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  • 1
    Publication Date: 2012-12-22
    Description: The presence of DNA in the cytoplasm of mammalian cells is a danger signal that triggers host immune responses such as the production of type I interferons. Cytosolic DNA induces interferons through the production of cyclic guanosine monophosphate-adenosine monophosphate (cyclic GMP-AMP, or cGAMP), which binds to and activates the adaptor protein STING. Through biochemical fractionation and quantitative mass spectrometry, we identified a cGAMP synthase (cGAS), which belongs to the nucleotidyltransferase family. Overexpression of cGAS activated the transcription factor IRF3 and induced interferon-beta in a STING-dependent manner. Knockdown of cGAS inhibited IRF3 activation and interferon-beta induction by DNA transfection or DNA virus infection. cGAS bound to DNA in the cytoplasm and catalyzed cGAMP synthesis. These results indicate that cGAS is a cytosolic DNA sensor that induces interferons by producing the second messenger cGAMP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863629/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863629/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Lijun -- Wu, Jiaxi -- Du, Fenghe -- Chen, Xiang -- Chen, Zhijian J -- AI-093967/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Feb 15;339(6121):786-91. doi: 10.1126/science.1232458. Epub 2012 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23258413" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Cell Line, Tumor ; Cyclic AMP/biosynthesis ; Cyclic GMP/biosynthesis ; Cytidine Triphosphate/metabolism ; Cytosol/enzymology/*immunology ; DNA/*immunology/metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Interferon Type I/*biosynthesis ; Interferon-beta/*biosynthesis ; Metabolic Networks and Pathways ; Mice ; Molecular Sequence Data ; Nucleotidyltransferases/genetics/isolation & purification/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2012-06-05
    Description: How environmental cues regulate adult stem cell and cancer cell activity through surface receptors is poorly understood. Angiopoietin-like proteins (ANGPTLs), a family of seven secreted glycoproteins, are known to support the activity of haematopoietic stem cells (HSCs) in vitro and in vivo. ANGPTLs also have important roles in lipid metabolism, angiogenesis and inflammation, but were considered 'orphan ligands' because no receptors were identified. Here we show that the immune-inhibitory receptor human leukocyte immunoglobulin-like receptor B2 (LILRB2) and its mouse orthologue paired immunoglobulin-like receptor (PIRB) are receptors for several ANGPTLs. LILRB2 and PIRB are expressed on human and mouse HSCs, respectively, and the binding of ANGPTLs to these receptors supported ex vivo expansion of HSCs. In mouse transplantation acute myeloid leukaemia models, a deficiency in intracellular signalling of PIRB resulted in increased differentiation of leukaemia cells, revealing that PIRB supports leukaemia development. Our study indicates an unexpected functional significance of classical immune-inhibitory receptors in maintenance of stemness of normal adult stem cells and in support of cancer development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367397/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367397/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Junke -- Umikawa, Masato -- Cui, Changhao -- Li, Jiyuan -- Chen, Xiaoli -- Zhang, Chaozheng -- Huynh, HoangDinh -- Kang, Xunlei -- Silvany, Robert -- Wan, Xuan -- Ye, Jingxiao -- Canto, Alberto Puig -- Chen, Shu-Hsia -- Wang, Huan-You -- Ward, E Sally -- Zhang, Cheng Cheng -- K01 CA 120099/CA/NCI NIH HHS/ -- K01 CA120099/CA/NCI NIH HHS/ -- K01 CA120099-03/CA/NCI NIH HHS/ -- K01 CA120099-04/CA/NCI NIH HHS/ -- K01 CA120099-05/CA/NCI NIH HHS/ -- K01 CA120099-06/CA/NCI NIH HHS/ -- R01 CA109322/CA/NCI NIH HHS/ -- R01 CA172268/CA/NCI NIH HHS/ -- England -- Nature. 2012 May 30;485(7400):656-60. doi: 10.1038/nature11095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Physiology and Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Disease Models, Animal ; Fetal Blood/cytology/metabolism ; HEK293 Cells ; Hematopoietic Stem Cells/*cytology/*metabolism ; Humans ; Leukemia/*metabolism/*pathology ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; Myeloid-Lymphoid Leukemia Protein ; Receptors, Immunologic/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2012-01-13
    Description: Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly following RB1 inactivation but the underlying mechanism is not known. Here we show that the retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulated. To identify the mutations that cooperate with RB1 loss, we performed whole-genome sequencing of retinoblastomas. The overall mutational rate was very low; RB1 was the only known cancer gene mutated. We then evaluated the role of RB1 in genome stability and considered non-genetic mechanisms of cancer pathway deregulation. For example, the proto-oncogene SYK is upregulated in retinoblastoma and is required for tumour cell survival. Targeting SYK with a small-molecule inhibitor induced retinoblastoma tumour cell death in vitro and in vivo. Thus, retinoblastomas may develop quickly as a result of the epigenetic deregulation of key cancer pathways as a direct or indirect result of RB1 loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289956/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289956/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jinghui -- Benavente, Claudia A -- McEvoy, Justina -- Flores-Otero, Jacqueline -- Ding, Li -- Chen, Xiang -- Ulyanov, Anatoly -- Wu, Gang -- Wilson, Matthew -- Wang, Jianmin -- Brennan, Rachel -- Rusch, Michael -- Manning, Amity L -- Ma, Jing -- Easton, John -- Shurtleff, Sheila -- Mullighan, Charles -- Pounds, Stanley -- Mukatira, Suraj -- Gupta, Pankaj -- Neale, Geoff -- Zhao, David -- Lu, Charles -- Fulton, Robert S -- Fulton, Lucinda L -- Hong, Xin -- Dooling, David J -- Ochoa, Kerri -- Naeve, Clayton -- Dyson, Nicholas J -- Mardis, Elaine R -- Bahrami, Armita -- Ellison, David -- Wilson, Richard K -- Downing, James R -- Dyer, Michael A -- CA21765/CA/NCI NIH HHS/ -- CA64402/CA/NCI NIH HHS/ -- EY014867/EY/NEI NIH HHS/ -- EY018599/EY/NEI NIH HHS/ -- GM81607/GM/NIGMS NIH HHS/ -- R01 CA155202/CA/NCI NIH HHS/ -- R01 EY014867/EY/NEI NIH HHS/ -- R01 EY014867-02/EY/NEI NIH HHS/ -- R01 EY018599/EY/NEI NIH HHS/ -- R01 EY018599-03/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jan 11;481(7381):329-34. doi: 10.1038/nature10733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237022" target="_blank"〉PubMed〈/a〉
    Keywords: Aneuploidy ; Animals ; Cell Death/drug effects ; Cell Line ; Cell Survival/drug effects ; Chromosomal Instability/genetics ; Epigenesis, Genetic/*genetics ; Gene Expression Regulation, Neoplastic ; Genes, Retinoblastoma/genetics ; *Genomics ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & ; inhibitors/genetics/metabolism ; Mice ; *Molecular Targeted Therapy ; Mutation/genetics ; Protein Kinase Inhibitors/*pharmacology/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors/genetics/metabolism ; Retinoblastoma/*drug therapy/*genetics/pathology ; Retinoblastoma Protein/deficiency/genetics ; Sequence Analysis, DNA ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-12-04
    Description: Ionic protein-lipid interactions are critical for the structure and function of membrane receptors, ion channels, integrins and many other proteins. However, the regulatory mechanism of these interactions is largely unknown. Here we show that Ca(2+) can bind directly to anionic phospholipids and thus modulate membrane protein function. The activation of T-cell antigen receptor-CD3 complex (TCR), a key membrane receptor for adaptive immunity, is regulated by ionic interactions between positively charged CD3epsilon/zeta cytoplasmic domains (CD3(CD)) and negatively charged phospholipids in the plasma membrane. Crucial tyrosines are buried in the membrane and are largely protected from phosphorylation in resting T cells. It is not clear how CD3(CD) dissociates from the membrane in antigen-stimulated T cells. The antigen engagement of even a single TCR triggers a Ca(2+) influx and TCR-proximal Ca(2+) concentration is higher than the average cytosolic Ca(2+) concentration. Our biochemical, live-cell fluorescence resonance energy transfer and NMR experiments showed that an increase in Ca(2+) concentration induced the dissociation of CD3(CD) from the membrane and the solvent exposure of tyrosine residues. As a consequence, CD3 tyrosine phosphorylation was significantly enhanced by Ca(2+) influx. Moreover, when compared with wild-type cells, Ca(2+) channel-deficient T cells had substantially lower levels of CD3 phosphorylation after stimulation. The effect of Ca(2+) on facilitating CD3 phosphorylation is primarily due to the charge of this ion, as demonstrated by the fact that replacing Ca(2+) with the non-physiological ion Sr(2+) resulted in the same feedback effect. Finally, (31)P NMR spectroscopy showed that Ca(2+) bound to the phosphate group in anionic phospholipids at physiological concentrations, thus neutralizing the negative charge of phospholipids. Rather than initiating CD3 phosphorylation, this regulatory pathway of Ca(2+) has a positive feedback effect on amplifying and sustaining CD3 phosphorylation and should enhance T-cell sensitivity to foreign antigens. Our study thus provides a new regulatory mechanism of Ca(2+) to T-cell activation involving direct lipid manipulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Xiaoshan -- Bi, Yunchen -- Yang, Wei -- Guo, Xingdong -- Jiang, Yan -- Wan, Chanjuan -- Li, Lunyi -- Bai, Yibing -- Guo, Jun -- Wang, Yujuan -- Chen, Xiangjun -- Wu, Bo -- Sun, Hongbin -- Liu, Wanli -- Wang, Junfeng -- Xu, Chenqi -- England -- Nature. 2013 Jan 3;493(7430):111-5. doi: 10.1038/nature11699. Epub 2012 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23201688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism/pharmacology ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Feedback, Physiological/drug effects ; Humans ; Jurkat Cells ; Lipid Bilayers/chemistry/metabolism ; *Lymphocyte Activation/drug effects ; Mice ; Phospholipids/*chemistry/*metabolism ; Phosphorylation/drug effects ; Receptor-CD3 Complex, Antigen, T-Cell/drug effects/immunology/*metabolism ; *Signal Transduction/drug effects ; Solvents/chemistry/metabolism ; Static Electricity ; T-Lymphocytes/drug effects/immunology/*metabolism ; Tyrosine/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-06-23
    Description: Medulloblastoma is a malignant childhood brain tumour comprising four discrete subgroups. Here, to identify mutations that drive medulloblastoma, we sequenced the entire genomes of 37 tumours and matched normal blood. One-hundred and thirty-six genes harbouring somatic mutations in this discovery set were sequenced in an additional 56 medulloblastomas. Recurrent mutations were detected in 41 genes not yet implicated in medulloblastoma; several target distinct components of the epigenetic machinery in different disease subgroups, such as regulators of H3K27 and H3K4 trimethylation in subgroups 3 and 4 (for example, KDM6A and ZMYM3), and CTNNB1-associated chromatin re-modellers in WNT-subgroup tumours (for example, SMARCA4 and CREBBP). Modelling of mutations in mouse lower rhombic lip progenitors that generate WNT-subgroup tumours identified genes that maintain this cell lineage (DDX3X), as well as mutated genes that initiate (CDH1) or cooperate (PIK3CA) in tumorigenesis. These data provide important new insights into the pathogenesis of medulloblastoma subgroups and highlight targets for therapeutic development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412905/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412905/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, Giles -- Parker, Matthew -- Kranenburg, Tanya A -- Lu, Charles -- Chen, Xiang -- Ding, Li -- Phoenix, Timothy N -- Hedlund, Erin -- Wei, Lei -- Zhu, Xiaoyan -- Chalhoub, Nader -- Baker, Suzanne J -- Huether, Robert -- Kriwacki, Richard -- Curley, Natasha -- Thiruvenkatam, Radhika -- Wang, Jianmin -- Wu, Gang -- Rusch, Michael -- Hong, Xin -- Becksfort, Jared -- Gupta, Pankaj -- Ma, Jing -- Easton, John -- Vadodaria, Bhavin -- Onar-Thomas, Arzu -- Lin, Tong -- Li, Shaoyi -- Pounds, Stanley -- Paugh, Steven -- Zhao, David -- Kawauchi, Daisuke -- Roussel, Martine F -- Finkelstein, David -- Ellison, David W -- Lau, Ching C -- Bouffet, Eric -- Hassall, Tim -- Gururangan, Sridharan -- Cohn, Richard -- Fulton, Robert S -- Fulton, Lucinda L -- Dooling, David J -- Ochoa, Kerri -- Gajjar, Amar -- Mardis, Elaine R -- Wilson, Richard K -- Downing, James R -- Zhang, Jinghui -- Gilbertson, Richard J -- P01 CA096832/CA/NCI NIH HHS/ -- P01CA96832/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01CA129541/CA/NCI NIH HHS/ -- England -- Nature. 2012 Aug 2;488(7409):43-8. doi: 10.1038/nature11213.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉St Jude Children's Research Hospital, Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CREB-Binding Protein/genetics ; Cadherins/genetics ; Cdh1 Proteins ; Cell Cycle Proteins/deficiency/genetics ; Cell Lineage ; Cerebellar Neoplasms/*classification/*genetics/pathology ; Child ; DEAD-box RNA Helicases/genetics ; DNA Copy Number Variations ; DNA Helicases/genetics ; DNA Mutational Analysis ; Disease Models, Animal ; Genome, Human/genetics ; Genomics ; Hedgehog Proteins/metabolism ; Histone Demethylases/genetics ; Histones/metabolism ; Humans ; Medulloblastoma/*classification/*genetics/pathology ; Methylation ; Mice ; Mutation/*genetics ; Nuclear Proteins/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Transcription Factors/genetics ; Wnt Proteins/metabolism ; beta Catenin/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-12-22
    Description: Cytosolic DNA induces type I interferons and other cytokines that are important for antimicrobial defense but can also result in autoimmunity. This DNA signaling pathway requires the adaptor protein STING and the transcription factor IRF3, but the mechanism of DNA sensing is unclear. We found that mammalian cytosolic extracts synthesized cyclic guanosine monophosphate-adenosine monophosphate (cyclic GMP-AMP, or cGAMP) in vitro from adenosine triphosphate and guanosine triphosphate in the presence of DNA but not RNA. DNA transfection or DNA virus infection of mammalian cells also triggered cGAMP production. cGAMP bound to STING, leading to the activation of IRF3 and induction of interferon-beta. Thus, cGAMP functions as an endogenous second messenger in metazoans and triggers interferon production in response to cytosolic DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3855410/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3855410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jiaxi -- Sun, Lijun -- Chen, Xiang -- Du, Fenghe -- Shi, Heping -- Chen, Chuo -- Chen, Zhijian J -- AI-093967/AI/NIAID NIH HHS/ -- GM-079554/GM/NIGMS NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- R01 GM079554/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Feb 15;339(6121):826-30. doi: 10.1126/science.1229963. Epub 2012 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23258412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Extracts/chemistry ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic GMP/*metabolism ; Cytosol/*immunology ; DNA/*immunology ; HEK293 Cells ; Herpesvirus 1, Human/immunology ; Humans ; *Immunity, Innate ; Interferon Regulatory Factor-3/metabolism ; Interferon-beta/biosynthesis ; Membrane Proteins/genetics/metabolism ; Mice ; Nucleotides, Cyclic/*metabolism ; RNA Interference ; Second Messenger Systems/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2012-04-06
    Description: Author(s): Z. Y. Zhao, X. G. Liu, Z. Z. He, X. M. Wang, C. Fan, W. P. Ke, Q. J. Li, L. M. Chen, X. Zhao, and X. F. Sun The very-low-temperature thermal conductivity ( κ ) is studied for BaCo 2 V 2 O 8 , a quasi-one-dimensional Ising-like antiferromagnet exhibiting an unusual magnetic-field-induced order-to-disorder transition. The nearly isotropic transport in the longitudinal field indicates that the magnetic excitations s... [Phys. Rev. B 85, 134412] Published Thu Apr 05, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 8
    Publication Date: 2012-05-31
    Description: Author(s): Q. J. Li, Z. Y. Zhao, H. D. Zhou, W. P. Ke, X. M. Wang, C. Fan, X. G. Liu, L. M. Chen, X. Zhao, and X. F. Sun We study the low-temperature heat transport of Nd 3 Ga 5 SiO 14 , which is a spin-liquid candidate, to probe the nature of the ground state and the effect of the magnetic field on the magnetic properties. The thermal conductivity ( κ ) shows a purely phononic transport in zero field. The external magnetic f... [Phys. Rev. B 85, 174438] Published Wed May 30, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
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  • 9
    Publication Date: 2012-11-17
    Description: Author(s): X. M. Wang, Z. Y. Zhao, C. Fan, X. G. Liu, Q. J. Li, F. B. Zhang, L. M. Chen, X. Zhao, and X. F. Sun We study the low-temperature heat transport, as well as the magnetization and the specific heat, of TmMnO 3 single crystals to probe the transitions of magnetic structure induced by magnetic field. It is found that the low- T thermal conductivity ( κ ) shows strong magnetic-field dependence and the over... [Phys. Rev. B 86, 174413] Published Fri Nov 16, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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