ALBERT

Description: The mechanisms by which expression of the beta-like globin genes are developmentally regulated are under intense investigation. The temporal control of human embryonic (epsilon) globin expression was analyzed. A 3.7-kilobase (kb) fragment that contained the entire human epsilon-globin gene was linked to a 2.5-kb cassette of the locus control region (LCR), and the developmental time of expression of this construct was studied in transgenic mice. The human epsilon-globin transgene was expressed in yolk sac-derived primitive erythroid cells, but not in fetal liver or bone marrow-derived definitive erythroid cells. The absence of epsilon gene expression in definitive erythroid cells suggests that the developmental regulation of the epsilon-globin gene depends only on the presence of the LCR and the epsilon-globin gene itself (that is, an autonomous negative control mechanism). The autonomy of epsilon-globin gene developmental control distinguishes it from the competitive mechanism of regulation of gamma and beta-globin genes, and therefore, suggests that at least two distinct mechanisms function in human hemoglobin switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raich, N -- Enver, T -- Nakamoto, B -- Josephson, B -- Papayannopoulou, T -- Stamatoyannopoulos, G -- DK 3132/DK/NIDDK NIH HHS/ -- HL 20899/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1147-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medical Genetics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251502" target="_blank"〉PubMed〈/a〉

Description: Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753175/" 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/PMC2753175/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Eun Young -- Chavakis, Emmanouil -- Czabanka, Marcus A -- Langer, Harald F -- Fraemohs, Line -- Economopoulou, Matina -- Kundu, Ramendra K -- Orlandi, Alessia -- Zheng, Ying Yi -- Prieto, Darue A -- Ballantyne, Christie M -- Constant, Stephanie L -- Aird, William C -- Papayannopoulou, Thalia -- Gahmberg, Carl G -- Udey, Mark C -- Vajkoczy, Peter -- Quertermous, Thomas -- Dimmeler, Stefanie -- Weber, Christian -- Chavakis, Triantafyllos -- AI067254/AI/NIAID NIH HHS/ -- R01 HL082927/HL/NHLBI NIH HHS/ -- Z01 BC010790-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 14;322(5904):1101-4. doi: 10.1126/science.1165218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19008446" target="_blank"〉PubMed〈/a〉

Description: The laboratory mouse shares the majority of its protein-coding genes with humans, making it the premier model organism in biomedical research, yet the two mammals differ in significant ways. To gain greater insights into both shared and species-specific transcriptional and cellular regulatory programs in the mouse, the Mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types. By comparing with the human genome, we not only confirm substantial conservation in the newly annotated potential functional sequences, but also find a large degree of divergence of sequences involved in transcriptional regulation, chromatin state and higher order chromatin organization. Our results illuminate the wide range of evolutionary forces acting on genes and their regulatory regions, and provide a general resource for research into mammalian biology and mechanisms of human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266106/" 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/PMC4266106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yue, Feng -- Cheng, Yong -- Breschi, Alessandra -- Vierstra, Jeff -- Wu, Weisheng -- Ryba, Tyrone -- Sandstrom, Richard -- Ma, Zhihai -- Davis, Carrie -- Pope, Benjamin D -- Shen, Yin -- Pervouchine, Dmitri D -- Djebali, Sarah -- Thurman, Robert E -- Kaul, Rajinder -- Rynes, Eric -- Kirilusha, Anthony -- Marinov, Georgi K -- Williams, Brian A -- Trout, Diane -- Amrhein, Henry -- Fisher-Aylor, Katherine -- Antoshechkin, Igor -- DeSalvo, Gilberto -- See, Lei-Hoon -- Fastuca, Meagan -- Drenkow, Jorg -- Zaleski, Chris -- Dobin, Alex -- Prieto, Pablo -- Lagarde, Julien -- Bussotti, Giovanni -- Tanzer, Andrea -- Denas, Olgert -- Li, Kanwei -- Bender, M A -- Zhang, Miaohua -- Byron, Rachel -- Groudine, Mark T -- McCleary, David -- Pham, Long -- Ye, Zhen -- Kuan, Samantha -- Edsall, Lee -- Wu, Yi-Chieh -- Rasmussen, Matthew D -- Bansal, Mukul S -- Kellis, Manolis -- Keller, Cheryl A -- Morrissey, Christapher S -- Mishra, Tejaswini -- Jain, Deepti -- Dogan, Nergiz -- Harris, Robert S -- Cayting, Philip -- Kawli, Trupti -- Boyle, Alan P -- Euskirchen, Ghia -- Kundaje, Anshul -- Lin, Shin -- Lin, Yiing -- Jansen, Camden -- Malladi, Venkat S -- Cline, Melissa S -- Erickson, Drew T -- Kirkup, Vanessa M -- Learned, Katrina -- Sloan, Cricket A -- Rosenbloom, Kate R -- Lacerda de Sousa, Beatriz -- Beal, Kathryn -- Pignatelli, Miguel -- Flicek, Paul -- Lian, Jin -- Kahveci, Tamer -- Lee, Dongwon -- Kent, W James -- Ramalho Santos, Miguel -- Herrero, Javier -- Notredame, Cedric -- Johnson, Audra -- Vong, Shinny -- Lee, Kristen -- Bates, Daniel -- Neri, Fidencio -- Diegel, Morgan -- Canfield, Theresa -- Sabo, Peter J -- Wilken, Matthew S -- Reh, Thomas A -- Giste, Erika -- Shafer, Anthony -- Kutyavin, Tanya -- Haugen, Eric -- Dunn, Douglas -- Reynolds, Alex P -- Neph, Shane -- Humbert, Richard -- Hansen, R Scott -- De Bruijn, Marella -- Selleri, Licia -- Rudensky, Alexander -- Josefowicz, Steven -- Samstein, Robert -- Eichler, Evan E -- Orkin, Stuart H -- Levasseur, Dana -- Papayannopoulou, Thalia -- Chang, Kai-Hsin -- Skoultchi, Arthur -- Gosh, Srikanta -- Disteche, Christine -- Treuting, Piper -- Wang, Yanli -- Weiss, Mitchell J -- Blobel, Gerd A -- Cao, Xiaoyi -- Zhong, Sheng -- Wang, Ting -- Good, Peter J -- Lowdon, Rebecca F -- Adams, Leslie B -- Zhou, Xiao-Qiao -- Pazin, Michael J -- Feingold, Elise A -- Wold, Barbara -- Taylor, James -- Mortazavi, Ali -- Weissman, Sherman M -- Stamatoyannopoulos, John A -- Snyder, Michael P -- Guigo, Roderic -- Gingeras, Thomas R -- Gilbert, David M -- Hardison, Ross C -- Beer, Michael A -- Ren, Bing -- Mouse ENCODE Consortium -- 095908/Wellcome Trust/United Kingdom -- 1U54HG007004/HG/NHGRI NIH HHS/ -- 3RC2HG005602/HG/NHGRI NIH HHS/ -- F31CA165863/CA/NCI NIH HHS/ -- F32HL110473/HL/NHLBI NIH HHS/ -- GM083337/GM/NIGMS NIH HHS/ -- GM085354/GM/NIGMS NIH HHS/ -- K99HL119617/HL/NHLBI NIH HHS/ -- P01 GM085354/GM/NIGMS NIH HHS/ -- P01 HL064190/HL/NHLBI NIH HHS/ -- P01 HL110860/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 DK065806/DK/NIDDK NIH HHS/ -- R01 DK096266/DK/NIDDK NIH HHS/ -- R01 ES024992/ES/NIEHS NIH HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R01 GM083337/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG007175/HG/NHGRI NIH HHS/ -- R01 HG007348/HG/NHGRI NIH HHS/ -- R01 HG007354/HG/NHGRI NIH HHS/ -- R01DK065806/DK/NIDDK NIH HHS/ -- R01HD043997-09/HD/NICHD NIH HHS/ -- R01HG003991/HG/NHGRI NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- R56 DK065806/DK/NIDDK NIH HHS/ -- RC2 HG005573/HG/NHGRI NIH HHS/ -- RC2HG005573/HG/NHGRI NIH HHS/ -- T32 GM081739/GM/NIGMS NIH HHS/ -- U01 HL099656/HL/NHLBI NIH HHS/ -- U01 HL099993/HL/NHLBI NIH HHS/ -- U54 HG006997/HG/NHGRI NIH HHS/ -- U54 HG006998/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Nov 20;515(7527):355-64. doi: 10.1038/nature13992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. [2] Department of Biochemistry and Molecular Biology, College of Medicine, The Pennsylvania State University, Hershey, Pennsylvania 17033, USA. ; Department of Genetics, Stanford University, 300 Pasteur Drive, MC-5477 Stanford, California 94305, USA. ; Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Center for Comparative Genomics and Bioinformatics, Huck Institutes of the Life Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Biological Science, 319 Stadium Drive, Florida State University, Tallahassee, Florida 32306-4295, USA. ; Functional Genomics, Cold Spring Harbor Laboratory, Bungtown Road, Cold Spring Harbor, New York 11724, USA. ; Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Division of Biology, California Institute of Technology, Pasadena, California 91125, USA. ; 1] Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. [2] Department of Theoretical Chemistry, Faculty of Chemistry, University of Vienna, Waehringerstrasse 17/3/303, A-1090 Vienna, Austria. ; Departments of Biology and Mathematics and Computer Science, Emory University, O. Wayne Rollins Research Center, 1510 Clifton Road NE, Atlanta, Georgia 30322, USA. ; 1] Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. [2] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. [2] Department of Radiation Oncology, University of Washington, Seattle, Washington 98195, USA. ; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. ; 1] Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. [2] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California 92697, USA. ; Center for Biomolecular Science and Engineering, School of Engineering, University of California Santa Cruz (UCSC), Santa Cruz, California 95064, USA. ; Departments of Obstetrics/Gynecology and Pathology, and Center for Reproductive Sciences, University of California San Francisco, San Francisco, California 94143, USA. ; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Yale University, Department of Genetics, PO Box 208005, 333 Cedar Street, New Haven, Connecticut 06520-8005, USA. ; Computer &Information Sciences &Engineering, University of Florida, Gainesville, Florida 32611, USA. ; McKusick-Nathans Institute of Genetic Medicine and Department of Biomedical Engineering, Johns Hopkins University, 733 N. Broadway, BRB 573 Baltimore, Maryland 21205, USA. ; 1] European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] Bill Lyons Informatics Centre, UCL Cancer Institute, University College London, London WC1E 6DD, UK. ; Department of Biological Structure, University of Washington, HSB I-516, 1959 NE Pacific Street, Seattle, Washington 98195, USA. ; MRC Molecular Haemotology Unit, University of Oxford, Oxford OX3 9DS, UK. ; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, New York 10065, USA. ; HHMI and Ludwig Center at Memorial Sloan Kettering Cancer Center, Immunology Program, Memorial Sloan Kettering Cancer Canter, New York, New York 10065, USA. ; Dana Farber Cancer Institute, Harvard Medical School, Cambridge, Massachusetts 02138, USA. ; University of Iowa Carver College of Medicine, Department of Internal Medicine, Iowa City, Iowa 52242, USA. ; Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pathology, University of Washington, Seattle, Washington 98195, USA. ; Department of Comparative Medicine, University of Washington, Seattle, Washington 98195, USA. ; Bioinformatics and Genomics program, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Hematology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] Division of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA. [2] Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Bioengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, Missouri 63108, USA. ; NHGRI, National Institutes of Health, 5635 Fishers Lane, Bethesda, Maryland 20892-9307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409824" target="_blank"〉PubMed〈/a〉

Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉

Description: To study the evolutionary dynamics of regulatory DNA, we mapped 〉1.3 million deoxyribonuclease I-hypersensitive sites (DHSs) in 45 mouse cell and tissue types, and systematically compared these with human DHS maps from orthologous compartments. We found that the mouse and human genomes have undergone extensive cis-regulatory rewiring that combines branch-specific evolutionary innovation and loss with widespread repurposing of conserved DHSs to alternative cell fates, and that this process is mediated by turnover of transcription factor (TF) recognition elements. Despite pervasive evolutionary remodeling of the location and content of individual cis-regulatory regions, within orthologous mouse and human cell types the global fraction of regulatory DNA bases encoding recognition sites for each TF has been strictly conserved. Our findings provide new insights into the evolutionary forces shaping mammalian regulatory DNA landscapes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337786/" 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/PMC4337786/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vierstra, Jeff -- Rynes, Eric -- Sandstrom, Richard -- Zhang, Miaohua -- Canfield, Theresa -- Hansen, R Scott -- Stehling-Sun, Sandra -- Sabo, Peter J -- Byron, Rachel -- Humbert, Richard -- Thurman, Robert E -- Johnson, Audra K -- Vong, Shinny -- Lee, Kristen -- Bates, Daniel -- Neri, Fidencio -- Diegel, Morgan -- Giste, Erika -- Haugen, Eric -- Dunn, Douglas -- Wilken, Matthew S -- Josefowicz, Steven -- Samstein, Robert -- Chang, Kai-Hsin -- Eichler, Evan E -- De Bruijn, Marella -- Reh, Thomas A -- Skoultchi, Arthur -- Rudensky, Alexander -- Orkin, Stuart H -- Papayannopoulou, Thalia -- Treuting, Piper M -- Selleri, Licia -- Kaul, Rajinder -- Groudine, Mark -- Bender, M A -- Stamatoyannopoulos, John A -- 1RC2HG005654/HG/NHGRI NIH HHS/ -- 2R01HD04399709/HD/NICHD NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 DK096266/DK/NIDDK NIH HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R01 HD043997/HD/NICHD NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- R37DK44746/DK/NIDDK NIH HHS/ -- RC2 HG005654/HG/NHGRI NIH HHS/ -- U54 HG007010/HG/NHGRI NIH HHS/ -- U54HG007010/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):1007-12. doi: 10.1126/science.1246426.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. ; Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA 98195, USA. ; Department of Biological Structure, University of Washington, Seattle, WA 98195, USA. ; Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. Howard Hughes Medical Institute. ; Division of Hematology, Department of Medicine, University of Washington, Seattle, WA 98195, USA. ; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. Howard Hughes Medical Institute. ; Medical Research Council (MRC) Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, UK. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. ; Howard Hughes Medical Institute. Division of Hematology/Oncology, Children's Hospital Boston and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA 02115, USA. ; Department of Comparative Medicine, University of Washington, Seattle, WA 98195, USA. ; Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY 10065, USA. ; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA 98195, USA. ; Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Department of Radiation Oncology, University of Washington, Seattle, WA 98109, USA. ; Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Department of Pediatrics, University of Washington, Seattle, WA 98195, USA. ; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. Division of Oncology, Department of Medicine, University of Washington, Seattle, WA 98195, USA. jstam@uw.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25411453" target="_blank"〉PubMed〈/a〉

Description: Arabinosylcytosine, a compound that inhibits DNA synthesis in rapidly dividing cells, stimulates fetal hemoglobin in adult baboons and produces significant perturbations in the pools of erythroid progenitors. It appears that changes in the kinetics of erythroid cell differentiation rather than direct action on the gamma genes underlie stimulation of fetal hemoglobin in the adult animals in vivo. These results also suggest that chemotherapeutic agents selected for their low carcinogenic or mutagenic potential could be used for therapeutic induction of fetal hemoglobin in patients with sickle cell anemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Torrealba de Ron, A -- Veith, R -- Knitter, G -- Stamatoyannopoulos, G -- GM 15253/GM/NIGMS NIH HHS/ -- HL-07093/HL/NHLBI NIH HHS/ -- HL-20899/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 May 11;224(4649):617-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200940" target="_blank"〉PubMed〈/a〉

Description: Erythroid colonies, raised from erythroid stem cells circulating in the peripheral blood of normal adult individuals, synthesize considerable amounts of fetal hemoglobin. In cultures from persons with sickling disorders, amounts of hemoglobin F that are known to inhibit sickling in vivo are produced. The results provide evidence that primitive erythroid progenitors are able to express the hemoglobin F production program and that cultures of mononuclear cells of the adult blood can be used to investigate the mechanisms involved in regulation of gamma-globin gene switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Nakamoto, B -- Buckley, J -- Kurachi, S -- Nute, P E -- Stamatoyannopoulos, G -- New York, N.Y. -- Science. 1978 Mar 24;199(4335):1349-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/628844" target="_blank"〉PubMed〈/a〉

Description: A new human erythroleukemia cell line has been established. This line, designated HEL, is capable of spontaneous and induced globin synthesis, producing mainly G gamma and A gamma chains. Embryonic chains (epsilon, zeta) and alpha chains are detectable in very small amounts; beta chains are undetectable. This line provides a new model system for studying aspects of erythroid cell differentiation and differential globin gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, P -- Papayannopoulou, T -- CA 18029/CA/NCI NIH HHS/ -- HL 20899/HL/NHLBI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1982 Jun 11;216(4551):1233-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6177045" target="_blank"〉PubMed〈/a〉