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  • 1
    Publication Date: 2008-12-06
    Description: Transcription initiation by RNA polymerase II (RNAPII) is thought to occur unidirectionally from most genes. Here, we present evidence of widespread divergent transcription at protein-encoding gene promoters. Transcription start site-associated RNAs (TSSa-RNAs) nonrandomly flank active promoters, with peaks of antisense and sense short RNAs at 250 nucleotides upstream and 50 nucleotides downstream of TSSs, respectively. Northern analysis shows that TSSa-RNAs are subsets of an RNA population 20 to 90 nucleotides in length. Promoter-associated RNAPII and H3K4-trimethylated histones, transcription initiation hallmarks, colocalize at sense and antisense TSSa-RNA positions; however, H3K79-dimethylated histones, characteristic of elongating RNAPII, are only present downstream of TSSs. These results suggest that divergent transcription over short distances is common for active promoters and may help promoter regions maintain a state poised for subsequent regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2692996/" 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/PMC2692996/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seila, Amy C -- Calabrese, J Mauro -- Levine, Stuart S -- Yeo, Gene W -- Rahl, Peter B -- Flynn, Ryan A -- Young, Richard A -- Sharp, Phillip A -- 5-F32-HD051190/HD/NICHD NIH HHS/ -- F32 HD051190-03/HD/NICHD NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- P01 CA042063/CA/NCI NIH HHS/ -- P01 CA042063-20/CA/NCI NIH HHS/ -- P01-CA42063/CA/NCI NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-35/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 GM034277/GM/NIGMS NIH HHS/ -- R01 GM034277-24/GM/NIGMS NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-05/HG/NHGRI NIH HHS/ -- R01-GM34277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1849-51. doi: 10.1126/science.1162253. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic Stem Cells/metabolism ; Gene Expression Regulation ; HeLa Cells ; Histones/metabolism ; Humans ; Methylation ; Mice ; *Promoter Regions, Genetic ; RNA/*genetics/metabolism ; RNA, Antisense/*genetics/metabolism ; Transcription Factors/metabolism ; Transcription Initiation Site ; *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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  • 2
    Publication Date: 2015-09-19
    Description: Autoantibodies target the RNA binding protein Ro60 in systemic lupus erythematosus (SLE) and Sjogren's syndrome. However, it is unclear whether Ro60 and its associated RNAs contribute to disease pathogenesis. We catalogued the Ro60-associated RNAs in human cell lines and found that among other RNAs, Ro60 bound an RNA motif derived from endogenous Alu retroelements. Alu transcripts were induced by type I interferon and stimulated proinflammatory cytokine secretion by human peripheral blood cells. Ro60 deletion resulted in enhanced expression of Alu RNAs and interferon-regulated genes. Anti-Ro60-positive SLE immune complexes contained Alu RNAs, and Alu transcripts were up-regulated in SLE whole blood samples relative to controls. These findings establish a link among the lupus autoantigen Ro60, Alu retroelements, and type I interferon.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4691329/" 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/PMC4691329/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hung, T -- Pratt, G A -- Sundararaman, B -- Townsend, M J -- Chaivorapol, C -- Bhangale, T -- Graham, R R -- Ortmann, W -- Criswell, L A -- Yeo, G W -- Behrens, T W -- HG004659/HG/NHGRI NIH HHS/ -- HG007005/HG/NHGRI NIH HHS/ -- NS075449/NS/NINDS NIH HHS/ -- R01 GM084317/GM/NIGMS NIH HHS/ -- R01 HG004659/HG/NHGRI NIH HHS/ -- R01 NS075449/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2015 Oct 23;350(6259):455-9. doi: 10.1126/science.aac7442. Epub 2015 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, South San Francisco, CA 94080, USA. behrens.tim@gene.com hungt2@gene.com geneyeo@ucsd.edu. ; Department of Cellular and Molecular Medicine, Institute for Genomic Medicine, Stem Cell Program, University of California at San Diego, Sanford Consortium for Regenerative Medicine, 2880 Torrey Pines Scenic Drive, La Jolla, CA 92037, USA. ; Genentech, South San Francisco, CA 94080, USA. ; Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, CA 94143, USA. ; Department of Cellular and Molecular Medicine, Institute for Genomic Medicine, Stem Cell Program, University of California at San Diego, Sanford Consortium for Regenerative Medicine, 2880 Torrey Pines Scenic Drive, La Jolla, CA 92037, USA. Department of Physiology, National University of Singapore, Singapore. Genome Institute of Singapore and Molecular Engineering Laboratory, Agency for Science, Technology and Research, Singapore. behrens.tim@gene.com hungt2@gene.com geneyeo@ucsd.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26382853" target="_blank"〉PubMed〈/a〉
    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
    Publication Date: 2016-04-29
    Description: Umbilical cord blood-derived haematopoietic stem cells (HSCs) are essential for many life-saving regenerative therapies. However, despite their advantages for transplantation, their clinical use is restricted because HSCs in cord blood are found only in small numbers. Small molecules that enhance haematopoietic stem and progenitor cell (HSPC) expansion in culture have been identified, but in many cases their mechanisms of action or the nature of the pathways they impinge on are poorly understood. A greater understanding of the molecular circuitry that underpins the self-renewal of human HSCs will facilitate the development of targeted strategies that expand HSCs for regenerative therapies. Whereas transcription factor networks have been shown to influence the self-renewal and lineage decisions of human HSCs, the post-transcriptional mechanisms that guide HSC fate have not been closely investigated. Here we show that overexpression of the RNA-binding protein Musashi-2 (MSI2) induces multiple pro-self-renewal phenotypes, including a 17-fold increase in short-term repopulating cells and a net 23-fold ex vivo expansion of long-term repopulating HSCs. By performing a global analysis of MSI2-RNA interactions, we show that MSI2 directly attenuates aryl hydrocarbon receptor (AHR) signalling through post-transcriptional downregulation of canonical AHR pathway components in cord blood HSPCs. Our study gives mechanistic insight into RNA networks controlled by RNA-binding proteins that underlie self-renewal and provides evidence that manipulating such networks ex vivo can enhance the regenerative potential of human HSCs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880456/" 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/PMC4880456/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rentas, Stefan -- Holzapfel, Nicholas T -- Belew, Muluken S -- Pratt, Gabriel A -- Voisin, Veronique -- Wilhelm, Brian T -- Bader, Gary D -- Yeo, Gene W -- Hope, Kristin J -- HG004659/HG/NHGRI NIH HHS/ -- MOP-126030/Canadian Institutes of Health Research/Canada -- NS075449/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Apr 28;532(7600):508-11. doi: 10.1038/nature17665.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biomedical Sciences, Stem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario L8S 4K1, Canada. ; Department of Cellular and Molecular Medicine, Institute for Genomic Medicine, University of California, San Diego, La Jolla, California 92037, USA. ; Bioinformatics Graduate Program, University of California, San Diego, La Jolla, California 92037, USA. ; The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec H3C 3J7, Canada. ; Department of Physiology, National University of Singapore and Molecular Engineering Laboratory, A*STAR, Singapore 138632, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27121842" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Cell Count ; *Cell Self Renewal/genetics ; Down-Regulation/genetics ; Female ; Fetal Blood/cytology ; Gene Knockdown Techniques ; Hematopoietic Stem Cells/*cytology/*metabolism ; Humans ; Male ; Mice ; Protein Binding ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/*metabolism ; Receptors, Aryl Hydrocarbon/genetics/*metabolism ; *Signal Transduction/genetics
    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: 2013-10-25
    Description: Identifying cellular and molecular differences between human and non-human primates (NHPs) is essential to the basic understanding of the evolution and diversity of our own species. Until now, preserved tissues have been the main source for most comparative studies between humans, chimpanzees (Pan troglodytes) and bonobos (Pan paniscus). However, these tissue samples do not fairly represent the distinctive traits of live cell behaviour and are not amenable to genetic manipulation. We propose that induced pluripotent stem (iPS) cells could be a unique biological resource to determine relevant phenotypical differences between human and NHPs, and that those differences could have potential adaptation and speciation value. Here we describe the generation and initial characterization of iPS cells from chimpanzees and bonobos as new tools to explore factors that may have contributed to great ape evolution. Comparative gene expression analysis of human and NHP iPS cells revealed differences in the regulation of long interspersed element-1 (L1, also known as LINE-1) transposons. A force of change in mammalian evolution, L1 elements are retrotransposons that have remained active during primate evolution. Decreased levels of L1-restricting factors APOBEC3B (also known as A3B) and PIWIL2 (ref. 7) in NHP iPS cells correlated with increased L1 mobility and endogenous L1 messenger RNA levels. Moreover, results from the manipulation of A3B and PIWIL2 levels in iPS cells supported a causal inverse relationship between levels of these proteins and L1 retrotransposition. Finally, we found increased copy numbers of species-specific L1 elements in the genome of chimpanzees compared to humans, supporting the idea that increased L1 mobility in NHPs is not limited to iPS cells in culture and may have also occurred in the germ line or embryonic cells developmentally upstream to germline specification during primate evolution. We propose that differences in L1 mobility may have differentially shaped the genomes of humans and NHPs and could have continuing adaptive significance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064720/" 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/PMC4064720/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marchetto, Maria C N -- Narvaiza, Inigo -- Denli, Ahmet M -- Benner, Christopher -- Lazzarini, Thomas A -- Nathanson, Jason L -- Paquola, Apua C M -- Desai, Keval N -- Herai, Roberto H -- Weitzman, Matthew D -- Yeo, Gene W -- Muotri, Alysson R -- Gage, Fred H -- AI074967/AI/NIAID NIH HHS/ -- GM084317/GM/NIGMS NIH HHS/ -- HG004659/HG/NHGRI NIH HHS/ -- MH08848/MH/NIMH NIH HHS/ -- MH094753/MH/NIMH NIH HHS/ -- NS075449/NS/NINDS NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 MH088485/MH/NIMH NIH HHS/ -- R01 MH094753/MH/NIMH NIH HHS/ -- R01 MH095741/MH/NIMH NIH HHS/ -- R01 NS075449/NS/NINDS NIH HHS/ -- England -- Nature. 2013 Nov 28;503(7477):525-9. doi: 10.1038/nature12686. Epub 2013 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins/metabolism ; Cell Line ; Cell Shape ; Cytidine Deaminase/metabolism ; Evolution, Molecular ; Genome, Human/genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Karyotyping ; Long Interspersed Nucleotide Elements/*genetics ; Mice, Nude ; Pan paniscus/*genetics/metabolism ; Pan troglodytes/*genetics/metabolism ; Pluripotent Stem Cells/cytology/*metabolism ; RNA, Messenger/analysis/genetics ; Sequence Analysis, RNA ; Species Specificity
    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: 2009-08-07
    Description: Long interspersed element 1 (LINE-1 or L1) retrotransposons have markedly affected the human genome. L1s must retrotranspose in the germ line or during early development to ensure their evolutionary success, yet the extent to which this process affects somatic cells is poorly understood. We previously demonstrated that engineered human L1s can retrotranspose in adult rat hippocampus progenitor cells in vitro and in the mouse brain in vivo. Here we demonstrate that neural progenitor cells isolated from human fetal brain and derived from human embryonic stem cells support the retrotransposition of engineered human L1s in vitro. Furthermore, we developed a quantitative multiplex polymerase chain reaction that detected an increase in the copy number of endogenous L1s in the hippocampus, and in several regions of adult human brains, when compared to the copy number of endogenous L1s in heart or liver genomic DNAs from the same donor. These data suggest that de novo L1 retrotransposition events may occur in the human brain and, in principle, have the potential to contribute to individual somatic mosaicism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909034/" 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/PMC2909034/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coufal, Nicole G -- Garcia-Perez, Jose L -- Peng, Grace E -- Yeo, Gene W -- Mu, Yangling -- Lovci, Michael T -- Morell, Maria -- O'Shea, K Sue -- Moran, John V -- Gage, Fred H -- GM069985/GM/NIGMS NIH HHS/ -- GM082970/GM/NIGMS NIH HHS/ -- MH082070/MH/NIMH NIH HHS/ -- NS048187/NS/NINDS NIH HHS/ -- P20 GM069985/GM/NIGMS NIH HHS/ -- P20 GM069985-010001/GM/NIGMS NIH HHS/ -- R01 GM060518/GM/NIGMS NIH HHS/ -- R01 GM082970/GM/NIGMS NIH HHS/ -- R01 GM082970-03/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Aug 27;460(7259):1127-31. doi: 10.1038/nature08248. Epub 2009 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19657334" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/genetics ; Brain/cytology ; Cell Line ; Chromatin Immunoprecipitation ; DNA Methylation ; Embryonic Stem Cells/*cytology/*metabolism ; Fetus/cytology ; Gene Dosage ; Humans ; Neurons/*cytology/*metabolism ; Polymerase Chain Reaction ; Retroelements/*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: 2012-08-07
    Description: Cockayne syndrome (CS) is a human premature aging disorder associated with neurological and developmental abnormalities, caused by mutations mainly in the CS group B gene ( ERCC6 ). At the molecular level, CS is characterized by a deficiency in the transcription-couple DNA repair pathway. To understand the role of this molecular pathway in a pluripotent cell and the impact of CSB mutation during human cellular development, we generated induced pluripotent stem cells (iPSCs) from CSB skin fibroblasts (CSB-iPSC). Here, we showed that the lack of functional CSB does not represent a barrier to genetic reprogramming. However, iPSCs derived from CSB patient's fibroblasts exhibited elevated cell death rate and higher reactive oxygen species (ROS) production. Moreover, these cellular phenotypes were accompanied by an up-regulation of TXNIP and TP53 transcriptional expression. Our findings suggest that CSB modulates cell viability in pluripotent stem cells, regulating the expression of TP53 and TXNIP and ROS production.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 7
    Publication Date: 2013-11-20
    Description: Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD). Here, we identify nuclear RNA foci containing the hexanucleotide expansion (GGGGCC) in patient cells, including white blood cells, fibroblasts, glia, and multiple neuronal cell types...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
    Publication Date: 2013-02-20
    Description: Transactivating response region DNA binding protein (TDP-43) is the major protein component of ubiquitinated inclusions found in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitinated inclusions. Two ALS-causing mutants (TDP-43Q331K and TDP-43M337V), but not wild-type human TDP-43, are shown here to provoke age-dependent, mutant-dependent, progressive motor axon...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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