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  • Cell Research
    Guangxiu Lu 1 2 Cell Research 2007 17 999 1007 doi 10 1038 cr 2007 97 published online 27 November 2007 Full Text PDF Homozygous human embryonic stem cells hESCs are thought to be better cell sources for hESC banking because their human leukocyte antigen HLA haplotype would strongly increase the degree of matching for certain populations with relatively smaller cohorts of cell lines Homozygous hESCs can be generated from parthenogenetic embryos but only heterozygous hESCs have been established using the current strategy to artificially activate the oocyte without second polar body extrusion Here we report the first successful derivation of a human homozygous ESC line chHES 32 from a one pronuclear oocyte following routine in vitro fertilization treatment chHES 32 cells express common markers and genes with normal hESCs They have been propagated in an undifferentiated state for more than a year P50 and have maintained a stable karyotype of 46 XX When differentiated in vivo and in vitro chHES 32 cells can form derivatives from all three embryonic germ layers The almost undetectable expression of five paternally expressed imprinted genes and their HLA genotype identical to the oocyte donor indicated their parthenogenetic origin Using genome wide single nucleotide polymorphism analysis and DNA fingerprinting the homozygosity of chHES 32 cells was further confirmed The results indicated that unwanted one pronuclear oocytes might be a potential source for human homozygous and parthenogenetic ESCs and suggested an alternative strategy for obtaining homozygous hESC lines from parthenogenetic haploid oocytes Derivation of human embryonic stem cell lines from parthenogenetic blastocysts Qingyun Mai 1 Yang Yu 1 2 3 Tao Li 1 Liu Wang 2 Mei jue Chen 4 Shu zhen Huang 4 Canquan Zhou 1 and Qi Zhou 2 Cell Research 2007 17 1008 1019 doi 10 1038 cr 2007 102 published online 11 December 2007 Full Text PDF Parthenogenesis is one of the main and most useful methods to derive embryonic stem cells ESCs which may be an important source of histocompatible cells and tissues for cell therapy Here we describe the derivation and characterization of two ESC lines hPES 1 and hPES 2 from in vitro developed blastocysts following parthenogenetic activation of human oocytes Typical ESC morphology was seen and the expression of ESC markers was as expected for alkaline phosphatase octamer binding transcription factor 4 stage specific embryonic antigen 3 stage specific embryonic antigen 4 TRA 1 60 and TRA 1 81 and there was absence of expression of negative markers such as stage specific embryonic antigen 1 Expression of genes specific for different embryonic germ layers was detected from the embryoid bodies EBs of both hESC lines suggesting their differentiation potential in vitro However in vivo only hPES 1 formed teratoma consisting of all three embryonic germ layers hPES 2 did not Interestingly after continuous proliferation for more than 100 passages hPES 1 cells still maintained a normal 46 XX karyotype hPES 2 displayed abnormalities such as chromosome translocation after long term passages Short Tandem Repeat STR results demonstrated

    Original URL path: http://www.cell-research.com/artsmore.asp?id=67 (2016-02-14)
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  • Cell Research
    in this pathway Each of these avenues of research has contributed significantly to our understanding of how the NER pathway works and how alterations in NER activity both positive and negative influence human biology Transcription coupled nucleotide excision repair in mammalian cells molecular mechanisms and biological effects Maria Fousteri 1 and Leon HF Mullenders 1 Cell Research 2008 18 73 84 doi 10 1038 cr 2008 6 published online 1 January 2008 Full Text PDF The encounter of elongating RNA polymerase II RNAPIIo with DNA lesions has severe consequences for the cell as this event provides a strong signal for P53 dependent apoptosis and cell cycle arrest To counteract prolonged blockage of transcription the cell removes the RNAPIIo blocking DNA lesions by transcription coupled repair TC NER a specialized subpathway of nucleotide excision repair NER Exposure of mice to UVB light or chemicals has elucidated that TC NER is a critical survival pathway protecting against acute toxic and long term effects cancer of genotoxic exposure Deficiency in TC NER is associated with mutations in the CSA and CSB genes giving rise to the rare human disorder Cockayne syndrome CS Recent data suggest that CSA and CSB play differential roles in mammalian TC NER CSB as a repair coupling factor to attract NER proteins chromatin remodellers and the CSA E3 ubiquitin ligase complex to the stalled RNAPIIo CSA is dispensable for attraction of NER proteins yet in cooperation with CSB is required to recruit XAB2 the nucleosomal binding protein HMGN1 and TFIIS The emerging picture of TC NER is complex repair of transcription blocking lesions occurs without displacement of the DNA damage stalled RNAPIIo and requires at least two essential assembly factors CSA and CSB the core NER factors except for XPC RAD23B and TC NER specific factors These and yet unidentified proteins will accomplish not only efficient repair of transcription blocking lesions but are also likely to contribute to DNA damage signalling events Mechanisms and functions of DNA mismatch repair Guo Min Li 1 Cell Research 2008 18 85 98 doi 10 1038 cr 2007 115 published online 24 December 2007 Full Text PDF DNA mismatch repair MMR is a highly conserved biological pathway that plays a key role in maintaining genomic stability The specificity of MMR is primarily for base base mismatches and insertion deletion mispairs generated during DNA replication and recombination MMR also suppresses homeologous recombination and was recently shown to play a role in DNA damage signaling in eukaryotic cells Escherichia coli MutS and MutL and their eukaryotic homologs MutSα and MutLα respectively are key players in MMR associated genome maintenance Many other protein components that participate in various DNA metabolic pathways such as PCNA and RPA are also essential for MMR Defects in MMR are associated with genome wide instability predisposition to certain types of cancer including hereditary non polyposis colorectal cancer resistance to certain chemotherapeutic agents and abnormalities in meiosis and sterility in mammalian systems Homologous recombination in DNA repair and DNA damage tolerance Xuan Li 1 and Wolf Dietrich Heyer 1 2 Cell Research 2008 18 99 113 doi 10 1038 cr 2008 1 published online 1 January 2008 Full Text PDF Homologous recombination HR comprises a series of interrelated pathways that function in the repair of DNA double stranded breaks DSBs and interstrand crosslinks ICLs In addition recombination provides critical support for DNA replication in the recovery of stalled or broken replication forks contributing to tolerance of DNA damage A central core of proteins most critically the RecA homolog Rad51 catalyzes the key reactions that typify HR homology search and DNA strand invasion The diverse functions of recombination are reflected in the need for context specific factors that perform supplemental functions in conjunction with the core proteins The inability to properly repair complex DNA damage and resolve DNA replication stress leads to genomic instability and contributes to cancer etiology Mutations in the BRCA2 recombination gene cause predisposition to breast and ovarian cancer as well as Fanconi anemia a cancer predisposition syndrome characterized by a defect in the repair of DNA interstrand crosslinks The cellular functions of recombination are also germane to DNA based treatment modalities of cancer which target replicating cells by the direct or indirect induction of DNA lesions that are substrates for recombination pathways This review focuses on mechanistic aspects of HR relating to DSB and ICL repair as well as replication fork support The endless tale of non homologous end joining Eric Weterings 1 and David J Chen 1 Cell Research 2008 18 114 124 doi 10 1038 cr 2008 3 published online 1 January 2008 Full Text PDF DNA double strand breaks DSBs are introduced in cells by ionizing radiation and reactive oxygen species In addition they are commonly generated during V D J recombination an essential aspect of the developing immune system Failure to effectively repair these DSBs can result in chromosome breakage cell death onset of cancer and defects in the immune system of higher vertebrates Fortunately all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs homologous recombination and non homologous end joining NHEJ The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule bring them together in a synaptic DNA protein complex and finally repair the DNA break In this review all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co operation of these enzymes during DSB repair is presented Flexibility in the order of action and in the enzymology of the nuclease polymerases and ligase of vertebrate nonhomologous DNA end joining relevance to cancer aging and the immune system Michael R Lieber 1 Haihui Lu 1 Jiafeng Gu 1 and Klaus Schwarz 2 Cell Research 2008 18 125 133 doi 10 1038 cr 2007 108 published online 18 December 2007 Full Text PDF Nonhomologous DNA end joining NHEJ is the primary pathway for repair of double strand DNA breaks in human cells and in multicellular eukaryotes

    Original URL path: http://www.cell-research.com/artsmore.asp?id=66 (2016-02-14)
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  • Cell Research
    1 Paul R Clarke 2 and Chuanmao Zhang 1 Cell Research 2008 18 268 280 doi 10 1038 cr 2008 11 published online 15 January 2008 Full Text PDF Cyclin B1 is a key regulatory protein controlling cell cycle progression in vertebrates Cyclin B1 binds CDK1 a cyclin dependent kinase catalytic subunit forming a complex that orchestrates mitosis through phosphorylation of key proteins Cyclin B1 regulates both the activation of CDK1 and its subcellular localization which may be critical for substrate selection Here we demonstrate that cyclin B1 is concentrated on the outer plate of the kinetochore during prometaphase This localization requires the cyclin box region of the protein Cyclin B1 is displaced from individual kinetochores to the spindle poles by microtubule attachment to the kinetochores and this displacement is dependent on the dynein dynactin complex Depletion of cyclin B1 by vector based siRNA causes inefficient attachment between kinetochores and microtubules and chromosome alignment defects and delays the onset of anaphase We conclude that cyclin B1 accumulates at kinetochores during prometaphase where it contributes to the correct attachment of microtubules to kinetochores and efficient alignment of the chromosomes most likely through localized phosphorylation of specific substrates by cyclin B1 CDK1 Cyclin B1 is then transported from each kinetochore as microtubule attachment is completed and this relocalization may redirect the activity of cyclin B1 CDK1 and contribute to inactivation of the spindle assembly checkpoint Preferential loss of mismatch repair function in refractory and relapsed acute myeloid leukemia potential contribution to AML progression Guogen Mao 1 Fenghua Yuan 1 Kimberly Absher 2 C Darrell Jennings 2 Dianna S Howard 3 Craig T Jordan 4 and Liya Gu 1 2 Cell Research 2008 18 281 289 doi 10 1038 cr 2008 14 published online 29 January 2008 Full Text PDF Acute myeloid leukemia AML is an aggressive hematological cancer Despite therapeutic regimens that lead to complete remission the vast majority of patients undergo relapse The molecular mechanisms underlying AML development and relapse remain incompletely defined To explore whether loss of DNA mismatch repair MMR function is involved in AML we screened two key MMR genes MSH2 and MLH1 for mutations and promoter hypermethylation in leukemia specimens from 53 AML patients and blood from 17 non cancer controls We show here that whereas no amino acid alteration or promoter hypermethylation was detected in all control samples 18 AML patients exhibited either mutations in MMR genes or hypermethylation in the MLH1 promoter In vitro functional MMR analysis revealed that almost all the mutations analyzed resulted in loss of MMR function MMR defects were significantly more frequent in patients with refractory or relapsed AML compared with newly diagnosed patients These observations suggest for the first time that the loss of MMR function is associated with refractory and relapsed AML and may contribute to disease pathogenesis SARS coronavirus entry into host cells through a novel clathrin and caveolae independent endocytic pathway Hongliang Wang 1 Peng Yang 1 Kangtai Liu 1 Feng Guo 1 Yanli Zhang 1 Gongyi

    Original URL path: http://www.cell-research.com/artsmore.asp?id=65 (2016-02-14)
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  • Cell Research
    the smallest size Among the three populations population A displayed the highest density of β1 integrin receptor contained the highest percentage of cells in G0 G1 phase showed the highest nucleus to cytoplasm ratio and possessed the highest colony formation efficiency CFE When injected into murine blastocysts these cells participated in multi tissue formation More significantly compared with a previous approach that sorted putative EpSCs according to β1 integrin antibody staining the viability of the EpSCs enriched by the improved approach was significantly enhanced Our results provide a putative strategy for the enrichment of human EpSCs and encourage further study into the role of cell size in stem cell biology Lethal 2 giant larvae is required in the follicle cells for formation of the initial AP asymmetry and the oocyte polarity during Drosophila oogenesis Qi Li Tianchi Xin Wenlian Chen Mingwei Zhu and Mingfa Li Cell Research 2008 18 372 384 doi 10 1038 cr 2008 25 published online 12 February 2008 Full Text PDF The intricately regulated differentiation of the somatic follicle cell lineages into distinct subpopulations with specific functions plays an essential role in Drosophila egg development At early oogenesis induction of the stalk cells generates the first anteroposterior AP asymmetry in the egg chamber by inducing the posterior localization of the oocyte Later the properly specified posterior follicle cells signal to polarize the oocyte along the AP and dorsoventral DV axes at mid oogenesis Here we show that lethal 2 giant larvae lgl a Drosophila tumor suppressor gene is required in the follicle cells for the differentiation of both stalk cells and posterior follicle cells Loss of function mutations in lgl cause oocyte mispositioning in the younger one of the fused chambers due to lack of the stalk Removal of lgl function from the posterior follicle cells using the FLP FRT system results in loss of the oocyte polarity that is elicited by the failure of those posterior cells to differentiate normally Thus we provide the first demonstration that lgl is implicated in the formation of the initial AP asymmetry and the patterning of the AP and DV axes in the oocyte by acting in the specification of a subset of somatic follicle cells FIT interacts with AtbHLH38 and AtbHLH39 in regulating iron uptake gene expression for iron homeostasis in Arabidopsis Youxi Yuan 1 2 Huilan Wu 1 Ning Wang 1 2 Jie Li 1 Weina Zhao 1 2 Juan Du 1 2 Daowen Wang 1 and Hong Qing Ling 1 Cell Research 2008 18 385 397 doi 10 1038 cr 2008 26 published online 12 February 2008 Full Text PDF Iron is an essential element for plant growth and development Iron homeostasis in plants is tightly regulated at both transcriptional and posttranscriptional level Several bHLH transcription factors involved in iron homeostasis have been identified recently However their regulatory mechanisms remain unknown In this work we demonstrate that the transcription factor FIT interacted with AtbHLH38 and AtbHLH39 and directly conferred the expression regulation of iron uptake genes

    Original URL path: http://www.cell-research.com/artsmore.asp?id=64 (2016-02-14)
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  • Cell Research
    membrane potential and cyto c release from mitochondria These apoptotic effects were inhibited by cyclosporine A CsA indicating that mutant TRX1 targeted to mPTP Alteration of TRX1 from its reduced form to oxidized form in vivo by 2 4 dinitrochlorobenzene DNCB a specific inhibitor of TRX reductase also sensitized HepG 2 cells to As 2 O 3 induced apoptosis These data suggest that TRX1 plays a central role in regulating apoptosis by blocking cyto c release and inactivation of TRX1 by either mutation or oxidization of the active site cysteines may sensitize tumor cells to As 2 O 3 induced apoptosis Is kinase activity essential for biological functions of BRI1 Weihui Xu 1 Juan Huang 1 2 Baohua Li 1 Jiayang Li 1 and Yonghong Wang 1 Cell Research 2008 18 472 478 doi 10 1038 cr 2008 36 published online 11 March 2008 Full Text PDF Brassinosteroids BRs are a major group of plant hormones that regulate plant growth and development BRI1 a protein localized to the plasma membrane functions as a BR receptor and it has been proposed that its kinase activity has an essential role in BR regulated plant growth and development Here we report the isolation and molecular characterization of a new allele of bri1 bri1 301 which shows moderate morphological phenotypes and a reduced response to BRs under normal growth conditions Sequence analysis identified a two base alteration from GG to AT resulting in a conversion of 989G to 989I in the BRI1 kinase domain An in vitro assay of kinase activity showed that bri1 301 has no detectable autophosphorylation activity or phosphorylation activity towards the BRI1 substrates TTL and BAK1 Furthermore our results suggest that bri1 301 even with extremely impaired kinase activity still retains partial function in regulating plant growth and development which raises the question of whether BRI1 kinase activity is essential for BR mediated growth and development in higher plants Migratory properties of cultured olfactory ensheathing cells by single cell migration assay Zhi hui Huang 1 2 Ying Wang 1 Li Cao 2 Zhi da Su 2 Yan ling Zhu 2 Yi zhang Chen 1 2 Xiao bing Yuan 3 and Cheng He 1 2 Cell Research 2008 18 479 490 doi 10 1038 cr 2008 38 published online 18 March 2008 Full Text PDF Olfactory ensheathing cells OECs are a unique type of glial cells that have axonal growth promoting properties OEC transplantation has emerged as a promising experimental therapy of axonal injuries and demyelinating diseases However some fundamental cellular properties of OECs remain unclear In this study we found that the distinct OEC subpopulations exhibited different migratory properties based on time lapse imaging of single isolated cells possibly due to their different cytoskeletal organizations Moreover OEC subpopulations displayed different attractive migratory responses to a gradient of lysophosphatidic acid LPA in single cell migration assays Finally we found that OEC subpopulations transformed into each other spontaneously Together these results demonstrate for the first time to our knowledge that distinct OEC

    Original URL path: http://www.cell-research.com/artsmore.asp?id=63 (2016-02-14)
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  • Cell Research
    which had been described to play a role in melanoma development The effect of let 7b on protein expression was due to targeting of 3 untranslated regions 3 UTRs of individual mRNAs as exemplified by reporter gene analyses for cyclin D1 In line with its downmodulating effects on cell cycle regulators let 7b inhibited cell cycle progression and anchorage independent growth of melanoma cells Taken together these findings not only point to new regulatory mechanisms of early melanoma development but also may open avenues for future targeted therapies of this tumor Maxi anion channel as a candidate pathway for osmosensitive ATP release from mouse astrocytes in primary culture Hong Tao Liu 1 2 3 Abduqodir H Toychiev 1 4 Nobuyuki Takahashi 1 4 Ravshan Z Sabirov 5 and Yasunobu Okada 1 4 Cell Research 2008 18 558 565 doi 10 1038 cr 2008 49 published online 15 April 2008 Full Text PDF In the present study we aimed to evaluate the pathways contributing to ATP release from mouse astrocytes during hypoosmotic stress We first examined the expression of mRNAs for proteins constituting possible ATP releasing pathways that have been suggested over the past several years In RT PCR analysis using both control and osmotically swollen astrocytes amplification of cDNA fragments of expected size was seen for connexins Cx32 Cx37 Cx43 pannexin 1 Px1 the P2X7 receptor MRP1 and MDR1 but not CFTR Inhibitors of exocytotic vesicular release gap junction hemi channels CFTR MRP1 MDR1 the P2X7 receptor and volume sensitive outwardly rectifying chloride channels had no significant effects on the massive ATP release from astrocytes In contrast the hypotonicity induced ATP release from astrocytes was most effectively inhibited by gadolinium 50 μM an inhibitor of the maxi anion channel which has recently been shown to serve as a pathway for ATP release from several other cell types Thus we propose that the maxi anion channel constitutes a major pathway for swelling induced ATP release from cultured mouse astrocytes as well AtTHIC a gene involved in thiamine biosynthesis in Arabidopsis thaliana Danyu Kong 1 2 Yuxing Zhu 1 2 Huilan Wu 1 Xudong Cheng 1 2 Hui Liang 1 and Hong Qing Ling 1 Cell Research 2008 18 566 576 doi 10 1038 cr 2008 35 published online 11 March 2008 Full Text PDF Thiamine vitamin B 1 is an essential compound for organisms It contains a pyrimidine ring structure and a thiazole ring structure These two moieties of thiamine are synthesized independently and then coupled together Here we report the molecular characterization of AtTHIC which is involved in thiamine biosynthesis in Arabidopsis AtTHIC is similar to Escherichia coli ThiC which is involved in pyrimidine biosynthesis in prokaryotes Heterologous expression of AtTHIC could functionally complement the thiC knock out mutant of E coli Downregulation of AtTHIC expression by T DNA insertion at its promoter region resulted in a drastic reduction of thiamine content in plants and the knock down mutant thic1 showed albino white leaves and lethal phenotypes under the normal

    Original URL path: http://www.cell-research.com/artsmore.asp?id=62 (2016-02-14)
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  • Cell Research
    member of the Ets family transcription factors ESE 1 as well as ESE 3 is upregulated by the inflammatory cytokines interleukin 1β IL 1β and tumor necrosis factor α TNF α in bronchial epithelial cell lines Treatment of these cells with IL 1β and TNF α resulted in a dramatic increase in mRNA expression for both ESE 1 and ESE 3 We demonstrate that the induced expression is mediated by activation of the transcription factor NF κB We have characterized the ESE 1 and ESE 3 promoters and have identified the NF κB binding sequences that are required for the cytokine induced expression In addition we also demonstrate that ESE 1 upregulates ESE 3 expression and downregulates its own induction by cytokines Finally we have shown that in Elf3 homologous to human ESE 1 knockout mice the expression of the inflammatory cytokine interleukin 6 IL 6 is downregulated Our findings suggest that ESE 1 and ESE 3 play an important role in airway inflammation Roscovitine sensitizes breast cancer cells to TRAIL induced apoptosis through a pleiotropic mechanism Gustavo Ortiz Ferrón 1 Rosario Yerbes 1 Adriana Eramo 2 Ana I López Pérez 1 Ruggero De Maria 2 and Abelardo López Rivas 1 Cell Research 2008 18 664 676 doi 10 1038 cr 2008 54 published online 06 May 2008 Full Text PDF The tumor necrosis factor TNF related apoptosis inducing ligand TRAIL APO2L is a member of the TNF gene superfamily that induces apoptosis upon engagement of cognate death receptors While TRAIL is relatively non toxic to normal cells it selectively induces apoptosis in many transformed cells Nevertheless breast tumor cells are particularly resistant to the effects of TRAIL Here we report that in combination with the cyclin dependent kinase inhibitor roscovitine exposure to TRAIL induced marked apoptosis in the majority of TRAIL resistant breast cancer cell lines examined Roscovitine facilitated TRAIL death inducing signaling complex formation and the activation of caspase 8 The cFLIP L and cFLIP S FLICE inhibitory proteins were significantly down regulated following exposure to roscovitine and indeed the knockdown of cFLIP isoforms by siRNA sensitized breast tumor cells to TRAIL induced apoptosis In addition we demonstrate that roscovitine strongly suppressed Mcl 1 expression and up regulated E2F1 protein levels in breast tumor cells Significantly the silencing of Mcl 1 by siRNA sensitized breast tumor cells to TRAIL induced apoptosis Furthermore the knockdown of E2F1 protein by siRNA reduced the sensitizing effect of roscovitine in TRAIL induced apoptosis In summary our results reveal a pleitropic mechanism for the pro apoptotic influence of roscovitine highlighting its potential as an antitumor agent in breast cancer in combination with TRAIL Gfi1 1 regulates hematopoietic lineage differentiation during zebrafish embryogenesis Wei Wei 1 Lu Wen 1 Peng Huang 1 Zheng Zhang 1 Yuanyuan Chen 1 An Xiao 1 Haigen Huang 2 Zuoyan Zhu 1 Bo Zhang 1 and Shuo Lin 1 2 Cell Research 2008 18 677 685 doi 10 1038 cr 2008 60 published online 27 May 2008 Full Text

    Original URL path: http://www.cell-research.com/artsmore.asp?id=61 (2016-02-14)
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  • Cell Research
    of macrophages However information regarding the signaling mechanism of TLR mediated phagocytosis is still limited Here we provide evidence that the stimulation of TLR4 with LPS leads to activation of multiple signaling pathways including MAP kinases phosphatidylinositide 3 kinase PI3K and small GTPases in the murine macrophage like cell line RAW264 7 Specific inhibition of Cdc42 Rac or p38 MAP kinase but not PI3K reduced TLR4 induced phagocytosis of bacteria Moreover we have found that either inhibition of actin polymerization by cytochalasin D or the knockdown of actin by RNAi markedly reduced the activation of Cdc42 and Rac by LPS TLR4 induced activation of Cdc42 and Rac appears to be independent of MyD88 Taken together our results described a novel actin Cdc42 Rac pathway through which TLRs can specifically provoke phagocytosis Role of the Arabidopsis thaliana NAC transcription factors ANAC019 and ANAC055 in regulating jasmonic acid signaled defense responses Qingyun Bu 1 Hongling Jiang 1 Chang Bao Li 1 2 Qingzhe Zhai 1 3 Jie Zhang 1 3 Xiaoyan Wu 1 Jiaqiang Sun 1 Qi Xie 1 and Chuanyou Li 1 Cell Research 2008 18 756 767 doi 10 1038 cr 2008 53 published online 22 April 2008 Full Text PDF Jasmonic acid JA is an important phytohormone that regulates plant defense responses against herbivore attack pathogen infection and mechanical wounding In this report we provided biochemical and genetic evidence to show that the Arabidopsis thaliana NAC family proteins ANAC019 and ANAC055 might function as transcription activators to regulate JA induced expression of defense genes The role of the two NAC genes in JA signaling was examined with the anac019 anac055 double mutant and with transgenic plants overexpressing ANAC019 or ANAC055 The anac019 anac055 double mutant plants showed attenuated JA induced VEGETATIVE STORAGE PROTEIN1 VSP1 and LIPOXYGENASE2 LOX2 expression whereas transgenic plants overexpressing the two NAC genes showed enhanced JA induced VSP1 and LOX2 expression That the JA induced expression of the two NAC genes depends on the function of COI1 and AtMYC2 together with the finding that overexpression of ANAC019 partially rescued the JA related phenotype of the atmyc2 2 mutant has led us to a hypothesis that the two NAC proteins act downstream of AtMYC2 to regulate JA signaled defense responses Further evidence to substantiate this idea comes from the observation that the response of the anac019 anac055 double mutant to a necrotrophic fungus showed high similarity to that of the atmyc2 2 mutant Membrane glycoprotein M6A promotes μ opioid receptor endocytosis and facilitates receptor sorting into the recycling pathway Ying Jian Liang Dai Fei Wu Ralf Stumm Volker H鰈lt and Thomas Koch Cell Research 2008 18 768 779 doi 10 1038 cr 2008 71 published online 24 June 2008 Full Text PDF The interaction of μ opioid receptor MOPr with the neuronal membrane glycoprotein M6a is known to facilitate MOPr endocytosis in human embryonic kidney 293 HEK293 cells To further study the role of M6a in the post endocytotic sorting of MOPr we investigated the agonist induced

    Original URL path: http://www.cell-research.com/artsmore.asp?id=60 (2016-02-14)
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