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  • 1
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    Systems-level dynamic analyses of fate change in murine embryonic stem cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-20
    Description: Molecular regulation of embryonic stem cell (ESC) fate involves a coordinated interaction between epigenetic, transcriptional and translational mechanisms. It is unclear how these different molecular regulatory mechanisms interact to regulate changes in stem cell fate. Here we present a dynamic systems-level study of cell fate change in murine ESCs following a well-defined perturbation. Global changes in histone acetylation, chromatin-bound RNA polymerase II, messenger RNA (mRNA), and nuclear protein levels were measured over 5 days after downregulation of Nanog, a key pluripotency regulator. Our data demonstrate how a single genetic perturbation leads to progressive widespread changes in several molecular regulatory layers, and provide a dynamic view of information flow in the epigenome, transcriptome and proteome. We observe that a large proportion of changes in nuclear protein levels are not accompanied by concordant changes in the expression of corresponding mRNAs, indicating important roles for translational and post-translational regulation of ESC fate. Gene-ontology analysis across different molecular layers indicates that although chromatin reconfiguration is important for altering cell fate, it is preceded by transcription-factor-mediated regulatory events. The temporal order of gene expression alterations shows the order of the regulatory network reconfiguration and offers further insight into the gene regulatory network. Our studies extend the conventional systems biology approach to include many molecular species, regulatory layers and temporal series, and underscore the complexity of the multilayer regulatory mechanisms responsible for changes in protein expression that determine stem cell fate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199216/" 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/PMC3199216/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Rong -- Markowetz, Florian -- Unwin, Richard D -- Leek, Jeffrey T -- Airoldi, Edoardo M -- MacArthur, Ben D -- Lachmann, Alexander -- Rozov, Roye -- Ma'ayan, Avi -- Boyer, Laurie A -- Troyanskaya, Olga G -- Whetton, Anthony D -- Lemischka, Ihor R -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A20007/GM/NIGMS NIH HHS/ -- P50 GM071558-020007/GM/NIGMS NIH HHS/ -- P50 GM071558-030007/GM/NIGMS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2009 Nov 19;462(7271):358-62. doi: 10.1038/nature08575.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. rlu@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19924215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Embryonic Stem Cells/*cytology/*metabolism ; Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Mice ; Proteome ; Time Factors
    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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    Design logic of a cannabinoid receptor signaling network that triggers neurite outgrowth (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: Cannabinoid receptor 1 (CB1R) regulates neuronal differentiation. To understand the logic underlying decision-making in the signaling network controlling CB1R-induced neurite outgrowth, we profiled the activation of several hundred transcription factors after cell stimulation. We assembled an in silico signaling network by connecting CB1R to 23 activated transcription factors. Statistical analyses of this network predicted a role for the breast cancer 1 protein BRCA1 in neuronal differentiation and a new pathway from CB1R through phosphoinositol 3-kinase to the transcription factor paired box 6 (PAX6). Both predictions were experimentally confirmed. Results of transcription factor activation experiments that used pharmacological inhibitors of kinases revealed a network organization of partial OR gates regulating kinases stacked above AND gates that control transcription factors, which together allow for distributed decision-making in CB1R-induced neurite outgrowth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776723/" 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/PMC2776723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bromberg, Kenneth D -- Ma'ayan, Avi -- Neves, Susana R -- Iyengar, Ravi -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- GM072853/GM/NIGMS NIH HHS/ -- GM54508/GM/NIGMS NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A2/GM/NIGMS NIH HHS/ -- P50 GM071558-01A20007/GM/NIGMS NIH HHS/ -- P50 GM071558-02/GM/NIGMS NIH HHS/ -- P50 GM071558-020007/GM/NIGMS NIH HHS/ -- P50 GM071558-030007/GM/NIGMS NIH HHS/ -- P50-071558/PHS HHS/ -- R01 GM054508/GM/NIGMS NIH HHS/ -- R01 GM054508-21/GM/NIGMS NIH HHS/ -- R01 GM072853/GM/NIGMS NIH HHS/ -- R01 GM072853-04/GM/NIGMS NIH HHS/ -- T32 CA88796/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):903-9. doi: 10.1126/science.1152662.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Cells, Cultured ; Computational Biology ; Computer Simulation ; Eye Proteins/metabolism ; Hippocampus/cytology ; Homeodomain Proteins/metabolism ; Metabolic Networks and Pathways ; Mice ; Neurites/*physiology ; Neurons/*cytology/metabolism ; Paired Box Transcription Factors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Interaction Mapping ; Rats ; Receptor, Cannabinoid, CB1/*metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Transcription Factors/antagonists & inhibitors/*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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  • 3
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    Formation of regulatory patterns during signal propagation in a Mammalian cellular network (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-16
    Description: We developed a model of 545 components (nodes) and 1259 interactions representing signaling pathways and cellular machines in the hippocampal CA1 neuron. Using graph theory methods, we analyzed ligand-induced signal flow through the system. Specification of input and output nodes allowed us to identify functional modules. Networking resulted in the emergence of regulatory motifs, such as positive and negative feedback and feedforward loops, that process information. Key regulators of plasticity were highly connected nodes required for the formation of regulatory motifs, indicating the potential importance of such motifs in determining cellular choices between homeostasis and plasticity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032439/" 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/PMC3032439/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma'ayan, Avi -- Jenkins, Sherry L -- Neves, Susana -- Hasseldine, Anthony -- Grace, Elizabeth -- Dubin-Thaler, Benjamin -- Eungdamrong, Narat J -- Weng, Gehzi -- Ram, Prahlad T -- Rice, J Jeremy -- Kershenbaum, Aaron -- Stolovitzky, Gustavo A -- Blitzer, Robert D -- Iyengar, Ravi -- DA15863/DA/NIDA NIH HHS/ -- GM-072853/GM/NIGMS NIH HHS/ -- GM-54508/GM/NIGMS NIH HHS/ -- GM-62754/GM/NIGMS NIH HHS/ -- GM-65065/GM/NIGMS NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A20007/GM/NIGMS NIH HHS/ -- P50 GM071558-020007/GM/NIGMS NIH HHS/ -- P50 GM071558-030007/GM/NIGMS NIH HHS/ -- R01 GM054508/GM/NIGMS NIH HHS/ -- R01 GM054508-12/GM/NIGMS NIH HHS/ -- R01 GM072853/GM/NIGMS NIH HHS/ -- R01 GM072853-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 12;309(5737):1078-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Biological Chemistry Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16099987" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Feedback, Physiological ; Glutamic Acid/metabolism ; Hippocampus/*cytology/physiology ; Homeostasis ; Ligands ; Long-Term Potentiation ; Mammals ; Mathematics ; Mitogen-Activated Protein Kinases/metabolism ; Models, Neurological ; Neuronal Plasticity ; Neurons/*physiology ; Norepinephrine/metabolism ; Protein Kinase C/metabolism ; Receptors, AMPA/metabolism ; *Signal Transduction ; Software ; Systems Biology
    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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    Patterns and rates of exonic de novo mutations in autism spectrum disorders (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-04-13
    Description: Autism spectrum disorders (ASD) are believed to have genetic and environmental origins, yet in only a modest fraction of individuals can specific causes be identified. To identify further genetic risk factors, here we assess the role of de novo mutations in ASD by sequencing the exomes of ASD cases and their parents (n = 175 trios). Fewer than half of the cases (46.3%) carry a missense or nonsense de novo variant, and the overall rate of mutation is only modestly higher than the expected rate. In contrast, the proteins encoded by genes that harboured de novo missense or nonsense mutations showed a higher degree of connectivity among themselves and to previous ASD genes as indexed by protein-protein interaction screens. The small increase in the rate of de novo events, when taken together with the protein interaction results, are consistent with an important but limited role for de novo point mutations in ASD, similar to that documented for de novo copy number variants. Genetic models incorporating these data indicate that most of the observed de novo events are unconnected to ASD; those that do confer risk are distributed across many genes and are incompletely penetrant (that is, not necessarily sufficient for disease). Our results support polygenic models in which spontaneous coding mutations in any of a large number of genes increases risk by 5- to 20-fold. Despite the challenge posed by such models, results from de novo events and a large parallel case-control study provide strong evidence in favour of CHD8 and KATNAL2 as genuine autism risk factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613847/" 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/PMC3613847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neale, Benjamin M -- Kou, Yan -- Liu, Li -- Ma'ayan, Avi -- Samocha, Kaitlin E -- Sabo, Aniko -- Lin, Chiao-Feng -- Stevens, Christine -- Wang, Li-San -- Makarov, Vladimir -- Polak, Paz -- Yoon, Seungtai -- Maguire, Jared -- Crawford, Emily L -- Campbell, Nicholas G -- Geller, Evan T -- Valladares, Otto -- Schafer, Chad -- Liu, Han -- Zhao, Tuo -- Cai, Guiqing -- Lihm, Jayon -- Dannenfelser, Ruth -- Jabado, Omar -- Peralta, Zuleyma -- Nagaswamy, Uma -- Muzny, Donna -- Reid, Jeffrey G -- Newsham, Irene -- Wu, Yuanqing -- Lewis, Lora -- Han, Yi -- Voight, Benjamin F -- Lim, Elaine -- Rossin, Elizabeth -- Kirby, Andrew -- Flannick, Jason -- Fromer, Menachem -- Shakir, Khalid -- Fennell, Tim -- Garimella, Kiran -- Banks, Eric -- Poplin, Ryan -- Gabriel, Stacey -- DePristo, Mark -- Wimbish, Jack R -- Boone, Braden E -- Levy, Shawn E -- Betancur, Catalina -- Sunyaev, Shamil -- Boerwinkle, Eric -- Buxbaum, Joseph D -- Cook, Edwin H Jr -- Devlin, Bernie -- Gibbs, Richard A -- Roeder, Kathryn -- Schellenberg, Gerard D -- Sutcliffe, James S -- Daly, Mark J -- KL2 RR024977/RR/NCRR NIH HHS/ -- P30 HD015052/HD/NICHD NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH089004/MH/NIMH NIH HHS/ -- R01 MH089025/MH/NIMH NIH HHS/ -- R01 MH089175/MH/NIMH NIH HHS/ -- R01 MH089208/MH/NIMH NIH HHS/ -- R01 MH089482/MH/NIMH NIH HHS/ -- R01MH084676/MH/NIMH NIH HHS/ -- R01MH089175/MH/NIMH NIH HHS/ -- R01MH089208/MH/NIMH NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- TL1 RR024978/RR/NCRR NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- UL1 RR024975/RR/NCRR NIH HHS/ -- England -- Nature. 2012 Apr 4;485(7397):242-5. doi: 10.1038/nature11011.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495311" target="_blank"〉PubMed〈/a〉
    Keywords: Autistic Disorder/*genetics ; Case-Control Studies ; DNA-Binding Proteins/*genetics ; Exome/genetics ; Exons/*genetics ; Family Health ; Genetic Predisposition to Disease/*genetics ; Humans ; Models, Genetic ; Multifactorial Inheritance/genetics ; Mutation/*genetics ; Phenotype ; Poisson Distribution ; Protein Interaction Maps ; Transcription Factors/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Synaptic, transcriptional and chromatin genes disrupted in autism (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-11-05
    Description: The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) 〈 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR 〈 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402723/" 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/PMC4402723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Rubeis, Silvia -- He, Xin -- Goldberg, Arthur P -- Poultney, Christopher S -- Samocha, Kaitlin -- Cicek, A Erucment -- Kou, Yan -- Liu, Li -- Fromer, Menachem -- Walker, Susan -- Singh, Tarinder -- Klei, Lambertus -- Kosmicki, Jack -- Shih-Chen, Fu -- Aleksic, Branko -- Biscaldi, Monica -- Bolton, Patrick F -- Brownfeld, Jessica M -- Cai, Jinlu -- Campbell, Nicholas G -- Carracedo, Angel -- Chahrour, Maria H -- Chiocchetti, Andreas G -- Coon, Hilary -- Crawford, Emily L -- Curran, Sarah R -- Dawson, Geraldine -- Duketis, Eftichia -- Fernandez, Bridget A -- Gallagher, Louise -- Geller, Evan -- Guter, Stephen J -- Hill, R Sean -- Ionita-Laza, Juliana -- Jimenz Gonzalez, Patricia -- Kilpinen, Helena -- Klauck, Sabine M -- Kolevzon, Alexander -- Lee, Irene -- Lei, Irene -- Lei, Jing -- Lehtimaki, Terho -- Lin, Chiao-Feng -- Ma'ayan, Avi -- Marshall, Christian R -- McInnes, Alison L -- Neale, Benjamin -- Owen, Michael J -- Ozaki, Noriio -- Parellada, Mara -- Parr, Jeremy R -- Purcell, Shaun -- Puura, Kaija -- Rajagopalan, Deepthi -- Rehnstrom, Karola -- Reichenberg, Abraham -- Sabo, Aniko -- Sachse, Michael -- Sanders, Stephan J -- Schafer, Chad -- Schulte-Ruther, Martin -- Skuse, David -- Stevens, Christine -- Szatmari, Peter -- Tammimies, Kristiina -- Valladares, Otto -- Voran, Annette -- Li-San, Wang -- Weiss, Lauren A -- Willsey, A Jeremy -- Yu, Timothy W -- Yuen, Ryan K C -- DDD Study -- Homozygosity Mapping Collaborative for Autism -- UK10K Consortium -- Cook, Edwin H -- Freitag, Christine M -- Gill, Michael -- Hultman, Christina M -- Lehner, Thomas -- Palotie, Aaarno -- Schellenberg, Gerard D -- Sklar, Pamela -- State, Matthew W -- Sutcliffe, James S -- Walsh, Christiopher A -- Scherer, Stephen W -- Zwick, Michael E -- Barett, Jeffrey C -- Cutler, David J -- Roeder, Kathryn -- Devlin, Bernie -- Daly, Mark J -- Buxbaum, Joseph D -- 5UL1 RR024975/RR/NCRR NIH HHS/ -- MH077139/MH/NIMH NIH HHS/ -- MH089482/MH/NIMH NIH HHS/ -- MH095034/MH/NIMH NIH HHS/ -- P30 HD15052/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH083565/MH/NIMH NIH HHS/ -- R01 MH089482/MH/NIMH NIH HHS/ -- R01 MH094400/MH/NIMH NIH HHS/ -- R01 MH095797/MH/NIMH NIH HHS/ -- R01 MH097849/MH/NIMH NIH HHS/ -- R01 MH100229/MH/NIMH NIH HHS/ -- R01 NS073601/NS/NINDS NIH HHS/ -- R01MH083565/MH/NIMH NIH HHS/ -- R01MH089208/MH/NIMH NIH HHS/ -- R37 MH057881/MH/NIMH NIH HHS/ -- RC2MH089952/MH/NIMH NIH HHS/ -- T32 HG002295/HG/NHGRI NIH HHS/ -- U01 MH100209/MH/NIMH NIH HHS/ -- U01 MH100229/MH/NIMH NIH HHS/ -- U01 MH100233/MH/NIMH NIH HHS/ -- U01 MH100239/MH/NIMH NIH HHS/ -- U01MH100209/MH/NIMH NIH HHS/ -- U01MH100229/MH/NIMH NIH HHS/ -- U01MH100233/MH/NIMH NIH HHS/ -- U01MH100239/MH/NIMH NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- UL1TR000445/TR/NCATS NIH HHS/ -- WT091310/Wellcome Trust/United Kingdom -- WT098051/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Nov 13;515(7526):209-15. doi: 10.1038/nature13772. Epub 2014 Oct 29.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363760" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Child Development Disorders, Pervasive/*genetics/pathology ; Chromatin/*genetics/metabolism ; Chromatin Assembly and Disassembly ; Exome/genetics ; Female ; Genetic Predisposition to Disease/*genetics ; Germ-Line Mutation/genetics ; Humans ; Male ; Molecular Sequence Data ; Mutation/*genetics ; Mutation, Missense/genetics ; Nerve Net/metabolism ; Odds Ratio ; Synapses/*metabolism ; Transcription, Genetic/*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
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    Fetal liver hematopoietic stem cell niches associate with portal vessels (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-12-05
    Description: Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver niche is not yet elucidated. We show that Nestin(+)NG2(+) pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin(+)NG2(+) cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1(+)Ephrin-B2(+) artery to EphB4(+) vein phenotype, associated with a loss of periportal Nestin(+)NG2(+) cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a periportal vascular niche with a fractal-like organization enabled by placental circulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4706788/" 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/PMC4706788/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, Jalal A -- Mendelson, Avital -- Kunisaki, Yuya -- Birbrair, Alexander -- Kou, Yan -- Arnal-Estape, Anna -- Pinho, Sandra -- Ciero, Paul -- Nakahara, Fumio -- Ma'ayan, Avi -- Bergman, Aviv -- Merad, Miriam -- Frenette, Paul S -- CA164468/CA/NCI NIH HHS/ -- DA033788/DA/NIDA NIH HHS/ -- DK056638/DK/NIDDK NIH HHS/ -- F30 943257/PHS HHS/ -- F32 HL123224/HL/NHLBI NIH HHS/ -- HL069438/HL/NHLBI NIH HHS/ -- HL097700/HL/NHLBI NIH HHS/ -- R01 CA173861/CA/NCI NIH HHS/ -- R01 CA190400/CA/NCI NIH HHS/ -- R01 DA033788/DA/NIDA NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- R01GM098316/GM/NIGMS NIH HHS/ -- T32 063754/PHS HHS/ -- U54 HL127624/HL/NHLBI NIH HHS/ -- U54CA189201/CA/NCI NIH HHS/ -- U54HL127624/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):176-80. doi: 10.1126/science.aad0084. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research. Albert Einstein College of Medicine, Bronx, NY, USA. Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research. Albert Einstein College of Medicine, Bronx, NY, USA. Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA. ; Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research. Albert Einstein College of Medicine, Bronx, NY, USA. ; Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA. ; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research. Albert Einstein College of Medicine, Bronx, NY, USA. Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA. paul.frenette@einstein.yu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26634440" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Ephrin-B2/analysis ; Female ; Hematopoietic Stem Cells/*physiology ; Liver/blood supply/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nestin/analysis ; Neuropilin-1/analysis ; Placental Circulation ; Portal System/chemistry/*embryology ; Pregnancy ; Proteoglycans/analysis ; Receptor, EphB4/analysis ; Stem Cell Niche/*physiology
    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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    Mesenchymal and haematopoietic stem cells form a unique bone marrow niche (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-13
    Description: The cellular constituents forming the haematopoietic stem cell (HSC) niche in the bone marrow are unclear, with studies implicating osteoblasts, endothelial and perivascular cells. Here we demonstrate that mesenchymal stem cells (MSCs), identified using nestin expression, constitute an essential HSC niche component. Nestin(+) MSCs contain all the bone-marrow colony-forming-unit fibroblastic activity and can be propagated as non-adherent 'mesenspheres' that can self-renew and expand in serial transplantations. Nestin(+) MSCs are spatially associated with HSCs and adrenergic nerve fibres, and highly express HSC maintenance genes. These genes, and others triggering osteoblastic differentiation, are selectively downregulated during enforced HSC mobilization or beta3 adrenoreceptor activation. Whereas parathormone administration doubles the number of bone marrow nestin(+) cells and favours their osteoblastic differentiation, in vivo nestin(+) cell depletion rapidly reduces HSC content in the bone marrow. Purified HSCs home near nestin(+) MSCs in the bone marrow of lethally irradiated mice, whereas in vivo nestin(+) cell depletion significantly reduces bone marrow homing of haematopoietic progenitors. These results uncover an unprecedented partnership between two distinct somatic stem-cell types and are indicative of a unique niche in the bone marrow made of heterotypic stem-cell pairs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146551/" 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/PMC3146551/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendez-Ferrer, Simon -- Michurina, Tatyana V -- Ferraro, Francesca -- Mazloom, Amin R -- Macarthur, Ben D -- Lira, Sergio A -- Scadden, David T -- Ma'ayan, Avi -- Enikolopov, Grigori N -- Frenette, Paul S -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A2/GM/NIGMS NIH HHS/ -- P50 GM071558-02/GM/NIGMS NIH HHS/ -- P50 GM071558-03/GM/NIGMS NIH HHS/ -- P50 GM071558-04/GM/NIGMS NIH HHS/ -- P50 GM071558-05/GM/NIGMS NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 DK056638-06A2/DK/NIDDK NIH HHS/ -- R01 DK056638-07/DK/NIDDK NIH HHS/ -- R01 DK056638-08/DK/NIDDK NIH HHS/ -- R01 DK056638-09/DK/NIDDK NIH HHS/ -- R01 DK056638-10/DK/NIDDK NIH HHS/ -- R01 DK056638-11/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL069438-05A2/HL/NHLBI NIH HHS/ -- R01 HL069438-06/HL/NHLBI NIH HHS/ -- R01 HL069438-06W1/HL/NHLBI NIH HHS/ -- R01 HL069438-07/HL/NHLBI NIH HHS/ -- R01 HL069438-08/HL/NHLBI NIH HHS/ -- R01 HL069438-09/HL/NHLBI NIH HHS/ -- R01 HL097819/HL/NHLBI NIH HHS/ -- R01 HL097819-01/HL/NHLBI NIH HHS/ -- R01 HL097819-02/HL/NHLBI NIH HHS/ -- R01 HL097819-03/HL/NHLBI NIH HHS/ -- R01DK056638/DK/NIDDK NIH HHS/ -- R01HL097819/HL/NHLBI NIH HHS/ -- R01HL69438/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Aug 12;466(7308):829-34. doi: 10.1038/nature09262.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA. simon.mendez-ferrer@cnic.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Division ; Cell Lineage/drug effects ; Cell Movement ; Cells, Cultured ; Chemokine CXCL12/metabolism ; Chondrocytes/cytology/drug effects ; Gene Expression Regulation/genetics ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects/metabolism ; Intermediate Filament Proteins/metabolism ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/*cytology/drug effects/metabolism ; Mice ; Mice, Transgenic ; Multipotent Stem Cells/cytology/drug effects/metabolism ; Nerve Tissue Proteins/metabolism ; Nestin ; Osteoblasts/cytology/drug effects/metabolism ; Parathyroid Hormone/pharmacology ; Stem Cell Niche/*cytology/drug effects/metabolism ; Stromal Cells/cytology/drug effects/metabolism ; Sympathetic Nervous System/physiology
    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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    GEO2Enrichr: browser extension and server app to extract gene sets from GEO and analyze them for biological functions (2015)
    Oxford University Press
    Details
    Publication Date: 2015-09-11
    Description: Motivation: Identification of differentially expressed genes is an important step in extracting knowledge from gene expression profiling studies. The raw expression data from microarray and other high-throughput technologies is deposited into the Gene Expression Omnibus (GEO) and served as Simple Omnibus Format in Text (SOFT) files. However, to extract and analyze differentially expressed genes from GEO requires significant computational skills. Results: Here we introduce GEO2Enrichr, a browser extension for extracting differentially expressed gene sets from GEO and analyzing those sets with Enrichr, an independent gene set enrichment analysis tool containing over 70 000 annotated gene sets organized into 75 gene-set libraries. GEO2Enrichr adds JavaScript code to GEO web-pages; this code scrapes user selected accession numbers and metadata, and then, with one click, users can submit this information to a web-server application that downloads the SOFT files, parses, cleans and normalizes the data, identifies the differentially expressed genes, and then pipes the resulting gene lists to Enrichr for downstream functional analysis. GEO2Enrichr opens a new avenue for adding functionality to major bioinformatics resources such GEO by integrating tools and resources without the need for a plug-in architecture. Importantly, GEO2Enrichr helps researchers to quickly explore hypotheses with little technical overhead, lowering the barrier of entry for biologists by automating data processing steps needed for knowledge extraction from the major repository GEO. Availability and implementation: GEO2Enrichr is an open source tool, freely available for installation as browser extensions at the Chrome Web Store and FireFox Add-ons. Documentation and a browser independent web application can be found at http://amp.pharm.mssm.edu/g2e/ . Contact: avi.maayan@mssm.edu
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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    Drug/Cell-line Browser: interactive canvas visualization of cancer drug/cell-line viability assay datasets (2014)
    Oxford University Press
    Details
    Publication Date: 2014-11-07
    Description: : Recently, several high profile studies collected cell viability data from panels of cancer cell lines treated with many drugs applied at different concentrations. Such drug sensitivity data for cancer cell lines provide suggestive treatments for different types and subtypes of cancer. Visualization of these datasets can reveal patterns that may not be obvious by examining the data without such efforts. Here we introduce Drug/Cell-line Browser (DCB), an online interactive HTML5 data visualization tool for interacting with three of the recently published datasets of cancer cell lines/drug-viability studies. DCB uses clustering and canvas visualization of the drugs and the cell lines, as well as a bar graph that summarizes drug effectiveness for the tissue of origin or the cancer subtypes for single or multiple drugs. DCB can help in understanding drug response patterns and prioritizing drug/cancer cell line interactions by tissue of origin or cancer subtype. Availability and implementation: DCB is an open source Web-based tool that is freely available at: http://www.maayanlab.net/LINCS/DCB Contact: avi.maayan@mssm.edu Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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    Ordered cyclic motifs contribute to dynamic stability in biological and engineered networks (2008)
    National Academy of Sciences
    Details
    Publication Date: 2008-11-25
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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