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  • 1
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    Dendrite development regulated by CREST, a calcium-regulated transcriptional activator (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: The lasting effects of neuronal activity on brain development involve calcium-dependent gene expression. Using a strategy called transactivator trap, we cloned a calcium-responsive transactivator called CREST (for calcium-responsive transactivator). CREST is a SYT-related nuclear protein that interacts with adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB)-binding protein (CBP) and is expressed in the developing brain. Mice that have a targeted disruption of the crest gene are viable but display defects in cortical and hippocampal dendrite development. Cortical neurons from crest mutant mice are compromised in calcium-dependent dendritic growth. Thus, calcium activation of CREST-mediated transcription helps regulate neuronal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aizawa, Hiroyuki -- Hu, Shu-Ching -- Bobb, Kathryn -- Balakrishnan, Karthik -- Ince, Gulayse -- Gurevich, Inga -- Cowan, Mitra -- Ghosh, Anirvan -- MH60598/MH/NIMH NIH HHS/ -- NS39993/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):197-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716005" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/cytology/embryology/growth & development/metabolism ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/metabolism ; Cloning, Molecular ; Dendrites/*physiology/ultrastructure ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Library ; Gene Targeting ; Humans ; In Situ Hybridization ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Nervous System/embryology/growth & development/metabolism ; Neurons/*physiology/ultrastructure ; Nuclear Proteins/metabolism ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection
    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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    Single-cell analysis reveals a stem-cell program in human metastatic breast cancer cells (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-09-30
    Description: Despite major advances in understanding the molecular and genetic basis of cancer, metastasis remains the cause of 〉90% of cancer-related mortality. Understanding metastasis initiation and progression is critical to developing new therapeutic strategies to treat and prevent metastatic disease. Prevailing theories hypothesize that metastases are seeded by rare tumour cells with unique properties, which may function like stem cells in their ability to initiate and propagate metastatic tumours. However, the identity of metastasis-initiating cells in human breast cancer remains elusive, and whether metastases are hierarchically organized is unknown. Here we show at the single-cell level that early stage metastatic cells possess a distinct stem-like gene expression signature. To identify and isolate metastatic cells from patient-derived xenograft models of human breast cancer, we developed a highly sensitive fluorescence-activated cell sorting (FACS)-based assay, which allowed us to enumerate metastatic cells in mouse peripheral tissues. We compared gene signatures in metastatic cells from tissues with low versus high metastatic burden. Metastatic cells from low-burden tissues were distinct owing to their increased expression of stem cell, epithelial-to-mesenchymal transition, pro-survival, and dormancy-associated genes. By contrast, metastatic cells from high-burden tissues were similar to primary tumour cells, which were more heterogeneous and expressed higher levels of luminal differentiation genes. Transplantation of stem-like metastatic cells from low-burden tissues showed that they have considerable tumour-initiating capacity, and can differentiate to produce luminal-like cancer cells. Progression to high metastatic burden was associated with increased proliferation and MYC expression, which could be attenuated by treatment with cyclin-dependent kinase (CDK) inhibitors. These findings support a hierarchical model for metastasis, in which metastases are initiated by stem-like cells that proliferate and differentiate to produce advanced metastatic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648562/" 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/PMC4648562/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawson, Devon A -- Bhakta, Nirav R -- Kessenbrock, Kai -- Prummel, Karin D -- Yu, Ying -- Takai, Ken -- Zhou, Alicia -- Eyob, Henok -- Balakrishnan, Sanjeev -- Wang, Chih-Yang -- Yaswen, Paul -- Goga, Andrei -- Werb, Zena -- CA136717/CA/NCI NIH HHS/ -- CA180039/CA/NCI NIH HHS/ -- K23 HL116657/HL/NHLBI NIH HHS/ -- R01 CA136717/CA/NCI NIH HHS/ -- R01 CA180039/CA/NCI NIH HHS/ -- England -- Nature. 2015 Oct 1;526(7571):131-5. doi: 10.1038/nature15260. Epub 2015 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, California 94143, USA. ; Department of Medicine, University of California, San Francisco, California 94143, USA. ; Department of Cell and Tissue Biology, University of California, San Francisco, California 94143, USA. ; Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan. ; Department of Cell and Molecular Biology, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26416748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/drug therapy/genetics/*pathology ; Cell Cycle/drug effects ; Cell Differentiation/drug effects/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Separation ; Cell Transformation, Neoplastic/drug effects/pathology ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Disease Models, Animal ; *Disease Progression ; Epithelial Cells/drug effects/pathology ; Epithelial-Mesenchymal Transition/genetics ; Flow Cytometry ; Gene Expression Profiling ; Genes, myc/genetics ; Humans ; Mesoderm/metabolism/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Metastasis/drug therapy/*pathology ; Neoplastic Stem Cells/drug effects/metabolism/*pathology ; *Single-Cell Analysis ; Xenograft Model Antitumor Assays
    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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  • 3
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    Stable recombination hotspots in birds (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-21
    Description: The DNA-binding protein PRDM9 has a critical role in specifying meiotic recombination hotspots in mice and apes, but it appears to be absent from other vertebrate species, including birds. To study the evolution and determinants of recombination in species lacking the gene that encodes PRDM9, we inferred fine-scale genetic maps from population resequencing data for two bird species: the zebra finch, Taeniopygia guttata, and the long-tailed finch, Poephila acuticauda. We found that both species have recombination hotspots, which are enriched near functional genomic elements. Unlike in mice and apes, most hotspots are shared between the two species, and their conservation seems to extend over tens of millions of years. These observations suggest that in the absence of PRDM9, recombination targets functional features that both enable access to the genome and constrain its evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singhal, Sonal -- Leffler, Ellen M -- Sannareddy, Keerthi -- Turner, Isaac -- Venn, Oliver -- Hooper, Daniel M -- Strand, Alva I -- Li, Qiye -- Raney, Brian -- Balakrishnan, Christopher N -- Griffith, Simon C -- McVean, Gil -- Przeworski, Molly -- 086786/Z/08/Z/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 100956/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Nov 20;350(6263):928-32. doi: 10.1126/science.aad0843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA. Department of Systems Biology, Columbia University, New York, NY 10032, USA. sonal.singhal1@gmail.com molly.przew@gmail.com. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK. ; Committee on Evolutionary Biology, University of Chicago, Chicago, IL 60637, USA. ; Department of Biological Sciences, Columbia University, New York, NY 10027, USA. ; China National Genebank, BGI-Shenzhen, Shenzhen 518083, China. ; Center for Biomolecular Science and Engineering, University of California-Santa Cruz, Santa Cruz, CA 95064, USA. ; Department of Biology, East Carolina University, Greenville, NC 27858, USA. ; Department of Biological Sciences, Macquarie University, Sydney, NSW 2109, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26586757" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Evolution, Molecular ; Finches/*genetics ; *Gene Expression Regulation ; Genome ; *Recombination, Genetic ; Repressor Proteins/*genetics ; Species Specificity
    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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    The genome of a songbird (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-03
    Description: The zebra finch is an important model organism in several fields with unique relevance to human neuroscience. Like other songbirds, the zebra finch communicates through learned vocalizations, an ability otherwise documented only in humans and a few other animals and lacking in the chicken-the only bird with a sequenced genome until now. Here we present a structural, functional and comparative analysis of the genome sequence of the zebra finch (Taeniopygia guttata), which is a songbird belonging to the large avian order Passeriformes. We find that the overall structures of the genomes are similar in zebra finch and chicken, but they differ in many intrachromosomal rearrangements, lineage-specific gene family expansions, the number of long-terminal-repeat-based retrotransposons, and mechanisms of sex chromosome dosage compensation. We show that song behaviour engages gene regulatory networks in the zebra finch brain, altering the expression of long non-coding RNAs, microRNAs, transcription factors and their targets. We also show evidence for rapid molecular evolution in the songbird lineage of genes that are regulated during song experience. These results indicate an active involvement of the genome in neural processes underlying vocal communication and identify potential genetic substrates for the evolution and regulation of this behaviour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187626/" 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/PMC3187626/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, Wesley C -- Clayton, David F -- Ellegren, Hans -- Arnold, Arthur P -- Hillier, Ladeana W -- Kunstner, Axel -- Searle, Steve -- White, Simon -- Vilella, Albert J -- Fairley, Susan -- Heger, Andreas -- Kong, Lesheng -- Ponting, Chris P -- Jarvis, Erich D -- Mello, Claudio V -- Minx, Pat -- Lovell, Peter -- Velho, Tarciso A F -- Ferris, Margaret -- Balakrishnan, Christopher N -- Sinha, Saurabh -- Blatti, Charles -- London, Sarah E -- Li, Yun -- Lin, Ya-Chi -- George, Julia -- Sweedler, Jonathan -- Southey, Bruce -- Gunaratne, Preethi -- Watson, Michael -- Nam, Kiwoong -- Backstrom, Niclas -- Smeds, Linnea -- Nabholz, Benoit -- Itoh, Yuichiro -- Whitney, Osceola -- Pfenning, Andreas R -- Howard, Jason -- Volker, Martin -- Skinner, Bejamin M -- Griffin, Darren K -- Ye, Liang -- McLaren, William M -- Flicek, Paul -- Quesada, Victor -- Velasco, Gloria -- Lopez-Otin, Carlos -- Puente, Xose S -- Olender, Tsviya -- Lancet, Doron -- Smit, Arian F A -- Hubley, Robert -- Konkel, Miriam K -- Walker, Jerilyn A -- Batzer, Mark A -- Gu, Wanjun -- Pollock, David D -- Chen, Lin -- Cheng, Ze -- Eichler, Evan E -- Stapley, Jessica -- Slate, Jon -- Ekblom, Robert -- Birkhead, Tim -- Burke, Terry -- Burt, David -- Scharff, Constance -- Adam, Iris -- Richard, Hugues -- Sultan, Marc -- Soldatov, Alexey -- Lehrach, Hans -- Edwards, Scott V -- Yang, Shiaw-Pyng -- Li, Xiaoching -- Graves, Tina -- Fulton, Lucinda -- Nelson, Joanne -- Chinwalla, Asif -- Hou, Shunfeng -- Mardis, Elaine R -- Wilson, Richard K -- BB/D013704/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E010652/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F007590/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0175091/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/I/00001425/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- R01 DC007218/DC/NIDCD NIH HHS/ -- R01 GM059290/GM/NIGMS NIH HHS/ -- R01 GM085233/GM/NIGMS NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 NS045264/NS/NINDS NIH HHS/ -- R01NS051820/NS/NINDS NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 1;464(7289):757-62. doi: 10.1038/nature08819.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center, Washington University School of Medicine, Campus Box 8501, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. wwarren@watson.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360741" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Animals ; Auditory Perception/genetics ; Brain/physiology ; Chickens/genetics ; Evolution, Molecular ; Female ; Finches/*genetics/physiology ; Gene Duplication ; Gene Regulatory Networks/genetics ; Genome/*genetics ; Male ; MicroRNAs/genetics ; Models, Animal ; Multigene Family/genetics ; Retroelements/genetics ; Sex Chromosomes/genetics ; Terminal Repeat Sequences/genetics ; Transcription, Genetic/genetics ; Vocalization, Animal/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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  • 5
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    Vibrational and rotational quenching of CO by collisions with H, He, and H2 (2006)
    In:  CASI
    Details
    Publication Date: 2019-07-11
    Description: Collisional quenching of molecular species is an important process in a variety of astrophysical environments including interstellar clouds, photodissociation regions, and cool stellar/planetary atmospheres. In this work, quantum mechanical scattering calculations are presented for the rotational and vibrational relaxation of rotationally-excited CO due to collisions with H, He and H2 for collision energies between 10(exp -6) and approx.15000/cm. The calculations were performed using the close-coupling approach and the l-labeled form of the coupled-states approximation. Cross sections and rate coefficients for the quenching of the v=0-2, j=0-6 levels of CO are presented and comparisons with previous calculations and measurements, where available, are provided.
    Keywords: Astrophysics
    Type: Proceedings of the NASA Laboratory Astrophysics Workshop; 288-291; NASA/CP-2006-214549
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  • 6
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    The Effect of Non-equilibrium Kinetics on Oxygen Chemistry in the Interstellar Medium (2006)
    In:  CASI
    Details
    Publication Date: 2019-07-11
    Description: It has been suggested that in photon-dominated regions, oxygen chemistry is initiated by the O+H2 yields OH+H reaction. The reaction has an energy barrier of about 0.4 eV with ground state reactants and it is slow at low temperatures. There is strong experimental evidence that vibrational excitation of the H2 molecule increases the reactivity significantly. We present extensive quantum calculations of cross sections and rate coefficients for the O+H2(v) reaction for v = 0 - 3 of the H2 molecule and show that the vibrational excitation of the molecule has a significant effect on reactivity, especially at low temperatures.
    Keywords: Astrophysics
    Type: Proceedings of the NASA Laboratory Astrophysics Workshop; 225-228; NASA/CP-2006-214549
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  • 7
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    Astrochemistry in the Early Universe: Collisional Rates for H on H2 (2006)
    In:  CASI
    Details
    Publication Date: 2019-07-11
    Description: We present preliminary results of a full quantum calculation of state to state cross sections for H on H2. These cross sections are calculated for v=0,4 j=0,15 for energies up to 3.0 eV. The cross sections are calculated on the BKMP2 potential surface (Boothroyd et al. 1996) with the ABC scattering code (Skouteris et al. 2000).
    Keywords: Astrophysics
    Type: Proceedings of the NASA Laboratory Astrophysics Workshop; 210-212; NASA/CP-2006-214549
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