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  • 1
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    Intersection of the RNA interference and X-inactivation pathways (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-07
    Description: In mammals, dosage compensation is achieved by X-chromosome inactivation (XCI) in the female. The noncoding Xist gene initiates silencing of the X chromosome, whereas its antisense partner Tsix blocks silencing. The complementarity of Xist and Tsix RNAs has long suggested a role for RNA interference (RNAi). Here, we report that murine Xist and Tsix form duplexes in vivo. During XCI, the duplexes are processed to small RNAs (sRNAs), most likely on the active X (Xa) in a Dicer-dependent manner. Deleting Dicer compromises sRNA production and derepresses Xist. Furthermore, without Dicer, Xist RNA cannot accumulate and histone 3 lysine 27 trimethylation is blocked on the inactive X (Xi). The defects are partially rescued by truncating Tsix. Thus, XCI and RNAi intersect, down-regulating Xist on Xa and spreading silencing on Xi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584363/" 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/PMC2584363/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Yuya -- Sun, Bryan K -- Lee, Jeannie T -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 6;320(5881):1336-41. doi: 10.1126/science.1157676.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital and Howard Hughes Medical Institute, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18535243" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cells, Cultured ; DEAD-box RNA Helicases/genetics/metabolism ; Embryonic Stem Cells ; Endoribonucleases/genetics/metabolism ; Female ; Histones/metabolism ; Male ; Methylation ; Mice ; *RNA Interference ; RNA, Double-Stranded/metabolism ; RNA, Long Noncoding ; RNA, Small Nuclear/metabolism ; RNA, Untranslated/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonuclease III ; X Chromosome/*genetics/metabolism ; *X Chromosome Inactivation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Polycomb proteins targeted by a short repeat RNA to the mouse X chromosome (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-01
    Description: To equalize X-chromosome dosages between the sexes, the female mammal inactivates one of her two X chromosomes. X-chromosome inactivation (XCI) is initiated by expression of Xist, a 17-kb noncoding RNA (ncRNA) that accumulates on the X in cis. Because interacting factors have not been isolated, the mechanism by which Xist induces silencing remains unknown. We discovered a 1.6-kilobase ncRNA (RepA) within Xist and identified the Polycomb complex, PRC2, as its direct target. PRC2 is initially recruited to the X by RepA RNA, with Ezh2 serving as the RNA binding subunit. The antisense Tsix RNA inhibits this interaction. RepA depletion abolishes full-length Xist induction and trimethylation on lysine 27 of histone H3 of the X. Likewise, PRC2 deficiency compromises Xist up-regulation. Therefore, RepA, together with PRC2, is required for the initiation and spread of XCI. We conclude that a ncRNA cofactor recruits Polycomb complexes to their target locus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748911/" 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/PMC2748911/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Jing -- Sun, Bryan K -- Erwin, Jennifer A -- Song, Ji-Joon -- Lee, Jeannie T -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- R01 GM110090/GM/NIGMS NIH HHS/ -- R01GM58839/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):750-6. doi: 10.1126/science.1163045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromatin Immunoprecipitation ; Electrophoretic Mobility Shift Assay ; Embryonic Stem Cells ; Female ; Fibroblasts ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Polycomb-Group Proteins ; Polymerase Chain Reaction ; RNA, Long Noncoding ; RNA, Untranslated/genetics/*metabolism ; Repetitive Sequences, Nucleic Acid ; Repressor Proteins/*metabolism ; Up-Regulation ; X Chromosome/*metabolism ; X Chromosome Inactivation
    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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    Advances in skin grafting and treatment of cutaneous wounds (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-22
    Description: The ability of the skin to repair itself after injury is vital to human survival and is disrupted in a spectrum of disorders. The process of cutaneous wound healing is complex, requiring a coordinated response by immune cells, hematopoietic cells, and resident cells of the skin. We review the classic paradigms of wound healing and evaluate how recent discoveries have enriched our understanding of this process. We evaluate current and experimental approaches to treating cutaneous wounds, with an emphasis on cell-based therapies and skin transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Bryan K -- Siprashvili, Zurab -- Khavari, Paul A -- F32 ARO63508/PHS HHS/ -- R01 AR045192/AR/NIAMS NIH HHS/ -- R01 AR055914/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):941-5. doi: 10.1126/science.1253836.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Epithelial Biology, Stanford University, Stanford, CA 94305, USA. ; Program in Epithelial Biology, Stanford University, Stanford, CA 94305, USA. Veterans Affairs Palo Alto Healthcare System, Palo Alto, CA 94304, USA. khavari@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25414301" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Engineering ; Humans ; Skin/*injuries ; Skin Transplantation/*trends ; Skin, Artificial ; Stem Cells ; Tissue Engineering ; Wound Healing/*physiology ; Wounds and Injuries/*surgery
    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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  • 4
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    Neutralization of HTLV-III/LAV replication by antiserum to thymosin alpha 1 (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-30
    Description: An antiserum prepared against thymosin alpha 1, a hormone secreted by the thymus gland, effectively neutralized the AIDS-associated virus [HTLV-III/LAV (clone BH-10)] and blocked its replication in H9 cells. Reverse transcriptase activity and expression of the HTLV-III/LAV antigens p15 and p24 were inhibited by purified immunoglobulin G preparations of antisera to thymosin alpha 1. The antiviral activity of the antiserum was found to be due to a region of homology between thymosin alpha 1 and p17, a product of the gag gene of HTLV-III/LAV. Comparison of the primary sequences of thymosin alpha 1 and the gag protein revealed a 44% to 50% homology in an 18-amino acid region, between positions 11 and 28 on thymosin alpha 1 and 92 and 109 on the gag protein. The effectiveness of the thymosin alpha 1 antiserum and of immunoglobulin G-enriched preparations in blocking replication of HTLV-III(BH-10) in H9 cells suggests a novel approach to the development of an AIDS vaccine. A vaccine directed against the gag protein might overcome the problem of genetic drift in the envelope region of the virus and be useful against all genetic variants of HTLV-III/LAV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarin, P S -- Sun, D K -- Thornton, A H -- Naylor, P H -- Goldstein, A L -- CA 24974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 30;232(4754):1135-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010464" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Adult ; Animals ; Child ; Deltaretrovirus/*drug effects/physiology ; Gene Products, gag ; Humans ; Immune Sera/immunology/*pharmacology ; Immunoglobulin G/immunology ; Rabbits/immunology ; Retroviridae Proteins/immunology ; Thymosin/*analogs & derivatives/immunology ; Virus Replication/*drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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