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  • 1
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    PTIP promotes chromatin changes critical for immunoglobulin class switch recombination (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here, we showed that activated B cells deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired trimethylation of histone 3 at lysine 4 (H3K4me3) and transcription initiation of downstream switch regions at the immunoglobulin heavy-chain (Igh) locus, leading to defective immunoglobulin class switching. We also showed that PTIP accumulation at DSBs contributes to class switch recombination (CSR) and genome stability independently of Igh switch transcription. These results demonstrate that PTIP promotes specific chromatin changes that control the accessibility of the Igh locus to CSR and suggest a nonredundant role for the MLL3-MLL4 complex in altering antibody effector function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008398/" 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/PMC3008398/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, Jeremy A -- Santos, Margarida Almeida -- Wang, Zhibin -- Zang, Chongzhi -- Schwab, Kristopher R -- Jankovic, Mila -- Filsuf, Darius -- Chen, Hua-Tang -- Gazumyan, Anna -- Yamane, Arito -- Cho, Young-Wook -- Sun, Hong-Wei -- Ge, Kai -- Peng, Weiqun -- Nussenzweig, Michel C -- Casellas, Rafael -- Dressler, Gregory R -- Zhao, Keji -- Nussenzweig, Andre -- Z01 AR041149-03/Intramural NIH HHS/ -- Z01 AR041149-04/Intramural NIH HHS/ -- Z01 DK047055-01/Intramural NIH HHS/ -- Z01 DK047055-02/Intramural NIH HHS/ -- Z01 DK075003-04/Intramural NIH HHS/ -- Z01 DK075003-05/Intramural NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- ZIA AR041149-05/Intramural NIH HHS/ -- ZIA DK075017-03/Intramural NIH HHS/ -- ZIADK047055-03/DK/NIDDK NIH HHS/ -- ZIADK075003-06/DK/NIDDK NIH HHS/ -- ZIADK075017-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):917-23. doi: 10.1126/science.1187942. Epub 2010 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity/genetics ; Carrier Proteins/genetics/*physiology ; Cytidine Deaminase/metabolism ; Dna ; Histones/metabolism ; Immunoglobulin Class Switching/genetics/*physiology ; Immunoglobulin Switch Region ; Methylation ; Mice ; Nuclear Proteins/genetics/*physiology ; Promoter Regions, Genetic ; Recombination, Genetic ; Transcriptional Activation
    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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    Dnmt3a-dependent nonpromoter DNA methylation facilitates transcription of neurogenic genes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-24
    Description: DNA methylation at proximal promoters facilitates lineage restriction by silencing cell type-specific genes. However, euchromatic DNA methylation frequently occurs in regions outside promoters. The functions of such nonproximal promoter DNA methylation are unclear. Here we show that the de novo DNA methyltransferase Dnmt3a is expressed in postnatal neural stem cells (NSCs) and is required for neurogenesis. Genome-wide analysis of postnatal NSCs indicates that Dnmt3a occupies and methylates intergenic regions and gene bodies flanking proximal promoters of a large cohort of transcriptionally permissive genes, many of which encode regulators of neurogenesis. Surprisingly, Dnmt3a-dependent nonproximal promoter methylation promotes expression of these neurogenic genes by functionally antagonizing Polycomb repression. Thus, nonpromoter DNA methylation by Dnmt3a may be used for maintaining active chromatin states of genes critical for development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539760/" 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/PMC3539760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Hao -- Coskun, Volkan -- Tao, Jifang -- Xie, Wei -- Ge, Weihong -- Yoshikawa, Kazuaki -- Li, En -- Zhang, Yi -- Sun, Yi Eve -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):444-8. doi: 10.1126/science.1190485.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Medical Pharmacology, University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. haowu7@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Brain/cytology/growth & development/*metabolism ; Chromatin Immunoprecipitation ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; *DNA Methylation ; DNA, Intergenic ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genome ; Histones/genetics/metabolism ; Mice ; Mice, Knockout ; Nervous System/growth & development ; Neurogenesis/*genetics ; Neuroglia/cytology ; Neurons/*cytology/metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Stem Cells/*metabolism ; *Transcription, Genetic
    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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    CRL4 complex regulates mammalian oocyte survival and reprogramming by activation of TET proteins (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The duration of a woman's reproductive period is determined by the size and persistence of a dormant oocyte pool. Specific oocyte genes are essential for follicle maintenance and female fertility. The mechanisms that regulate the expression of these genes are poorly understood. We found that a cullin-ring finger ligase-4 (CRL4) complex was crucial in this process. Oocyte-specific deletion of the CRL4 linker protein DDB1 or its substrate adaptor VPRBP (also known as DCAF1) caused rapid oocyte loss, premature ovarian insufficiency, and silencing of fertility maintaining genes. CRL4(VPRBP) activates the TET methylcytosine dioxygenases, which are involved in female germ cell development and zygote genome reprogramming. Hence, CRL4(VPRBP) ubiquitin ligase is a guardian of female reproductive life in germ cells and a maternal reprogramming factor after fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Chao -- Zhang, Yin-Li -- Pan, Wei-Wei -- Li, Xiao-Meng -- Wang, Zhong-Wei -- Ge, Zhao-Jia -- Zhou, Jian-Jie -- Cang, Yong -- Tong, Chao -- Sun, Qing-Yuan -- Fan, Heng-Yu -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1518-21. doi: 10.1126/science.1244587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Institute and Innovation Center for Cell Biology, Zhejiang University, Hangzhou 310058, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Cell Survival/genetics/physiology ; Cellular Reprogramming/*genetics ; Cullin Proteins/genetics/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dioxygenases/genetics/*metabolism ; Female ; Fertility/*genetics ; Gene Silencing ; Gonadal Dysgenesis/genetics ; HeLa Cells ; Humans ; Mice ; Mice, Knockout ; Oocytes/*physiology ; Ovary/physiopathology ; Proto-Oncogene 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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  • 4
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    Inactivation of the mouse Huntington's disease gene homolog Hdh (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-21
    Description: Huntington's disease (HD) is a dominant neurodegenerative disorder caused by expansion of a CAG repeat in the gene encoding huntingtin, a protein of unknown function. To distinguish between "loss of function" and "gain of function" models of HD, the murine HD homolog Hdh was inactivated by gene targeting. Mice heterozygous for Hdh inactivation were phenotypically normal, whereas homozygosity resulted in embryonic death. Homozygotes displayed abnormal gastrulation at embryonic day 7.5 and were resorbing by day 8.5. Thus, huntingtin is critical early in embryonic development, before the emergence of the nervous system. That Hdh inactivation does not mimic adult HD neuropathology suggests that the human disease involves a gain of function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duyao, M P -- Auerbach, A B -- Ryan, A -- Persichetti, F -- Barnes, G T -- McNeil, S M -- Ge, P -- Vonsattel, J P -- Gusella, J F -- Joyner, A L -- NS16367/NS/NINDS NIH HHS/ -- NS32765/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 21;269(5222):407-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurogenetics Unit, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Ectoderm/cytology ; Embryonic and Fetal Development ; Female ; Gene Targeting ; Genotype ; Heterozygote ; Homozygote ; Humans ; Huntington Disease/*genetics ; Male ; Mesoderm/cytology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Tissue Proteins/*genetics/physiology ; Nuclear Proteins/*genetics/physiology ; Phenotype ; Stem Cells/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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    Pluripotent stem cells induced from mouse somatic cells by small-molecule compounds (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-23
    Description: Pluripotent stem cells can be induced from somatic cells, providing an unlimited cell resource, with potential for studying disease and use in regenerative medicine. However, genetic manipulation and technically challenging strategies such as nuclear transfer used in reprogramming limit their clinical applications. Here, we show that pluripotent stem cells can be generated from mouse somatic cells at a frequency up to 0.2% using a combination of seven small-molecule compounds. The chemically induced pluripotent stem cells resemble embryonic stem cells in terms of their gene expression profiles, epigenetic status, and potential for differentiation and germline transmission. By using small molecules, exogenous "master genes" are dispensable for cell fate reprogramming. This chemical reprogramming strategy has potential use in generating functional desirable cell types for clinical applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hou, Pingping -- Li, Yanqin -- Zhang, Xu -- Liu, Chun -- Guan, Jingyang -- Li, Honggang -- Zhao, Ting -- Ye, Junqing -- Yang, Weifeng -- Liu, Kang -- Ge, Jian -- Xu, Jun -- Zhang, Qiang -- Zhao, Yang -- Deng, Hongkui -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):651-4. doi: 10.1126/science.1239278. Epub 2013 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Life Sciences and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/genetics ; Cell Engineering/*methods ; Cellular Reprogramming/*drug effects/genetics ; Epithelial-Mesenchymal Transition/drug effects/genetics ; Fibroblasts/cytology/*drug effects ; Gene Expression Profiling ; Green Fluorescent Proteins/genetics ; Induced Pluripotent Stem Cells/*cytology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Octamer Transcription Factor-3/genetics/metabolism ; Promoter Regions, Genetic/drug effects ; Small Molecule Libraries/chemistry/*pharmacology
    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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