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  • 1
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0020-7608
    Keywords: Computational Chemistry and Molecular Modeling ; Atomic, Molecular and Optical Physics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: The weak hydrogen bonded systems H2CO⃛HX (X = F, Cl, Br, and I) have been studied by means of ab initio MO method with pseudopotential approximation. The stabilization energies of these hydrogen bonds are 8.96, 4.12, 3.00, and 2.21 kcal/mol, respectively. The interaction eneraction energies are farther decomposed according to Morokuma's energy decomposing scheme. It is found that the title complexes are mainly electrostatic, although the contribution of charge transfer is also significant.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2011-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Yi -- Lakowicz, Joseph R -- England -- Nature. 2011 Apr 14;472(7342):178-9. doi: 10.1038/472178a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21490666" target="_blank"〉PubMed〈/a〉
    Keywords: Gases/chemistry ; Molecular Conformation ; Motion ; Polymers/*chemistry ; Solvents/chemistry ; Spectrum Analysis/*methods
    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: 2012-06-09
    Description: Radial glial cells are the primary neural progenitor cells in the developing neocortex. Consecutive asymmetric divisions of individual radial glial progenitor cells produce a number of sister excitatory neurons that migrate along the elongated radial glial fibre, resulting in the formation of ontogenetic columns. Moreover, sister excitatory neurons in ontogenetic columns preferentially develop specific chemical synapses with each other rather than with nearby non-siblings. Although these findings provide crucial insight into the emergence of functional columns in the neocortex, little is known about the basis of this lineage-dependent assembly of excitatory neuron microcircuits at single-cell resolution. Here we show that transient electrical coupling between radially aligned sister excitatory neurons regulates the subsequent formation of specific chemical synapses in the neocortex. Multiple-electrode whole-cell recordings showed that sister excitatory neurons preferentially form strong electrical coupling with each other rather than with adjacent non-sister excitatory neurons during early postnatal stages. This preferential coupling allows selective electrical communication between sister excitatory neurons, promoting their action potential generation and synchronous firing. Interestingly, although this electrical communication largely disappears before the appearance of chemical synapses, blockade of the electrical communication impairs the subsequent formation of specific chemical synapses between sister excitatory neurons in ontogenetic columns. These results suggest a strong link between lineage-dependent transient electrical coupling and the assembly of precise excitatory neuron microcircuits in the neocortex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3599787/" 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/PMC3599787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Yong-Chun -- He, Shuijin -- Chen, She -- Fu, Yinghui -- Brown, Keith N -- Yao, Xing-Hua -- Ma, Jian -- Gao, Kate P -- Sosinsky, Gina E -- Huang, Kun -- Shi, Song-Hai -- R01 DA024681/DA/NIDA NIH HHS/ -- R01 GM065937/GM/NIGMS NIH HHS/ -- R01 GM072881/GM/NIGMS NIH HHS/ -- R01DA024681/DA/NIDA NIH HHS/ -- R01GM065947/GM/NIGMS NIH HHS/ -- R21 MH083624/MH/NIMH NIH HHS/ -- R21MH083624/MH/NIMH NIH HHS/ -- R21NS072483/NS/NINDS NIH HHS/ -- England -- Nature. 2012 May 2;486(7401):113-7. doi: 10.1038/nature10958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurobiology, State Key Laboratory of Medical Neurobiology, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. ycyu@fudan.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678291" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Animals, Newborn ; *Cell Lineage ; *Electric Conductivity ; Electrical Synapses/metabolism/*physiology ; Gap Junctions/drug effects/*metabolism ; Meclofenamic Acid/pharmacology ; Mice ; Models, Neurological ; Neocortex/*cytology ; Neurons/*cytology/drug effects/*physiology ; Synaptic Transmission
    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: 2013-10-05
    Description: Interpreting variants, especially noncoding ones, in the increasing number of personal genomes is challenging. We used patterns of polymorphisms in functionally annotated regions in 1092 humans to identify deleterious variants; then we experimentally validated candidates. We analyzed both coding and noncoding regions, with the former corroborating the latter. We found regions particularly sensitive to mutations ("ultrasensitive") and variants that are disruptive because of mechanistic effects on transcription-factor binding (that is, "motif-breakers"). We also found variants in regions with higher network centrality tend to be deleterious. Insertions and deletions followed a similar pattern to single-nucleotide variants, with some notable exceptions (e.g., certain deletions and enhancers). On the basis of these patterns, we developed a computational tool (FunSeq), whose application to ~90 cancer genomes reveals nearly a hundred candidate noncoding drivers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3947637/" 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/PMC3947637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khurana, Ekta -- Fu, Yao -- Colonna, Vincenza -- Mu, Xinmeng Jasmine -- Kang, Hyun Min -- Lappalainen, Tuuli -- Sboner, Andrea -- Lochovsky, Lucas -- Chen, Jieming -- Harmanci, Arif -- Das, Jishnu -- Abyzov, Alexej -- Balasubramanian, Suganthi -- Beal, Kathryn -- Chakravarty, Dimple -- Challis, Daniel -- Chen, Yuan -- Clarke, Declan -- Clarke, Laura -- Cunningham, Fiona -- Evani, Uday S -- Flicek, Paul -- Fragoza, Robert -- Garrison, Erik -- Gibbs, Richard -- Gumus, Zeynep H -- Herrero, Javier -- Kitabayashi, Naoki -- Kong, Yong -- Lage, Kasper -- Liluashvili, Vaja -- Lipkin, Steven M -- MacArthur, Daniel G -- Marth, Gabor -- Muzny, Donna -- Pers, Tune H -- Ritchie, Graham R S -- Rosenfeld, Jeffrey A -- Sisu, Cristina -- Wei, Xiaomu -- Wilson, Michael -- Xue, Yali -- Yu, Fuli -- 1000 Genomes Project Consortium -- Dermitzakis, Emmanouil T -- Yu, Haiyuan -- Rubin, Mark A -- Tyler-Smith, Chris -- Gerstein, Mark -- 085532/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 095908/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- CA167824/CA/NCI NIH HHS/ -- G12 MD007579/MD/NIMHD NIH HHS/ -- G12 RR003050/RR/NCRR NIH HHS/ -- GM104424/GM/NIGMS NIH HHS/ -- HG005718/HG/NHGRI NIH HHS/ -- HG007000/HG/NHGRI NIH HHS/ -- P20 MD006899/MD/NIMHD NIH HHS/ -- R01 CA166661/CA/NCI NIH HHS/ -- R01 HG002898/HG/NHGRI NIH HHS/ -- R01CA152057/CA/NCI NIH HHS/ -- R01HG4719/HG/NHGRI NIH HHS/ -- U01 CA111275/CA/NCI NIH HHS/ -- U01 HG005718/HG/NHGRI NIH HHS/ -- U01HG6513/HG/NHGRI NIH HHS/ -- U41 HG007000/HG/NHGRI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- UL1 TR000457/TR/NCATS NIH HHS/ -- WT085532/Wellcome Trust/United Kingdom -- WT095908/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):1235587. doi: 10.1126/science.1235587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092746" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites/genetics ; *Genetic Variation ; Genome, Human ; Genomics ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Molecular Sequence Annotation/*methods ; Mutation ; Neoplasms/*genetics ; Polymorphism, Single Nucleotide ; Population/genetics ; RNA, Untranslated/genetics ; Selection, 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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  • 6
    Publication Date: 2011-02-05
    Description: Genomic structural variants (SVs) are abundant in humans, differing from other forms of variation in extent, origin and functional impact. Despite progress in SV characterization, the nucleotide resolution architecture of most SVs remains unknown. We constructed a map of unbalanced SVs (that is, copy number variants) based on whole genome DNA sequencing data from 185 human genomes, integrating evidence from complementary SV discovery approaches with extensive experimental validations. Our map encompassed 22,025 deletions and 6,000 additional SVs, including insertions and tandem duplications. Most SVs (53%) were mapped to nucleotide resolution, which facilitated analysing their origin and functional impact. We examined numerous whole and partial gene deletions with a genotyping approach and observed a depletion of gene disruptions amongst high frequency deletions. Furthermore, we observed differences in the size spectra of SVs originating from distinct formation mechanisms, and constructed a map of SV hotspots formed by common mechanisms. Our analytical framework and SV map serves as a resource for sequencing-based association studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077050/" 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/PMC3077050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mills, Ryan E -- Walter, Klaudia -- Stewart, Chip -- Handsaker, Robert E -- Chen, Ken -- Alkan, Can -- Abyzov, Alexej -- Yoon, Seungtai Chris -- Ye, Kai -- Cheetham, R Keira -- Chinwalla, Asif -- Conrad, Donald F -- Fu, Yutao -- Grubert, Fabian -- Hajirasouliha, Iman -- Hormozdiari, Fereydoun -- Iakoucheva, Lilia M -- Iqbal, Zamin -- Kang, Shuli -- Kidd, Jeffrey M -- Konkel, Miriam K -- Korn, Joshua -- Khurana, Ekta -- Kural, Deniz -- Lam, Hugo Y K -- Leng, Jing -- Li, Ruiqiang -- Li, Yingrui -- Lin, Chang-Yun -- Luo, Ruibang -- Mu, Xinmeng Jasmine -- Nemesh, James -- Peckham, Heather E -- Rausch, Tobias -- Scally, Aylwyn -- Shi, Xinghua -- Stromberg, Michael P -- Stutz, Adrian M -- Urban, Alexander Eckehart -- Walker, Jerilyn A -- Wu, Jiantao -- Zhang, Yujun -- Zhang, Zhengdong D -- Batzer, Mark A -- Ding, Li -- Marth, Gabor T -- McVean, Gil -- Sebat, Jonathan -- Snyder, Michael -- Wang, Jun -- Ye, Kenny -- Eichler, Evan E -- Gerstein, Mark B -- Hurles, Matthew E -- Lee, Charles -- McCarroll, Steven A -- Korbel, Jan O -- 1000 Genomes Project -- 062023/Wellcome Trust/United Kingdom -- 077009/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- 077192/Wellcome Trust/United Kingdom -- 085532/Wellcome Trust/United Kingdom -- G0701805/Medical Research Council/United Kingdom -- G1000758/Medical Research Council/United Kingdom -- P01 HG004120/HG/NHGRI NIH HHS/ -- P41 HG004221/HG/NHGRI NIH HHS/ -- P41 HG004221-01/HG/NHGRI NIH HHS/ -- P41 HG004221-02/HG/NHGRI NIH HHS/ -- P41 HG004221-03/HG/NHGRI NIH HHS/ -- P41 HG004221-03S1/HG/NHGRI NIH HHS/ -- P41 HG004221-03S2/HG/NHGRI NIH HHS/ -- P41 HG004221-03S3/HG/NHGRI NIH HHS/ -- R01 GM059290/GM/NIGMS NIH HHS/ -- R01 GM081533/GM/NIGMS NIH HHS/ -- R01 GM081533-01A1/GM/NIGMS NIH HHS/ -- R01 GM081533-02/GM/NIGMS NIH HHS/ -- R01 GM081533-03/GM/NIGMS NIH HHS/ -- R01 GM081533-04/GM/NIGMS NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG004719/HG/NHGRI NIH HHS/ -- R01 HG004719-01/HG/NHGRI NIH HHS/ -- R01 HG004719-02/HG/NHGRI NIH HHS/ -- R01 HG004719-02S1/HG/NHGRI NIH HHS/ -- R01 HG004719-03/HG/NHGRI NIH HHS/ -- R01 HG004719-04/HG/NHGRI NIH HHS/ -- R01 MH091350/MH/NIMH NIH HHS/ -- RC2 HG005552/HG/NHGRI NIH HHS/ -- RC2 HG005552-01/HG/NHGRI NIH HHS/ -- RC2 HG005552-02/HG/NHGRI NIH HHS/ -- U01 HG005209/HG/NHGRI NIH HHS/ -- U01 HG005209-01/HG/NHGRI NIH HHS/ -- U01 HG005209-02/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 3;470(7332):59-65. doi: 10.1038/nature09708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21293372" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Copy Number Variations/*genetics ; Gene Duplication/genetics ; Genetic Predisposition to Disease/genetics ; *Genetics, Population ; Genome, Human/*genetics ; *Genomics ; Genotype ; Humans ; Mutagenesis, Insertional/genetics ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Deletion/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2011-07-22
    Description: The seminal importance of DNA sequencing to the life sciences, biotechnology and medicine has driven the search for more scalable and lower-cost solutions. Here we describe a DNA sequencing technology in which scalable, low-cost semiconductor manufacturing techniques are used to make an integrated circuit able to directly perform non-optical DNA sequencing of genomes. Sequence data are obtained by directly sensing the ions produced by template-directed DNA polymerase synthesis using all-natural nucleotides on this massively parallel semiconductor-sensing device or ion chip. The ion chip contains ion-sensitive, field-effect transistor-based sensors in perfect register with 1.2 million wells, which provide confinement and allow parallel, simultaneous detection of independent sequencing reactions. Use of the most widely used technology for constructing integrated circuits, the complementary metal-oxide semiconductor (CMOS) process, allows for low-cost, large-scale production and scaling of the device to higher densities and larger array sizes. We show the performance of the system by sequencing three bacterial genomes, its robustness and scalability by producing ion chips with up to 10 times as many sensors and sequencing a human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothberg, Jonathan M -- Hinz, Wolfgang -- Rearick, Todd M -- Schultz, Jonathan -- Mileski, William -- Davey, Mel -- Leamon, John H -- Johnson, Kim -- Milgrew, Mark J -- Edwards, Matthew -- Hoon, Jeremy -- Simons, Jan F -- Marran, David -- Myers, Jason W -- Davidson, John F -- Branting, Annika -- Nobile, John R -- Puc, Bernard P -- Light, David -- Clark, Travis A -- Huber, Martin -- Branciforte, Jeffrey T -- Stoner, Isaac B -- Cawley, Simon E -- Lyons, Michael -- Fu, Yutao -- Homer, Nils -- Sedova, Marina -- Miao, Xin -- Reed, Brian -- Sabina, Jeffrey -- Feierstein, Erika -- Schorn, Michelle -- Alanjary, Mohammad -- Dimalanta, Eileen -- Dressman, Devin -- Kasinskas, Rachel -- Sokolsky, Tanya -- Fidanza, Jacqueline A -- Namsaraev, Eugeni -- McKernan, Kevin J -- Williams, Alan -- Roth, G Thomas -- Bustillo, James -- R01 HG005094/HG/NHGRI NIH HHS/ -- England -- Nature. 2011 Jul 20;475(7356):348-52. doi: 10.1038/nature10242.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ion Torrent by Life Technologies, Suite 100, 246 Goose Lane, Guilford, Connecticut 06437, USA. Jonathan.Rothberg@Lifetech.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21776081" target="_blank"〉PubMed〈/a〉
    Keywords: Escherichia coli/genetics ; Genome, Bacterial/*genetics ; Genome, Human/*genetics ; Genomics/*instrumentation/*methods ; Humans ; Light ; Male ; Rhodopseudomonas/genetics ; *Semiconductors ; Sequence Analysis, DNA/*instrumentation/*methods ; Vibrio/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2012-09-08
    Description: Transcription factors bind in a combinatorial fashion to specify the on-and-off states of genes; the ensemble of these binding events forms a regulatory network, constituting the wiring diagram for a cell. To examine the principles of the human transcriptional regulatory network, we determined the genomic binding information of 119 transcription-related factors in over 450 distinct experiments. We found the combinatorial, co-association of transcription factors to be highly context specific: distinct combinations of factors bind at specific genomic locations. In particular, there are significant differences in the binding proximal and distal to genes. We organized all the transcription factor binding into a hierarchy and integrated it with other genomic information (for example, microRNA regulation), forming a dense meta-network. Factors at different levels have different properties; for instance, top-level transcription factors more strongly influence expression and middle-level ones co-regulate targets to mitigate information-flow bottlenecks. Moreover, these co-regulations give rise to many enriched network motifs (for example, noise-buffering feed-forward loops). Finally, more connected network components are under stronger selection and exhibit a greater degree of allele-specific activity (that is, differential binding to the two parental alleles). The regulatory information obtained in this study will be crucial for interpreting personal genome sequences and understanding basic principles of human biology and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4154057/" 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/PMC4154057/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerstein, Mark B -- Kundaje, Anshul -- Hariharan, Manoj -- Landt, Stephen G -- Yan, Koon-Kiu -- Cheng, Chao -- Mu, Xinmeng Jasmine -- Khurana, Ekta -- Rozowsky, Joel -- Alexander, Roger -- Min, Renqiang -- Alves, Pedro -- Abyzov, Alexej -- Addleman, Nick -- Bhardwaj, Nitin -- Boyle, Alan P -- Cayting, Philip -- Charos, Alexandra -- Chen, David Z -- Cheng, Yong -- Clarke, Declan -- Eastman, Catharine -- Euskirchen, Ghia -- Frietze, Seth -- Fu, Yao -- Gertz, Jason -- Grubert, Fabian -- Harmanci, Arif -- Jain, Preti -- Kasowski, Maya -- Lacroute, Phil -- Leng, Jing -- Lian, Jin -- Monahan, Hannah -- O'Geen, Henriette -- Ouyang, Zhengqing -- Partridge, E Christopher -- Patacsil, Dorrelyn -- Pauli, Florencia -- Raha, Debasish -- Ramirez, Lucia -- Reddy, Timothy E -- Reed, Brian -- Shi, Minyi -- Slifer, Teri -- Wang, Jing -- Wu, Linfeng -- Yang, Xinqiong -- Yip, Kevin Y -- Zilberman-Schapira, Gili -- Batzoglou, Serafim -- Sidow, Arend -- Farnham, Peggy J -- Myers, Richard M -- Weissman, Sherman M -- Snyder, Michael -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32GM008283-24/GM/NIGMS NIH HHS/ -- U01 HG004695/HG/NHGRI NIH HHS/ -- U54 HG004558/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Sep 6;489(7414):91-100. doi: 10.1038/nature11245.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Computational Biology and Bioinformatics, Yale University, New Haven, Connecticut 06520, USA. mark.gerstein@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22955619" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Line ; DNA/*genetics ; *Encyclopedias as Topic ; GATA1 Transcription Factor/metabolism ; Gene Expression Profiling ; Gene Regulatory Networks/*genetics ; Genome, Human/*genetics ; Genomics ; Humans ; K562 Cells ; *Molecular Sequence Annotation ; Organ Specificity ; Phosphorylation/genetics ; Polymorphism, Single Nucleotide/genetics ; Protein Interaction Maps ; RNA, Untranslated/genetics/metabolism ; Regulatory Sequences, Nucleic Acid/*genetics ; Selection, Genetic/genetics ; Transcription Factors/*metabolism ; Transcription Initiation Site
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2014-01-28
    Description: The mammary epithelium undergoes profound morphogenetic changes during development. Architecturally, it comprises two primary lineages, the inner luminal and outer myoepithelial cell layers. Two opposing concepts on the nature of mammary stem cells (MaSCs) in the postnatal gland have emerged. One model, based on classical transplantation assays, postulates that bipotent MaSCs have a key role in coordinating ductal epithelial expansion and maintenance in the adult gland, whereas the second model proposes that only unipotent MaSCs identified by lineage tracing contribute to these processes. Through clonal cell-fate mapping studies using a stochastic multicolour cre reporter combined with a new three-dimensional imaging strategy, we provide evidence for the existence of bipotent MaSCs as well as distinct long-lived progenitor cells. The cellular dynamics at different developmental stages support a model in which both stem and progenitor cells drive morphogenesis during puberty, whereas bipotent MaSCs coordinate ductal homeostasis and remodelling of the mouse adult gland.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rios, Anne C -- Fu, Nai Yang -- Lindeman, Geoffrey J -- Visvader, Jane E -- England -- Nature. 2014 Feb 20;506(7488):322-7. doi: 10.1038/nature12948. Epub 2014 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia [3]. ; 1] Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medicine, The University of Melbourne, Parkville, Victoria 3010, Australia [3] Department of Medical Oncology and Familial Cancer Centre, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia. ; 1] Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24463516" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Tracking ; Clone Cells/cytology/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Humans ; Keratin-14/metabolism ; Mammary Glands, Animal/*cytology ; Mammary Glands, Human/*cytology ; Mice ; Morphogenesis ; Multipotent Stem Cells/*cytology/metabolism ; Puberty ; Receptors, G-Protein-Coupled/metabolism ; Sexual Maturation ; Transcription Factors/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2018-10-11
    Description: Salmonella enterica serovar Typhimurium ( S. Typhimurium) is one of the most used models for bacterial pathogenesis and successful infection requires its adaptation to the low oxygen environment in host gastrointestinal tracts. Central to this process is the Arc ( a erobic r espiratory c ontrol) two-component regulatory system that contains a sensor kinase ArcB and a response regulator ArcA. Nevertheless, a comprehensive profile of the ArcA regulon on the proteome level is still lacking in S. Typhimurium. Here we quantitatively profiled Salmonella proteome during anaerobiosis in an arcA -deleting mutant compared with its parental strain. In addition to known processes under its control, notably we found that ArcA represses ethanolamine utilization by directly binding to the promoter region of the eut operon. Furthermore, we found opposing changes of several bacterial genes on the protein and transcript levels in the arcA -deleting mutant including the virulence genes of Salmonella pathogenicity island 1 (SPI-1), thereby indicating potentially prevalent post-transcriptional regulatory mechanisms. Altogether, our study provides important new insights into ArcA-dependent bacterial physiology and virulence during Salmonella anaerobiosis.
    Print ISSN: 1535-9476
    Electronic ISSN: 1535-9484
    Topics: Biology , Medicine
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