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  • 1
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    Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-22
    Description: Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X chromosome (Deltam) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in Deltam female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967734/" 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/PMC2967734/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Jongdae -- Bossenz, Michael -- Chung, Young -- Ma, Hong -- Byron, Meg -- Taniguchi-Ishigaki, Naoko -- Zhu, Xiaochun -- Jiao, Baowei -- Hall, Lisa L -- Green, Michael R -- Jones, Stephen N -- Hermans-Borgmeyer, Irm -- Lawrence, Jeanne B -- Bach, Ingolf -- 5 P30 DK32520/DK/NIDDK NIH HHS/ -- DK32520/DK/NIDDK NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 CA131158/CA/NCI NIH HHS/ -- R01 CA131158-04/CA/NCI NIH HHS/ -- R01 GM033977/GM/NIGMS NIH HHS/ -- R01 GM053234/GM/NIGMS NIH HHS/ -- R01CA131158/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Oct 21;467(7318):977-81. doi: 10.1038/nature09457.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS), Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Congenic ; Blastocyst/metabolism ; Cell Line ; Chromosomes, Mammalian/*genetics ; Embryo Loss/genetics ; Fathers ; Female ; Gene Silencing ; *Genomic Imprinting ; Male ; Mice ; Mice, Transgenic ; *Mothers ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Repressor Proteins/deficiency/genetics/*metabolism ; Ubiquitin-Protein Ligases ; X Chromosome/*genetics ; X Chromosome Inactivation/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    CKAMP44: a brain-specific protein attenuating short-term synaptic plasticity in the dentate gyrus (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: CKAMP44, identified here by a proteomic approach, is a brain-specific type I transmembrane protein that associates with AMPA receptors in synaptic spines. CKAMP44 expressed in Xenopus oocytes reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl-D-aspartate (NMDA) receptor-mediated currents. Mouse hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance, and overexpression of CKAMP44 led to stronger and faster AMPA receptor desensitization, slower recovery from desensitization, and a reduction in the paired-pulse ratio of AMPA currents. By contrast, dentate gyrus granule cells exhibited strong CKAMP44 expression, and CKAMP44 knockout increased the paired-pulse ratio of AMPA currents in lateral and medial perforant path-granule cell synapses. CKAMP44 thus modulates short-term plasticity at specific excitatory synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Engelhardt, Jakob -- Mack, Volker -- Sprengel, Rolf -- Kavenstock, Netta -- Li, Ka Wan -- Stern-Bach, Yael -- Smit, August B -- Seeburg, Peter H -- Monyer, Hannah -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1518-22. doi: 10.1126/science.1184178. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neurobiology, University of Heidelberg, 6910 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/metabolism ; Calcium Channels/metabolism ; Dendritic Spines/metabolism ; Dentate Gyrus/cytology/*metabolism ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Guanylate Kinase ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Miniature Postsynaptic Potentials ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neural Inhibition ; *Neuronal Plasticity ; Neurons/*metabolism ; Oocytes/metabolism ; Patch-Clamp Techniques ; Perforant Pathway ; Protein Interaction Domains and Motifs ; Protein Isoforms/genetics/metabolism ; Proteomics ; Pyramidal Cells/metabolism ; Receptors, AMPA/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Synapses/*physiology ; *Synaptic Transmission ; Xenopus laevis
    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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  • 3
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    RLIM is dispensable for X-chromosome inactivation in the mouse embryonic epiblast (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-05-30
    Description: In female mice, two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Beginning at the four-cell stage, imprinted XCI (iXCI) exclusively silences the paternal X chromosome. Later, around implantation, epiblast cells of the inner cell mass that give rise to the embryo reactivate the paternal X chromosome and undergo a random form of XCI (rXCI). Xist, a long non-coding RNA crucial for both forms of XCI, is activated by the ubiquitin ligase RLIM (also known as Rnf12). Although RLIM is required for triggering iXCI in mice, its importance for rXCI has been controversial. Here we show that RLIM levels are downregulated in embryonic cells undergoing rXCI. Using mouse genetics we demonstrate that female cells lacking RLIM from pre-implantation stages onwards show hallmarks of XCI, including Xist clouds and H3K27me3 foci, and have full embryogenic potential. These results provide evidence that RLIM is dispensable for rXCI, indicating that in mice an RLIM-independent mechanism activates Xist in the embryo proper.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105192/" 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/PMC4105192/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, JongDae -- Wallingford, Mary C -- Gallant, Judith -- Marcho, Chelsea -- Jiao, Baowei -- Byron, Meg -- Bossenz, Michael -- Lawrence, Jeanne B -- Jones, Stephen N -- Mager, Jesse -- Bach, Ingolf -- CA077735/CA/NCI NIH HHS/ -- CA131158/CA/NCI NIH HHS/ -- DK32520/DK/NIDDK NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 CA131158/CA/NCI NIH HHS/ -- R01 GM053234/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Jul 3;511(7507):86-9. doi: 10.1038/nature13286. Epub 2014 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS), Worcester, Massachusetts 01605, USA. ; Veterinary & Animal Sciences, University of Massachusetts Amherst, Amherst, Massachusetts 01003, USA. ; Department of Cell and Developmental Biology, UMMS, Worcester, Massachusetts 01605, USA. ; 1] Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS), Worcester, Massachusetts 01605, USA [2] Kunming Institute of Zoology, Chinese Academy of Science, Kunming 650223, China. ; Ortenau Klinikum Lahr-Ettenheim, Institut fur Pathologie, 77933 Lahr, Germany. ; 1] Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS), Worcester, Massachusetts 01605, USA [2] Program in Molecular Medicine, UMMS, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Down-Regulation ; Embryo Implantation ; Embryo, Mammalian/embryology/metabolism ; Female ; Germ Layers/*embryology/*metabolism ; Histones/chemistry/metabolism ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Methylation ; Mice ; Mice, Knockout ; RNA, Long Noncoding/genetics ; Ubiquitin-Protein Ligases/genetics/*metabolism ; X Chromosome Inactivation/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Ligand-induced autoregulation of IFN-gamma receptor beta chain expression in T helper cell subsets (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-17
    Description: Interferon gamma (IFN-gamma) responsiveness in certain cells depends on the state of cellular differentiation or activation. Here an in vitro developmental system was used to show that IFN-gamma produced during generation of the CD4+ T helper cell type 1 (TH1) subset extinguishes expression of the IFN-gamma receptor beta subunit, resulting in TH1 cells that are unresponsive to IFN-gamma. This beta chain loss also occurred in IFN-gamma-treated TH2 cells and thus represents a specific response of CD4+ T cells to IFN-gamma rather than a TH1-specific differentiation event. These results define a mechanism of cellular desensitization where a cytokine down-regulates expression of a receptor subunit required primarily for signaling and not ligand binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bach, E A -- Szabo, S J -- Dighe, A S -- Ashkenazi, A -- Aguet, M -- Murphy, K M -- Schreiber, R D -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1215-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*biosynthesis ; Cell Differentiation ; Cell Line ; Cytokines/biosynthesis ; Down-Regulation ; Gene Expression ; Genes, MHC Class I ; Interferon-gamma/*pharmacology ; Ligands ; Mice ; Mice, Transgenic ; Receptors, Interferon/*biosynthesis ; Th1 Cells/cytology/immunology/*metabolism ; Th2 Cells/cytology/immunology/*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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  • 5
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    Control of memory formation through regulated expression of a CaMKII transgene (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: One of the major limitations in the use of genetically modified mice for studying cognitive functions is the lack of regional and temporal control of gene function. To overcome these limitations, a forebrain-specific promoter was combined with the tetracycline transactivator system to achieve both regional and temporal control of transgene expression. Expression of an activated calcium-independent form of calcium-calmodulin-dependent kinase II (CaMKII) resulted in a loss of hippocampal long-term potentiation in response to 10-hertz stimulation and a deficit in spatial memory, a form of explicit memory. Suppression of transgene expression reversed both the physiological and the memory deficit. When the transgene was expressed at high levels in the lateral amygdala and the striatum but not other forebrain structures, there was a deficit in fear conditioning, an implicit memory task, that also was reversible. Thus, the CaMKII signaling pathway is critical for both explicit and implicit memory storage, in a manner that is independent of its potential role in development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayford, M -- Bach, M E -- Huang, Y Y -- Wang, L -- Hawkins, R D -- Kandel, E R -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, and Howard Hughes Medical Institute, 722 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939850" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology ; Animals ; Brain/*physiology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Conditioning (Psychology) ; Corpus Striatum/physiology ; Doxycycline/pharmacology ; Fear ; *Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Hippocampus/physiology ; Long-Term Potentiation ; Maze Learning ; Memory/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuronal Plasticity ; Promoter Regions, Genetic ; Prosencephalon/physiology ; Signal Transduction ; Transgenes
    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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  • 6
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    The true challenge of giant marine reserves (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, David M -- Bach, Pascal -- Bonhommeau, Sylvain -- Chassot, Emmanuel -- Chavance, Pierre -- Dagorn, Laurent -- Davies, Tim -- Dueri, Sibylle -- Fletcher, Rick -- Fonteneau, Alain -- Fromentin, Jean-Marc -- Gaertner, Daniel -- Hampton, John -- Hilborn, Ray -- Hobday, Alistair -- Kearney, Robert -- Kleiber, Pierre -- Lehodey, Patrick -- Marsac, Francis -- Maury, Olivier -- Mees, Chris -- Menard, Frederic -- Pearce, John -- Sibert, John -- New York, N.Y. -- Science. 2013 May 17;340(6134):810-1. doi: 10.1126/science.340.6134.810-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; Fisheries/*legislation & jurisprudence ; *Fishes
    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
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    Histocompatibility and isoenzyme differences in commercially supplied "BALB/c" mice (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-07-23
    Description: BALB/c mice obtained commercially were found to differ significantly from the standard phenotype of BALB/c strain mice. Isoenzyme tests and H-2 haplotype analyses indicated that the majority of mice from two of the three sources tested appeared mixed, frequently heterozygous, and did not consistently express either the expected H-2 or glucose phosphate isomerase type.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahan, B -- Auerbach, R -- Alter, B J -- Bach, F H -- New York, N.Y. -- Science. 1982 Jul 23;217(4557):379-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6953593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity Tests, Immunologic ; Female ; Flow Cytometry ; Genetic Markers ; Glucose-6-Phosphate Isomerase/genetics ; H-2 Antigens/genetics/immunology ; Inbreeding ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred BALB C/*genetics ; Phenotype
    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
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    H-2 antigen class: effect on mouse islet allograft rejection (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-18
    Description: Rejection of mouse pancreatic islet allografts occurred in a high percentage of donor recipient combinations identical for H-21-region antigens and differing at H-2K and H-2K + H-2D without I-region disparities. The results suggest that disparities in major histocompatibility complex antigens of class I (H-2K and H-2D) alone are capable of eliciting islet allograft rejection, and that lack of a stimulus from class II (I-region) alloantigens does not ensure permanent islet allograft survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrow, C E -- Sutherland, D E -- Steffes, M W -- Najarian, J S -- Bach, F H -- AI 18326/AI/NIAID NIH HHS/ -- AI/GM 17687/AI/NIAID NIH HHS/ -- AM 13083/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1337-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6402817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Graft Rejection ; H-2 Antigens/*immunology ; Histocompatibility Antigens Class II/*immunology ; *Islets of Langerhans Transplantation ; Major Histocompatibility Complex ; Mice ; T-Lymphocytes/immunology
    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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