectively were found to be potential dual coding transcripts Most transcripts showed low conservation among species Interestingly dual coding transcripts were significantly enriched for transcripts from the zinc

    Original URL path: http://www.cell-research.com/artsmore.asp?id=39 (2016-02-14)
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  • Cell Research
    crystallography and NMR respectively The Arabidopsis P450 protein CYP82C2 modulates jasmonate induced root growth inhibition defense gene expression and indole glucosinolate biosynthesis Fang Liu 1 Hongling Jiang 1 Songqing Ye 2 Wen Ping Chen 2 Wenxing Liang 1 Yingxiu Xu 1 1 Bo Sun 3 Jiaqiang Sun 1 Qiaomei Wang 3 Jerry D Cohen 2 and Chuanyou Li 1 Cell Research 2010 20 539 552 doi 10 1038 cr 2010 36 published online 30 March 2010 Full Text PDF Jasmonic acid JA is a fatty acid derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens Molecular genetic studies have established that JA also performs a critical role in several aspects of plant development Here we describe the characterization of the Arabidopsis mutant jasmonic acid hypersensitive1 1 jah1 1 which is defective in several aspects of JA responses Although the mutant exhibits increased sensitivity to JA in root growth inhibition it shows decreased expression of JA inducible defense genes and reduced resistance to the necrotrophic fungus Botrytis cinerea Gene cloning studies indicate that these defects are caused by a mutation in the cytochrome P450 protein CYP82C2 We provide evidence showing that the compromised resistance of the jah1 1 mutant to B cinerea is accompanied by decreased expression of JA induced defense genes and reduced accumulation of JA induced indole glucosinolates IGs Conversely the enhanced resistance to B cinerea in CYP82C2 overexpressing plants is accompanied by increased expression of JA induced defense genes and elevated levels of JA induced IGs We demonstrate that CYP82C2 affects JA induced accumulation of the IG biosynthetic precursor tryptophan Trp but not the JA induced IAA or pathogen induced camalexin Together our results support a hypothesis that CYP82C2 may act in the metabolism of Trp derived secondary metabolites under conditions in which JA levels are elevated The jah1 1 mutant should thus be important in future studies toward understanding the mechanisms underlying the complexity of JA mediated differential responses which are important for plants to adapt their growth to the ever changing environments VL30 retrotransposition signals activation of a caspase independent and p53 dependent death pathway associated with mitochondrial and lysosomal damage Dimitrios Noutsopoulos 1 Georgios Markopoulos 1 Georgios Vartholomatos 2 Evangelos Kolettas 3 Nicolaos Kolaitis 2 and Theodore Tzavaras 1 Cell Research 2010 20 553 562 doi 10 1038 cr 2010 48 published online 13 April 2010 Full Text PDF The impact of long terminal repeat LTR retrotransposition on cell fate is unknown Here we investigated the effect of VL30 retrotransposition on cell death in SV40 transformed mouse SVTT1 cells Transfection of a VL30 retrotransposon decreased the clonogenicity of SVTT1 by 17 fold as compared to parental NIH3T3 cells Correlated levels of retrotransposition frequency and cell death rates were found in retrotransposition positive SVTT1 cloned cells exhibiting DNA fragmentation nuclear condensation multinucleation and cytoplasmic vacuolization Analysis of activation of effector caspases revealed a caspase independent cell death mechanism However cell death was associated with p53 induction and

    Original URL path: http://www.cell-research.com/artsmore.asp?id=38 (2016-02-14)
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  • Cell Research
    induces a Zipper like entry mechanism Consequently Salmonella seems to be the first bacterium found to be able to induce both Zipper and Trigger mechanisms to invade host cells BNIP3 is essential for mediating 6 thioguanine and 5 fluorouracil induced autophagy following DNA mismatch repair processing Xuehuo Zeng 1 2 and Timothy J Kinsella 1 2 Cell Research 2010 20 665 675 doi 10 1038 cr 2010 40 published online 6 April 2010 Full Text PDF DNA mismatch repair MMR processes the chemically induced mispairs following treatment with clinically important nucleoside analogs such as 6 thioguanine 6 TG and 5 fluorouracil 5 FU MMR processing of these drugs has been implicated in activation of a prolonged G2 M cell cycle arrest for repair and later induction of apoptosis and or autophagy for irreparable DNA damage In this study we investigated the role of B cl2 and adenovirus E1B N ineteen kilodalton I nteracting P rotein BNIP3 in the activation of autophagy and the temporal relationship between a G2 M cell cycle arrest and the activation of BNIP3 mediated autophagy following MMR processing of 6 TG and 5 FU We found that BNIP3 protein levels are upregulated in a MLH1 MMR dependent manner following 6 TG and 5 FU treatment Subsequent small interfering RNA siRNA mediated BNIP3 knockdown abrogates 6 TG induced autophagy We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6 TG and 5 FU induced upregulation of BNIP3 protein levels and autophagy Furthermore suppression of Checkpoint kinase 1 Chk1 expression with a subsequent reduction in 6 TG induced G2 M cell cycle arrest by Chk1 siRNA promotes the extent of 6 TG induced autophagy These findings suggest that BNIP3 mediates 6 TG and 5 FU induced autophagy in a p53 and mTOR dependent manner Additionally the duration of Chk1 activated G2 M cell cycle arrest determines the level of autophagy following MMR processing of these nucleoside analogs Hypoxia induces PGC 1α expression and mitochondrial biogenesis in the myocardium of TOF patients Lingyun Zhu 1 Qiang Wang 2 Lin Zhang 1 Zhixiang Fang 1 Fang Zhao 3 Zhiyuan Lv 1 Zuguang Gu 1 Junfeng Zhang 1 Jin Wang 1 Ke Zen 1 Yang Xiang 1 Dongjin Wang 2 and Chen Yu Zhang 1 Cell Research 2010 20 676 687 doi 10 1038 cr 2010 46 published online 6 April 2010 Full Text PDF PGC 1α a potent transcriptional coactivator is the major regulator of mitochondrial biogenesis and activity in the cardiac muscle The dysregulation of PGC 1α and its target genes has been reported to be associated with congenital and acquired heart diseases By examining myocardium samples from patients with Tetralogy of Fallot we show here that PGC 1α expression levels are markedly increased in patients compared with healthy controls and positively correlated with the severity of cyanosis Furthermore hypoxia significantly induced the expression of PGC 1α and mitochondrial biogenesis in cultured cardiac myocytes Mechanistic studies suggest that hypoxia induced PGC 1α expression

    Original URL path: http://www.cell-research.com/artsmore.asp?id=37 (2016-02-14)
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  • Cell Research
    pathogenesis of gastric cancer PHF8 is a histone H3K9me2 demethylase regulating rRNA synthesis Ziqi Zhu 1 2 Yanru Wang 1 2 3 Xia Li 1 2 Yiqin Wang 1 2 Longyong Xu 1 2 Xiang Wang 2 Tianliang Sun 2 Xiaobin Dong 2 Lulu Chen 2 Hailei Mao 1 2 3 Yi Yu 1 2 Jingsong Li 2 4 Pin Adele Chen 2 and Charlie Degui Chen 1 2 Cell Research 2010 20 794 801 doi 10 1038 cr 2010 75 published online 8 June 2010 Full Text PDF Dimethylation of histone H3 lysine 9 H3K9me2 is an important epigenetic mark associated with transcription repression Here we identified PHF8 a JmjC domain containing protein as a histone demethylase specific for this repressing mark Recombinant full length wild type protein could remove methylation from H3K9me2 but mutation of a conserved histidine to alanine H247A abolished the demethylase activity Overexpressed exogenous PHF8 was colocalized with B23 staining Endogenous PHF8 was also colocalized with B23 and fibrillarin two well established nucleolus proteins suggesting that PHF8 is localized in the nucleolus and may regulate rRNA transcription Indeed PHF8 bound to the promoter region of the rDNA gene Knockdown of PHF8 reduced the expression of rRNA and overexpression of the gene resulted in upregulation of rRNA transcript Concomitantly H3K9me2 level was elevated in the promoter region of the rDNA gene in PHF8 knockdown cells and reduced significantly when the wild type but not the catalytically inactive H247A mutant PHF8 was overexpressed Thus our study identified a histone demethylase for H3K9me2 that regulates rRNA transcription The ubiquitin specific protease 17 is involved in virus triggered type I IFN signaling Rui Chen Lu Zhang Bo Zhong Bo Tan Yu Liu and Hong Bing Shu Cell Research 2010 20 802 811 doi 10 1038 cr 2010 41 published online 6 April 2010 Full Text PDF Viral infection initiates a series of signaling cascades that activate the transcription factors nuclear factor kappa B and interferon regulatory factor 3 which collaborate to induce transcription of genes for type I interferons IFNs and other cytokines Here we report that the deubiquitinating enzyme ubiquitin specific protease 17 USP17 is required for virus induced RIG I and melanoma differentiation associated protein 5 MDA5 mediated type I IFN signaling Knockdown of endogenous USP17 inhibited virus cytoplasmic poly I C and poly dA dT induced activation of the IFN β promoter and cellular antiviral responses We further found that knockdown of USP17 inhibited RIG I and MDA5 induced but not downstream activator induced activation of the IFN β promoter which was correlated with an increase in ubiquitination levels of RIG I and MDA5 Taken together our findings suggest that USP17 functions through deubiquitination of RIG I and MDA5 to regulate virus induced type I IFN signaling The molecular cell death machinery in the simple cnidarian Hydra includes an expanded caspase family and pro and anti apoptotic Bcl 2 proteins Margherita Lasi 1 Barbara Pauly 1 Nikola Schmidt 1 Mihai Cikala 1 Beate Stiening 1 Tina

    Original URL path: http://www.cell-research.com/artsmore.asp?id=36 (2016-02-14)
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