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  • 1
    Publication Date: 2013-01-03
    Description: Author(s): H.-C. Su, M.-J. Huang, H.-J. Lin, C.-H. Lee, C.-T. Chen, C.-H. Liu, H.-F. Hsu, K.-W. Lin, and J. van Lierop The overall and element specific magnetism in an exchange biased [Ni 80 Fe 20 /Mn] 3 film system, with film layers 3.5 nm thick, has been studied to examine the magnetism between interfacial Mn, Ni, and Fe spins. Field-cooling the film results in large exchange bias loop shifts at temperatures from 2 to ... [Phys. Rev. B 87, 014402] Published Wed Jan 02, 2013
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 2
    Publication Date: 2011-06-01
    Description: Author(s): R. H. Liu, J. S. Zhang, P. Cheng, X. G. Luo, J. J. Ying, Y. J. Yan, M. Zhang, A. F. Wang, Z. J. Xiang, G. J. Ye, and X. H. Chen The new layered manganese oxychalcogenides (LaO) 2 Mn 2 Se 2 O and (BaF) 2 Mn 2 Se 2 O, isostructural to (LaO) 2 Fe 2 Se 2 O, were synthesized by solid state reaction method. The single crystals of the former compound were also successfully grown using fusion method. The polycrystalline samples show the semiconductin... [Phys. Rev. B 83, 174450] Published Tue May 31, 2011
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 3
    Publication Date: 2012-07-19
    Description: Author(s): S. Le Gall, J. Cucchiara, M. Gottwald, C. Berthelot, C.-H. Lambert, Y. Henry, D. Bedau, D. B. Gopman, H. Liu, A. D. Kent, J. Z. Sun, W. Lin, D. Ravelosona, J. A. Katine, Eric E. Fullerton, and S. Mangin The spin-torque switching of metallic nanopillar spin valves showing strong perpendicular anisotropy are studied. The magnetic states of the layers depend on extrinsic parameters such as the magnetic field and the dc current applied to the device. A state diagram presents a comprehensive graph of th... [Phys. Rev. B 86, 014419] Published Wed Jul 18, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 4
    Publication Date: 2012-06-20
    Description: Author(s): H. Liu, D. Bedau, J. Z. Sun, S. Mangin, E. E. Fullerton, J. A. Katine, and A. D. Kent We present a two-current-pulse temporal correlation experiment to study the intrinsic subnanosecond nonequilibrium magnetic dynamics of a nanomagnet during and following a pulse excitation. This method is applied to a model spin-transfer system, a spin-valve nanopillar with perpendicular magnetic an... [Phys. Rev. B 85, 220405] Published Tue Jun 19, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
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  • 5
    Publication Date: 2011-11-29
    Description: Author(s): R. H. Liu, M. Zhang, P. Cheng, Y. J. Yan, Z. J. Xiang, J. J. Ying, X. F. Wang, A. F. Wang, G. J. Ye, X. G. Luo, and X. H. Chen [Phys. Rev. B 84, 184432] Published Mon Nov 28, 2011
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 6
    Publication Date: 2001-04-03
    Description: We report the development of a pseudorabies virus that can be used for retrograde tracing from selected neurons. This virus encodes a green fluorescent protein marker and replicates only in neurons that express the Cre recombinase and in neurons in synaptic contact with the originally infected cells. The virus was injected into the arcuate nucleus of mice that express Cre only in those neurons that express neuropeptide Y or the leptin receptor. Sectioning of the brains revealed that these neurons receive inputs from neurons in other regions of the hypothalamus, as well as the amygdala, cortex, and other brain regions. These data suggest that higher cortical centers modulate leptin signaling in the hypothalamus. This method of neural tracing may prove useful in studies of other complex neural circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeFalco, J -- Tomishima, M -- Liu, H -- Zhao, C -- Cai, X -- Marth, J D -- Enquist, L -- Friedman, J M -- DK48247/DK/NIDDK NIH HHS/ -- R01133506/PHS HHS/ -- R01DK41096/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Mar 30;291(5513):2608-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11283374" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Arcuate Nucleus of Hypothalamus/cytology/*physiology/virology ; Brain/cytology/*physiology/virology ; Brain Mapping ; Carrier Proteins/genetics/metabolism ; Chromosomes, Artificial, Bacterial ; *Eating ; Gene Expression ; Green Fluorescent Proteins ; Herpesvirus 1, Suid/*genetics/physiology ; Hypothalamus/cytology/*physiology/virology ; Integrases/genetics/metabolism ; Luminescent Proteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurons/*metabolism/virology ; Neuropeptide Y/genetics/metabolism ; *Receptors, Cell Surface ; Receptors, Leptin ; Recombinant Fusion Proteins/metabolism ; Recombination, Genetic ; *Viral Proteins ; Virus Replication ; tau Proteins/genetics/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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  • 7
    Publication Date: 2001-09-22
    Description: SLAP-130/Fyb (SLP-76-associated phosphoprotein or Fyn-binding protein; also known as Fyb/Slap) is a hematopoietic-specific adapter, which associates with and modulates function of SH2-containing leukocyte phosphoprotein of 76 kilodaltons (SLP-76). T cells from mice lacking SLAP-130/Fyb show markedly impaired proliferation following CD3 engagement. In addition, the T cell receptor (TCR) in SLAP-130/Fyb mutant cells fails to enhance integrin-dependent adhesion. Although TCR-induced actin polymerization is normal, TCR-stimulated clustering of the integrin LFA-1 is defective in SLAP-130/Fyb-deficient cells. These data indicate that SLAP-130/Fyb is important for coupling TCR-mediated actin cytoskeletal rearrangement with activation of integrin function, and for T cells to respond fully to activating signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peterson, E J -- Woods, M L -- Dmowski, S A -- Derimanov, G -- Jordan, M S -- Wu, J N -- Myung, P S -- Liu, Q H -- Pribila, J T -- Freedman, B D -- Shimizu, Y -- Koretzky, G A -- R01 AI060921/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2001 Sep 21;293(5538):2263-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Abramson Family Cancer Research Institute, Department of Medicine, School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11567141" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/metabolism ; Antigens, CD3/immunology ; Antigens, Differentiation, T-Lymphocyte/metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Adhesion ; Cell Membrane/metabolism ; Immunologic Capping ; Intercellular Adhesion Molecule-1/metabolism ; Interleukin-2/biosynthesis/pharmacology ; Lectins, C-Type ; Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/*physiology ; Mice ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/genetics/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Receptors, Interleukin-2/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/metabolism/*physiology
    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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  • 8
    Publication Date: 2010-09-08
    Description: Cell cycle checkpoints are implemented to safeguard the genome, avoiding the accumulation of genetic errors. Checkpoint loss results in genomic instability and contributes to the evolution of cancer. Among G1-, S-, G2- and M-phase checkpoints, genetic studies indicate the role of an intact S-phase checkpoint in maintaining genome integrity. Although the basic framework of the S-phase checkpoint in multicellular organisms has been outlined, the mechanistic details remain to be elucidated. Human chromosome-11 band-q23 translocations disrupting the MLL gene lead to poor prognostic leukaemias. Here we assign MLL as a novel effector in the mammalian S-phase checkpoint network and identify checkpoint dysfunction as an underlying mechanism of MLL leukaemias. MLL is phosphorylated at serine 516 by ATR in response to genotoxic stress in the S phase, which disrupts its interaction with, and hence its degradation by, the SCF(Skp2) E3 ligase, leading to its accumulation. Stabilized MLL protein accumulates on chromatin, methylates histone H3 lysine 4 at late replication origins and inhibits the loading of CDC45 to delay DNA replication. Cells deficient in MLL showed radioresistant DNA synthesis and chromatid-type genomic abnormalities, indicative of S-phase checkpoint dysfunction. Reconstitution of Mll(-/-) (Mll also known as Mll1) mouse embryonic fibroblasts with wild-type but not S516A or DeltaSET mutant MLL rescues the S-phase checkpoint defects. Moreover, murine myeloid progenitor cells carrying an Mll-CBP knock-in allele that mimics human t(11;16) leukaemia show a severe radioresistant DNA synthesis phenotype. MLL fusions function as dominant negative mutants that abrogate the ATR-mediated phosphorylation/stabilization of wild-type MLL on damage to DNA, and thus compromise the S-phase checkpoint. Together, our results identify MLL as a key constituent of the mammalian DNA damage response pathway and show that deregulation of the S-phase checkpoint incurred by MLL translocations probably contributes to the pathogenesis of human MLL leukaemias.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940944/" 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/PMC2940944/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Han -- Takeda, Shugaku -- Kumar, Rakesh -- Westergard, Todd D -- Brown, Eric J -- Pandita, Tej K -- Cheng, Emily H-Y -- Hsieh, James J-D -- CA119008/CA/NCI NIH HHS/ -- CA123232/CA/NCI NIH HHS/ -- CA129537/CA/NCI NIH HHS/ -- R01 CA119008/CA/NCI NIH HHS/ -- R01 CA119008-01/CA/NCI NIH HHS/ -- R01 CA119008-02/CA/NCI NIH HHS/ -- R01 CA119008-03/CA/NCI NIH HHS/ -- R01 CA119008-04/CA/NCI NIH HHS/ -- R01 CA119008-05/CA/NCI NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):343-6. doi: 10.1038/nature09350. Epub 2010 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20818375" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA Damage ; DNA Replication/physiology ; Genes, Dominant/genetics ; Genomic Instability/physiology ; Histone-Lysine N-Methyltransferase ; Histones/chemistry/metabolism ; Humans ; Leukemia/genetics ; Lysine/metabolism ; Methylation ; Mice ; Myeloid Progenitor Cells/metabolism ; Myeloid-Lymphoid Leukemia Protein/chemistry/deficiency/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Binding ; Protein-Serine-Threonine Kinases/*metabolism ; S Phase/*physiology ; S-Phase Kinase-Associated Proteins/metabolism ; Signal Transduction ; Translocation, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2009-05-01
    Description: Mice deficient in the Polycomb repressor Bmi1 develop numerous abnormalities including a severe defect in stem cell self-renewal, alterations in thymocyte maturation and a shortened lifespan. Previous work has implicated de-repression of the Ink4a/Arf (also known as Cdkn2a) locus as mediating many of the aspects of the Bmi1(-/-) phenotype. Here we demonstrate that cells derived from Bmi1(-/-) mice also have impaired mitochondrial function, a marked increase in the intracellular levels of reactive oxygen species and subsequent engagement of the DNA damage response pathway. Furthermore, many of the deficiencies normally observed in Bmi1(-/-) mice improve after either pharmacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage response pathway by Chk2 (also known as Chek2) deletion. These results demonstrate that Bmi1 has an unexpected role in maintaining mitochondrial function and redox homeostasis and indicate that the Polycomb family of proteins can coordinately regulate cellular metabolism with stem and progenitor cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721521/" 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/PMC4721521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jie -- Cao, Liu -- Chen, Jichun -- Song, Shiwei -- Lee, In Hye -- Quijano, Celia -- Liu, Hongjun -- Keyvanfar, Keyvan -- Chen, Haoqian -- Cao, Long-Yue -- Ahn, Bong-Hyun -- Kumar, Neil G -- Rovira, Ilsa I -- Xu, Xiao-Ling -- van Lohuizen, Maarten -- Motoyama, Noboru -- Deng, Chu-Xia -- Finkel, Toren -- R00 AG032356/AG/NIA NIH HHS/ -- Z01 HL005012-11/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 May 21;459(7245):387-92. doi: 10.1038/nature08040. Epub 2009 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19404261" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/pharmacology ; Animals ; Antioxidants/pharmacology ; Checkpoint Kinase 2 ; *DNA Damage/genetics ; Female ; Male ; Mice ; Mitochondria/*metabolism ; Nuclear Proteins/deficiency/genetics/*metabolism ; Oxidation-Reduction/drug effects ; Polycomb Repressive Complex 1 ; Protein-Serine-Threonine Kinases/deficiency/genetics ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Repressor Proteins/genetics/*metabolism ; Stem Cells/cytology/drug effects/metabolism ; Thymus Gland/cytology/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2010-06-18
    Description: Sialic acid acetylesterase (SIAE) is an enzyme that negatively regulates B lymphocyte antigen receptor signalling and is required for the maintenance of immunological tolerance in mice. Heterozygous loss-of-function germline rare variants and a homozygous defective polymorphic variant of SIAE were identified in 24/923 subjects of European origin with relatively common autoimmune disorders and in 2/648 controls of European origin. All heterozygous loss-of-function SIAE mutations tested were capable of functioning in a dominant negative manner. A homozygous secretion-defective polymorphic variant of SIAE was catalytically active, lacked the ability to function in a dominant negative manner, and was seen in eight autoimmune subjects but in no control subjects. The odds ratio for inheriting defective SIAE alleles was 8.6 in all autoimmune subjects, 8.3 in subjects with rheumatoid arthritis, and 7.9 in subjects with type I diabetes. Functionally defective SIAE rare and polymorphic variants represent a strong genetic link to susceptibility in relatively common human autoimmune disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900412/" 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/PMC2900412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surolia, Ira -- Pirnie, Stephan P -- Chellappa, Vasant -- Taylor, Kendra N -- Cariappa, Annaiah -- Moya, Jesse -- Liu, Haoyuan -- Bell, Daphne W -- Driscoll, David R -- Diederichs, Sven -- Haider, Khaleda -- Netravali, Ilka -- Le, Sheila -- Elia, Roberto -- Dow, Ethan -- Lee, Annette -- Freudenberg, Jan -- De Jager, Philip L -- Chretien, Yves -- Varki, Ajit -- MacDonald, Marcy E -- Gillis, Tammy -- Behrens, Timothy W -- Bloch, Donald -- Collier, Deborah -- Korzenik, Joshua -- Podolsky, Daniel K -- Hafler, David -- Murali, Mandakolathur -- Sands, Bruce -- Stone, John H -- Gregersen, Peter K -- Pillai, Shiv -- AI 064930/AI/NIAID NIH HHS/ -- AI 068759/AI/NIAID NIH HHS/ -- AI 076505/AI/NIAID NIH HHS/ -- AR 022263/AR/NIAMS NIH HHS/ -- AR 044422/AR/NIAMS NIH HHS/ -- AR 058481/AR/NIAMS NIH HHS/ -- NS 32765/NS/NINDS NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI064930/AI/NIAID NIH HHS/ -- R01 AI064930-04/AI/NIAID NIH HHS/ -- R01 AI068759/AI/NIAID NIH HHS/ -- R01 AI068759-05/AI/NIAID NIH HHS/ -- R01 AI076505/AI/NIAID NIH HHS/ -- R01 AI076505-02/AI/NIAID NIH HHS/ -- R01 AR044422/AR/NIAMS NIH HHS/ -- R01 AR044422-13/AR/NIAMS NIH HHS/ -- RC1 AR058481/AR/NIAMS NIH HHS/ -- RC1 AR058481-01/AR/NIAMS NIH HHS/ -- England -- Nature. 2010 Jul 8;466(7303):243-7. doi: 10.1038/nature09115. Epub 2010 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20555325" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetylesterase/*genetics/metabolism/secretion ; Alleles ; Animals ; Antibodies, Antinuclear/blood ; Arthritis, Rheumatoid/enzymology/genetics ; Autoimmune Diseases/*enzymology/*genetics ; Autoimmunity/*genetics ; B-Lymphocytes/metabolism ; Biocatalysis ; Carboxylic Ester Hydrolases/*genetics/metabolism/secretion ; Case-Control Studies ; Cell Line ; Diabetes Mellitus, Type 1/enzymology/genetics ; Europe/ethnology ; Exons/genetics ; Genetic Predisposition to Disease/*genetics ; Germ-Line Mutation/*genetics ; Humans ; Mice ; N-Acetylneuraminic Acid/*metabolism ; Odds Ratio ; Polymorphism, Single Nucleotide/genetics ; Sample Size ; Sequence Analysis, DNA
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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