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  • Cell Research
    mitochondrial networks through KIF5B mediated dynamic tubulation of mitochondria We found that KIF5B pulls thin highly dynamic tubules out of mitochondria Fusion of these dynamic tubules which is mediated by mitofusins gives rise to the mitochondrial network We further demonstrated that dynamic tubulation and fusion is sufficient for mitochondrial network formation by reconstituting mitochondrial networks in vitro using purified fusion competent mitochondria recombinant KIF5B and polymerized microtubules Interestingly KIF5B only controls network formation in the peripheral zone of the cell indicating that the mitochondrial network is divided into subzones which may be constructed by different mechanisms Our data not only uncover an essential mechanism for mitochondrial network formation but also reveal that different parts of the mitochondrial network are formed by different mechanisms Siglec1 suppresses antiviral innate immune response by inducing TBK1 degradation via the ubiquitin ligase TRIM27 FREE Qingliang Zheng 1 Jin Hou 2 Ye Zhou 2 Yingyun Yang 3 Bing Xie 1 and Xuetao Cao 1 2 3 10 1038 cr 2015 108 Full Text PDF Type I interferon IFN production plays pivotal roles in host antiviral innate immune responses but an excessive production of type I IFN leads to the development of immunopathological conditions Investigations on the regulatory mechanisms underlying host type I IFN production are currently of great interest Here we found that the expression of lectin family member Siglec1 was upregulated by viral infection in macrophages which was dependent on the IFN JAK STAT1 signaling pathway Siglec1 was found to negatively regulate viral infection triggered type I IFN production Mechanistically Siglec1 associates with DAP12 to recruit and activate the scaffolding function of SHP2 SHP2 then recruits E3 ubiquitin ligase TRIM27 which induces TBK1 degradation via K48 linked ubiquitination at Lys251 and Lys372 Therefore viral infection induced upregulation of Siglec1 feedback loop inhibits type I IFN production and suppresses antiviral innate immune responses Our study outlines a novel mechanism of negative regulation of type I IFN production which may help virus to escape immune elimination Acute inflammation stimulates a regenerative response in the neonatal mouse heart OPEN Chunyong Han 1 Yu Nie 1 Hong Lian 1 Rui Liu 1 Feng He 1 Huihui Huang 1 and Shengshou Hu 1 10 1038 cr 2015 110 Full Text PDF Cardiac injury in neonatal 1 day old mice stimulates a regenerative response characterized by reactive cardiomyocyte proliferation which is distinguished from the fibrotic repair process in adults Acute inflammation occurs immediately after heart injury and has generally been believed to exert a negative effect on heart regeneration by promoting scar formation in adults however little is known about the role of acute inflammation in the cardiac regenerative response in neonatal mice Here we show that acute inflammation induced cardiomyocyte proliferation after apical intramyocardial microinjection of immunogenic zymosan A particles into the neonatal mouse heart We also found that cardiac injury induced regenerative response was suspended after immunosuppression in neonatal mice and that cardiomyocytes could not be reactivated to proliferate after neonatal heart injury in the absence of interleukin 6

    Original URL path: http://www.cell-research.com/artsmore.asp?id=189 (2016-02-14)
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  • Cell Research
    OPEN Chen Song Zhang 1 Qi Liu 1 Mengqi Li 1 Shu Yong Lin 1 Yongying Peng 1 Di Wu 1 Terytty Yang Li 1 Qiang Fu 2 Weiping Jia 3 Xinjun Wang 4 Teng Ma 1 Yue Zong 1 Jiwen Cui 1 Chengfei Pu 1 Guili Lian 1 Huiling Guo 1 Zhiyun Ye 1 and Sheng Cai Lin 1 10 1038 cr 2015 90 Full Text PDF Hypoxia inducible factors HIFs are master regulators of adaptive responses to low oxygen and their α subunits are rapidly degraded through the ubiquitination dependent proteasomal pathway after hydroxylation Aberrant accumulation or activation of HIFs is closely linked to many types of cancer However how hydroxylation of HIFα and its delivery to the ubiquitination machinery are regulated remains unclear Here we show that Rho related BTB domain containing protein 3 RHOBTB3 directly interacts with the hydroxylase PHD2 to promote HIFα hydroxylation RHOBTB3 also directly interacts with the von Hippel Lindau VHL protein a component of the E3 ubiquitin ligase complex facilitating ubiquitination of HIFα Remarkably RHOBTB3 dimerizes with LIMD1 and constructs a RHOBTB3 LIMD1 PHD2 VHL HIFα complex to effect the maximal degradation of HIFα Hypoxia reduces the RHOBTB3 centered complex formation resulting in an accumulation of HIFα Importantly the expression level of RHOBTB3 is greatly reduced in human renal carcinomas and RHOBTB3 deficiency significantly elevates the Warburg effect and accelerates xenograft growth Our work thus reveals that RHOBTB3 serves as a scaffold to organize a multi subunit complex that promotes the hydroxylation ubiquitination and degradation of HIFα Crystal structure of the Ego1 Ego2 Ego3 complex and its role in promoting Rag GTPase dependent TORC1 signaling FREE Katie Powis 1 Tianlong Zhang 2 Nicolas Panchaud 1 Rong Wang 2 Claudio De Virgilio 1 and Jianping Ding 2 10 1038 cr 2015 86 Full Text PDF The target of rapamycin complex 1 TORC1 integrates various hormonal and nutrient signals to regulate cell growth proliferation and differentiation Amino acid dependent activation of TORC1 is mediated via the yeast EGO complex EGOC consisting of Gtr1 Gtr2 Ego1 and Ego3 Here we identify the previously uncharacterized Ycr075w a Ego2 protein as an additional EGOC component that is required for the integrity and localization of the heterodimeric Gtr1 Gtr2 GTPases equivalent to mammalian Rag GTPases We also report the crystal structure of the Ego1 Ego2 Ego3 ternary complex EGO TC at 2 4 Å resolution in which Ego2 and Ego3 form a heterodimer flanked along one side by Ego1 Structural data also reveal the structural conservation of protein components between the yeast EGO TC and the human Ragulator which acts as a GEF for Rag GTPases Interestingly however artificial tethering of Gtr1 Gtr2 to the vacuolar membrane is sufficient to activate TORC1 in response to amino acids even in the absence of the EGO TC Our structural and functional data therefore support a model in which the EGO TC acts as a scaffold for Rag GTPases in TORC1 signaling Substrate bound structure of the E coli multidrug resistance

    Original URL path: http://www.cell-research.com/artsmore.asp?id=188 (2016-02-14)
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  • Cell Research
    1 4 Ji Wei 1 Chen Hong Ding 1 Ren Xin Feng 1 Xin Zeng 1 Yue Xiang Chen 1 Jin Ding 3 Lei Qiu 2 Zhen Lin Hu 2 Xin Zhang 1 Hong Yang Wang 3 Jun Ping Zhang 2 and Wei Fen Xie 1 10 1038 cr 2015 84 Full Text PDF Hepatocytes are critical for the maintenance of liver homeostasis but its involvement in hepatic fibrogenesis remains elusive Hepatocyte nuclear factor 1α HNF1α is a liver enriched transcription factor that plays a key role in hepatocyte function Our previous study revealed a significant inhibitory effect of HNF1α on hepatocellular carcinoma In this study we report that the expression of HNF1α is significantly repressed in both human and rat fibrotic liver Knockdown of HNF1α in the liver significantly aggravates hepatic fibrogenesis in either dimethylnitrosamine DMN or bile duct ligation BDL model in rats In contrast forced expression of HNF1α markedly alleviates hepatic fibrosis HNF1α regulates the transcriptional expression of SH2 domain containing phosphatase 1 SHP 1 via directly binding to SHP 1 promoter in hepatocytes Inhibition of SHP 1 expression abrogates the anti fibrotic effect of HNF1α in DMN treated rats Moreover HNF1α repression in primary hepatocytes leads to the activation of NF κB and JAK STAT pathways and initiates an inflammatory feedback circuit consisting of HNF1α SHP 1 STAT3 p65 miR 21 and miR 146a which sustains the deregulation of HNF1α in hepatocytes More interestingly a coordinated crosstalk between hepatocytes and hepatic stellate cells HSCs participates in this positive feedback circuit and facilitates the progression of hepatocellular damage Our findings demonstrate that impaired hepatocytes play an active role in hepatic fibrogenesis Early intervention of HNF1α regulated inflammatory feedback loop in hepatocytes may have beneficial effects in the treatment of chronic liver diseases Mutation of kri1l causes definitive hematopoiesis failure via PERK dependent excessive autophagy induction OPEN Xiao E Jia 1 4 Ke Ma 1 Tao Xu 1 Lei Gao 1 Shuang Wu 1 Cong Fu 1 Wenjuan Zhang 1 Zhizhang Wang 1 Kaiyu Liu 6 Mei Dong 1 Changbin Jing 1 Chunguang Ren 1 Zhiwei Dong 1 Yi Chen 2 Yi Jin 2 Qiuhua Huang 2 Xing Chang 1 9 Min Deng1 Li Li 8 Lingfei Luo 8 Jun Zhu 7 9 Yongjun Dang 6 Hung Chun Chang 5 Leonard I Zon 3 Yi Zhou 3 Saijuan Chen 2 9 and Weijun Pan 1 9 10 1038 cr 2015 81 Full Text PDF Dysregulation of ribosome biogenesis causes human diseases such as Diamond Blackfan anemia del 5q syndrome and bone marrow failure However the mechanisms of blood disorders in these diseases remain elusive Through genetic mapping molecular cloning and mechanism characterization of the zebrafish mutant cas002 we reveal a novel connection between ribosomal dysfunction and excessive autophagy in the regulation of hematopoietic stem progenitor cells HSPCs cas002 carries a recessive lethal mutation in kri1l gene that encodes an essential component of rRNA small subunit processome We show that Kri1l is required for normal ribosome biogenesis expansion of

    Original URL path: http://www.cell-research.com/artsmore.asp?id=187 (2016-02-14)
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  • Cell Research
    been identified in Neurofibromatosis type 2 and other cancer patients Despite more than two decades of research the upstream regulator of Merlin in the Hippo pathway remains unknown Here we show by high resolution crystal structures that the Lats1 2 binding site on the Merlin FERM domain is physically blocked by Merlin s auto inhibitory tail Angiomotin binding releases the auto inhibition and promotes Merlin s binding to Lats1 2 Phosphorylation of Ser518 outside the Merlin s auto inhibitory tail does not obviously alter Merlin s conformation but instead prevents angiomotin from binding and thus inhibits Hippo pathway kinase activation Cancer causing mutations clustered in the angiomotin binding domain impair angiomotin mediated Merlin activation Our findings reveal that angiomotin and Merlin respectively interface cortical actin filaments and core kinases in Hippo signaling and allow construction of a complete Hippo signaling pathway Activity induced synaptic delivery of the GluN2A containing NMDA receptor is dependent on endoplasmic reticulum chaperone Bip and involved in fear memory FREE Xiao min Zhang 1 2 Xun yi Yan 1 Bin Zhang 1 Qian Yang 1 Mao Ye 1 Wei Cao 1 Wen bin Qiang 1 Li jun Zhu 1 Yong lan Du 1 Xing xing Xu 1 Jia sheng Wang 1 Fei Xu 1 Wei Lu 3 Shuang Qiu 1 Wei Yang 1 and Jian hong Luo 1 10 1038 cr 2015 75 Full Text PDF The N methyl D aspartate receptor NMDAR in adult forebrain is a heterotetramer mainly composed of two GluN1 subunits and two GluN2A and or GluN2B subunits The synaptic expression and relative numbers of GluN2A and GluN2B containing NMDARs play critical roles in controlling Ca2 dependent signaling and synaptic plasticity Previous studies have suggested that the synaptic trafficking of NMDAR subtypes is differentially regulated but the precise molecular mechanism is not yet clear In this study we demonstrated that Bip an endoplasmic reticulum ER chaperone selectively interacted with GluN2A and mediated the neuronal activity induced assembly and synaptic incorporation of the GluN2A containing NMDAR from dendritic ER Furthermore the GluN2A specific synaptic trafficking was effectively disrupted by peptides interrupting the interaction between Bip and GluN2A Interestingly fear conditioning in mice was disrupted by intraperitoneal injection of the interfering peptide before training In summary we have uncovered a novel mechanism for the activity dependent supply of synaptic GluN2A containing NMDARs and demonstrated its relevance to memory formation High mobility group protein mediated transcription requires DNA damage marker γ H2AX FREE Indrabahadur Singh 1 Nihan Ozturk 1 Julio Cordero 1 Aditi Mehta 1 Diya Hasan 1 Claudia Cosentino 2 Carlos Sebastian 2 Marcus Krüger 3 Mario Looso 4 Gianni Carraro 5 Saverio Bellusci 6 9 10 Werner Seeger 7 10 Thomas Braun 8 10 Raul Mostoslavsky 2 and Guillermo Barreto 1 9 10 10 1038 cr 2015 67 Full Text PDF The eukaryotic genome is organized into chromatins the physiological template for DNA dependent processes including replication recombination repair and transcription Chromatin mediated transcription regulation involves DNA methylation chromatin remodeling and histone modifications

    Original URL path: http://www.cell-research.com/artsmore.asp?id=186 (2016-02-14)
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  • Cell Research
    protection during SE Park7 interacts with p47phox to direct NADPH oxidase dependent ROS production and protect against sepsis FREE Wenjun Liu 1 Hailong Wu 1 Lili Chen 1 Yankai Wen 1 Xiaoni Kong 1 and Wei Qiang Gao 1 10 1038 cr 2015 63 Full Text PDF Inappropriate inflammation responses contribute to mortality during sepsis Through Toll like receptors TLRs reactive oxygen species ROS produced by NADPH oxidase could modulate the inflammation responses Parkinson disease autosomal recessive early onset 7 Park7 has a cytoprotective role by eliminating ROS However whether Park7 could modulate inflammation responses and mortality in sepsis is unclear Here we show that compared with wild type mice Park7 mice had significantly increased mortality and bacterial burdens in sepsis model along with markedly decreased systemic and local inflammation and drastically impaired macrophage phagocytosis and bacterial killing abilities Surprisingly LPS and phorbol 12 myristate 13 acetate stimulation failed to induce ROS and proinflammatory cytokine production in Park7 macrophages and Park7 deficient RAW264 7 cells Through its C terminus Park7 binds to p47phox a subunit of the NADPH oxidase to promote NADPH oxidase dependent production of ROS Restoration of Park7 expression rescues ROS production and improves survival in LPS induced sepsis Together our study shows that Park7 has a protective role against sepsis by controlling macrophage activation NADPH oxidase activation and inflammation responses Methylation dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics FREE Gi Bang Koo 1 2 Michael J Morgan 3 Da Gyum Lee 1 Woo Jung Kim 1 2 Jung Ho Yoon 1 2 Ja Seung Koo 4 Seung Il Kim 5 Soo Jung Kim 6 Mi Kwon Son 6 Soon Sun Hong 6 Jean M Mulcahy Levy 7 Daniel A Pollyea 8 Craig T Jordan 8 Pearlly Yan 9 David Frankhouser 9 Deedra Nicolet 9 10 Kati Maharry 9 10 Guido Marcucci 9 Kyeong Sook Choi 1 2 Hyeseong Cho 1 2 Andrew Thorburn 3 and You Sun Kim 1 2 10 1038 cr 2015 56 Full Text PDF Receptor interacting protein kinase 3 RIP3 or RIPK3 is an essential part of the cellular machinery that executes programmed or regulated necrosis Here we show that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy induced cell death However we show that RIP3 expression is often silenced in cancer cells due to genomic methylation near its transcriptional start site thus RIP3 dependent activation of MLKL and downstream programmed necrosis during chemotherapeutic death is largely repressed Nevertheless treatment with hypomethylating agents restores RIP3 expression and thereby promotes sensitivity to chemotherapeutics in a RIP3 dependent manner RIP3 expression is reduced in tumors compared to normal tissue in 85 of breast cancer patients suggesting that RIP3 deficiency is positively selected during tumor growth development Since hypomethylating agents are reasonably well tolerated in patients we propose that RIP3 deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional chemotherapeutics Structural organization of an

    Original URL path: http://www.cell-research.com/artsmore.asp?id=184 (2016-02-14)
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  • Cell Research
    Vol 20 Num 1 February 2010 Vol 20 Num 2 March 2010 Vol 20 Num 3 April 2010 Vol 20 Num 4 May 2010 Vol 20 Num 5 June 2010 Vol 20 Num 6 July 2010 Vol 20 Num 7 August 2010 Vol 20 Num 8 September 2010 Vol 20 Num 9 October 2010 Vol 20 Num 10 November 2010 Vol 20 Num 11 December 2010 Vol 20 Num 12

    Original URL path: http://www.cell-research.com/archive_1.asp?year=2010 (2016-02-14)
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  • Cell Research
    Vol 21 Num 1 February 2011 Vol 21 Num 2 March 2011 Vol 21 Num 3 April 2011 Vol 21 Num 4 May 2011 Vol 21 Num 5 June 2011 Vol 21 Num 6 July 2011 Vol 21 Num 7 August 2011 Vol 21 Num 8 September 2011 Vol 21 Num 9 October 2011 Vol 21 Num 10 November 2011 Vol 21 Num 11 December 2011 Vol 21 Num 12

    Original URL path: http://www.cell-research.com/archive_1.asp?year=2011 (2016-02-14)
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  • Cell Research
    Vol 22 Num 1 February 2012 Vol 22 Num 2 March 2012 Vol 22 Num 3 April 2012 Vol 22 Num 4 May 2012 Vol 22 Num 5 June 2012 Vol 22 Num 6 July 2012 Vol 22 Num 7 August 2012 Vol 22 Num 8 September 2012 Vol 22 Num 9 October 2012 Vol 22 Num 10 November 2012 Vol 22 Num 11 December 2012 Vol 22 Num 12

    Original URL path: http://www.cell-research.com/archive_1.asp?year=2012 (2016-02-14)
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