ALBERT

Description: Mutations in the BRCA2 (breast cancer susceptibility gene 2) tumor suppressor lead to chromosomal instability due to defects in the repair of double-strand DNA breaks (DSBs) by homologous recombination, but BRCA2's role in this process has been unclear. Here, we present the 3.1 angstrom crystal structure of a approximately 90-kilodalton BRCA2 domain bound to DSS1, which reveals three oligonucleotide-binding (OB) folds and a helix-turn-helix (HTH) motif. We also (i) demonstrate that this BRCA2 domain binds single-stranded DNA, (ii) present its 3.5 angstrom structure bound to oligo(dT)9, (iii) provide data that implicate the HTH motif in dsDNA binding, and (iv) show that BRCA2 stimulates RAD51-mediated recombination in vitro. These findings establish that BRCA2 functions directly in homologous recombination and provide a structural and biochemical basis for understanding the loss of recombination-mediated DSB repair in BRCA2-associated cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Haijuan -- Jeffrey, Philip D -- Miller, Julie -- Kinnucan, Elspeth -- Sun, Yutong -- Thoma, Nicolas H -- Zheng, Ning -- Chen, Phang-Lang -- Lee, Wen-Hwa -- Pavletich, Nikola P -- New York, N.Y. -- Science. 2002 Sep 13;297(5588):1837-48.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Sloan-Kettering Division, Joan and Sanford I. Weill Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12228710" target="_blank"〉PubMed〈/a〉

Description: Non-human primates are valuable for modelling human disorders and for developing therapeutic strategies; however, little work has been reported in establishing transgenic non-human primate models of human diseases. Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor impairment, cognitive deterioration and psychiatric disturbances followed by death within 10-15 years of the onset of the symptoms. HD is caused by the expansion of cytosine-adenine-guanine (CAG, translated into glutamine) trinucleotide repeats in the first exon of the human huntingtin (HTT) gene. Mutant HTT with expanded polyglutamine (polyQ) is widely expressed in the brain and peripheral tissues, but causes selective neurodegeneration that is most prominent in the striatum and cortex of the brain. Although rodent models of HD have been developed, these models do not satisfactorily parallel the brain changes and behavioural features observed in HD patients. Because of the close physiological, neurological and genetic similarities between humans and higher primates, monkeys can serve as very useful models for understanding human physiology and diseases. Here we report our progress in developing a transgenic model of HD in a rhesus macaque that expresses polyglutamine-expanded HTT. Hallmark features of HD, including nuclear inclusions and neuropil aggregates, were observed in the brains of the HD transgenic monkeys. Additionally, the transgenic monkeys showed important clinical features of HD, including dystonia and chorea. A transgenic HD monkey model may open the way to understanding the underlying biology of HD better, and to the development of potential therapies. Moreover, our data suggest that it will be feasible to generate valuable non-human primate models of HD and possibly other human genetic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652570/" 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/PMC2652570/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Shang-Hsun -- Cheng, Pei-Hsun -- Banta, Heather -- Piotrowska-Nitsche, Karolina -- Yang, Jin-Jing -- Cheng, Eric C H -- Snyder, Brooke -- Larkin, Katherine -- Liu, Jun -- Orkin, Jack -- Fang, Zhi-Hui -- Smith, Yoland -- Bachevalier, Jocelyne -- Zola, Stuart M -- Li, Shi-Hua -- Li, Xiao-Jiang -- Chan, Anthony W S -- R01 AG019206/AG/NIA NIH HHS/ -- R01 AG019206-07/AG/NIA NIH HHS/ -- R01 NS036232/NS/NINDS NIH HHS/ -- R01 NS036232-09/NS/NINDS NIH HHS/ -- R01 NS041669/NS/NINDS NIH HHS/ -- R01 NS041669-07/NS/NINDS NIH HHS/ -- England -- Nature. 2008 Jun 12;453(7197):921-4. doi: 10.1038/nature06975. Epub 2008 May 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yerkes National Primate Research Center, Emory University, Atlanta, Georgia 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18488016" target="_blank"〉PubMed〈/a〉

Description: The RecA family of ATPases mediates homologous recombination, a reaction essential for maintaining genomic integrity and for generating genetic diversity. RecA, ATP and single-stranded DNA (ssDNA) form a helical filament that binds to double-stranded DNA (dsDNA), searches for homology, and then catalyses the exchange of the complementary strand, producing a new heteroduplex. Here we have solved the crystal structures of the Escherichia coli RecA-ssDNA and RecA-heteroduplex filaments. They show that ssDNA and ATP bind to RecA-RecA interfaces cooperatively, explaining the ATP dependency of DNA binding. The ATP gamma-phosphate is sensed across the RecA-RecA interface by two lysine residues that also stimulate ATP hydrolysis, providing a mechanism for DNA release. The DNA is underwound and stretched globally, but locally it adopts a B-DNA-like conformation that restricts the homology search to Watson-Crick-type base pairing. The complementary strand interacts primarily through base pairing, making heteroduplex formation strictly dependent on complementarity. The underwound, stretched filament conformation probably evolved to destabilize the donor duplex, freeing the complementary strand for homology sampling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhucheng -- Yang, Haijuan -- Pavletich, Nikola P -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 May 22;453(7194):489-4. doi: 10.1038/nature06971.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497818" target="_blank"〉PubMed〈/a〉

Description: The balance between stem cell self-renewal and differentiation is controlled by intrinsic factors and niche signals. In the Drosophila melanogaster ovary, some intrinsic factors promote germline stem cell (GSC) self-renewal, whereas others stimulate differentiation. However, it remains poorly understood how the balance between self-renewal and differentiation is controlled. Here we use D. melanogaster ovarian GSCs to demonstrate that the differentiation factor Bam controls the functional switch of the COP9 complex from self-renewal to differentiation via protein competition. The COP9 complex is composed of eight Csn subunits, Csn1-8, and removes Nedd8 modifications from target proteins. Genetic results indicated that the COP9 complex is required intrinsically for GSC self-renewal, whereas other Csn proteins, with the exception of Csn4, were also required for GSC progeny differentiation. Bam-mediated Csn4 sequestration from the COP9 complex via protein competition inactivated the self-renewing function of COP9 and allowed other Csn proteins to promote GSC differentiation. Therefore, this study reveals a protein-competition-based mechanism for controlling the balance between stem cell self-renewal and differentiation. Because numerous self-renewal factors are ubiquitously expressed throughout the stem cell lineage in various systems, protein competition may function as an important mechanism for controlling the self-renewal-to-differentiation switch.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Lei -- Wang, Su -- Lu, Tinglin -- Weng, Changjiang -- Song, Xiaoqing -- Park, Joseph K -- Sun, Jin -- Yang, Zhi-Hao -- Yu, Junjing -- Tang, Hong -- McKearin, Dennis M -- Chamovitz, Daniel A -- Ni, Jianquan -- Xie, Ting -- GM64428/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Oct 9;514(7521):233-6. doi: 10.1038/nature13562.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China [3]. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA [3]. ; 1] Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China [2]. ; Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA. ; 1] Department of Molecular Biology and Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA. ; Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China. ; Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China. ; Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25119050" target="_blank"〉PubMed〈/a〉

Description: A single-base pair resolution silkworm genetic variation map was constructed from 40 domesticated and wild silkworms, each sequenced to approximately threefold coverage, representing 99.88% of the genome. We identified ~16 million single-nucleotide polymorphisms, many indels, and structural variations. We find that the domesticated silkworms are clearly genetically differentiated from the wild ones, but they have maintained large levels of genetic variability, suggesting a short domestication event involving a large number of individuals. We also identified signals of selection at 354 candidate genes that may have been important during domestication, some of which have enriched expression in the silk gland, midgut, and testis. These data add to our understanding of the domestication processes and may have applications in devising pest control strategies and advancing the use of silkworms as efficient bioreactors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951477/" 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/PMC3951477/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xia, Qingyou -- Guo, Yiran -- Zhang, Ze -- Li, Dong -- Xuan, Zhaoling -- Li, Zhuo -- Dai, Fangyin -- Li, Yingrui -- Cheng, Daojun -- Li, Ruiqiang -- Cheng, Tingcai -- Jiang, Tao -- Becquet, Celine -- Xu, Xun -- Liu, Chun -- Zha, Xingfu -- Fan, Wei -- Lin, Ying -- Shen, Yihong -- Jiang, Lan -- Jensen, Jeffrey -- Hellmann, Ines -- Tang, Si -- Zhao, Ping -- Xu, Hanfu -- Yu, Chang -- Zhang, Guojie -- Li, Jun -- Cao, Jianjun -- Liu, Shiping -- He, Ningjia -- Zhou, Yan -- Liu, Hui -- Zhao, Jing -- Ye, Chen -- Du, Zhouhe -- Pan, Guoqing -- Zhao, Aichun -- Shao, Haojing -- Zeng, Wei -- Wu, Ping -- Li, Chunfeng -- Pan, Minhui -- Li, Jingjing -- Yin, Xuyang -- Li, Dawei -- Wang, Juan -- Zheng, Huisong -- Wang, Wen -- Zhang, Xiuqing -- Li, Songgang -- Yang, Huanming -- Lu, Cheng -- Nielsen, Rasmus -- Zhou, Zeyang -- Wang, Jian -- Xiang, Zhonghuai -- Wang, Jun -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 HG003229-05/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):433-6. doi: 10.1126/science.1176620. Epub 2009 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Sericultural Laboratory of Agricultural Ministry, College of Biotechnology, Southwest University, Chongqing 400715, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713493" target="_blank"〉PubMed〈/a〉

Description: Residents of the Tibetan Plateau show heritable adaptations to extreme altitude. We sequenced 50 exomes of ethnic Tibetans, encompassing coding sequences of 92% of human genes, with an average coverage of 18x per individual. Genes showing population-specific allele frequency changes, which represent strong candidates for altitude adaptation, were identified. The strongest signal of natural selection came from endothelial Per-Arnt-Sim (PAS) domain protein 1 (EPAS1), a transcription factor involved in response to hypoxia. One single-nucleotide polymorphism (SNP) at EPAS1 shows a 78% frequency difference between Tibetan and Han samples, representing the fastest allele frequency change observed at any human gene to date. This SNP's association with erythrocyte abundance supports the role of EPAS1 in adaptation to hypoxia. Thus, a population genomic survey has revealed a functionally important locus in genetic adaptation to high altitude.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711608/" 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/PMC3711608/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Xin -- Liang, Yu -- Huerta-Sanchez, Emilia -- Jin, Xin -- Cuo, Zha Xi Ping -- Pool, John E -- Xu, Xun -- Jiang, Hui -- Vinckenbosch, Nicolas -- Korneliussen, Thorfinn Sand -- Zheng, Hancheng -- Liu, Tao -- He, Weiming -- Li, Kui -- Luo, Ruibang -- Nie, Xifang -- Wu, Honglong -- Zhao, Meiru -- Cao, Hongzhi -- Zou, Jing -- Shan, Ying -- Li, Shuzheng -- Yang, Qi -- Asan -- Ni, Peixiang -- Tian, Geng -- Xu, Junming -- Liu, Xiao -- Jiang, Tao -- Wu, Renhua -- Zhou, Guangyu -- Tang, Meifang -- Qin, Junjie -- Wang, Tong -- Feng, Shuijian -- Li, Guohong -- Huasang -- Luosang, Jiangbai -- Wang, Wei -- Chen, Fang -- Wang, Yading -- Zheng, Xiaoguang -- Li, Zhuo -- Bianba, Zhuoma -- Yang, Ge -- Wang, Xinping -- Tang, Shuhui -- Gao, Guoyi -- Chen, Yong -- Luo, Zhen -- Gusang, Lamu -- Cao, Zheng -- Zhang, Qinghui -- Ouyang, Weihan -- Ren, Xiaoli -- Liang, Huiqing -- Zheng, Huisong -- Huang, Yebo -- Li, Jingxiang -- Bolund, Lars -- Kristiansen, Karsten -- Li, Yingrui -- Zhang, Yong -- Zhang, Xiuqing -- Li, Ruiqiang -- Li, Songgang -- Yang, Huanming -- Nielsen, Rasmus -- Wang, Jun -- Wang, Jian -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 MH084695/MH/NIMH NIH HHS/ -- R01HG003229/HG/NHGRI NIH HHS/ -- R01MHG084695/PHS HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):75-8. doi: 10.1126/science.1190371.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BGI-Shenzhen, Shenzhen 518083, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595611" target="_blank"〉PubMed〈/a〉

Description: A number of human cancers harbor somatic point mutations in the genes encoding isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2). These mutations alter residues in the enzyme active sites and confer a gain-of-function in cancer cells, resulting in the accumulation and secretion of the oncometabolite (R)-2-hydroxyglutarate (2HG). We developed a small molecule, AGI-6780, that potently and selectively inhibits the tumor-associated mutant IDH2/R140Q. A crystal structure of AGI-6780 complexed with IDH2/R140Q revealed that the inhibitor binds in an allosteric manner at the dimer interface. The results of steady-state enzymology analysis were consistent with allostery and slow-tight binding by AGI-6780. Treatment with AGI-6780 induced differentiation of TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro. These data provide proof-of-concept that inhibitors targeting mutant IDH2/R140Q could have potential applications as a differentiation therapy for cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fang -- Travins, Jeremy -- DeLaBarre, Byron -- Penard-Lacronique, Virginie -- Schalm, Stefanie -- Hansen, Erica -- Straley, Kimberly -- Kernytsky, Andrew -- Liu, Wei -- Gliser, Camelia -- Yang, Hua -- Gross, Stefan -- Artin, Erin -- Saada, Veronique -- Mylonas, Elena -- Quivoron, Cyril -- Popovici-Muller, Janeta -- Saunders, Jeffrey O -- Salituro, Francesco G -- Yan, Shunqi -- Murray, Stuart -- Wei, Wentao -- Gao, Yi -- Dang, Lenny -- Dorsch, Marion -- Agresta, Sam -- Schenkein, David P -- Biller, Scott A -- Su, Shinsan M -- de Botton, Stephane -- Yen, Katharine E -- New York, N.Y. -- Science. 2013 May 3;340(6132):622-6. doi: 10.1126/science.1234769. Epub 2013 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agios Pharmaceuticals, Cambridge, MA 02139-4169, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23558173" target="_blank"〉PubMed〈/a〉

Description: Serotonin or 5-hydroxytryptamine (5-HT) regulates a wide spectrum of human physiology through the 5-HT receptor family. We report the crystal structures of the human 5-HT1B G protein-coupled receptor bound to the agonist antimigraine medications ergotamine and dihydroergotamine. The structures reveal similar binding modes for these ligands, which occupy the orthosteric pocket and an extended binding pocket close to the extracellular loops. The orthosteric pocket is formed by residues conserved in the 5-HT receptor family, clarifying the family-wide agonist activity of 5-HT. Compared with the structure of the 5-HT2B receptor, the 5-HT1B receptor displays a 3 angstrom outward shift at the extracellular end of helix V, resulting in a more open extended pocket that explains subtype selectivity. Together with docking and mutagenesis studies, these structures provide a comprehensive structural basis for understanding receptor-ligand interactions and designing subtype-selective serotonergic drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644373/" 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/PMC3644373/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Chong -- Jiang, Yi -- Ma, Jinming -- Wu, Huixian -- Wacker, Daniel -- Katritch, Vsevolod -- Han, Gye Won -- Liu, Wei -- Huang, Xi-Ping -- Vardy, Eyal -- McCorvy, John D -- Gao, Xiang -- Zhou, X Edward -- Melcher, Karsten -- Zhang, Chenghai -- Bai, Fang -- Yang, Huaiyu -- Yang, Linlin -- Jiang, Hualiang -- Roth, Bryan L -- Cherezov, Vadim -- Stevens, Raymond C -- Xu, H Eric -- P50 GM073197/GM/NIGMS NIH HHS/ -- R01 DA027170/DA/NIDA NIH HHS/ -- R01 DA27170/DA/NIDA NIH HHS/ -- R01 DK071662/DK/NIDDK NIH HHS/ -- R01 MH061887/MH/NIMH NIH HHS/ -- R01 MH61887/MH/NIMH NIH HHS/ -- U19 MH082441/MH/NIMH NIH HHS/ -- U19 MH82441/MH/NIMH NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 3;340(6132):610-4. doi: 10.1126/science.1232807. Epub 2013 Mar 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23519210" target="_blank"〉PubMed〈/a〉

Description: Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390078/" 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/PMC4390078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Guojie -- Li, Cai -- Li, Qiye -- Li, Bo -- Larkin, Denis M -- Lee, Chul -- Storz, Jay F -- Antunes, Agostinho -- Greenwold, Matthew J -- Meredith, Robert W -- Odeen, Anders -- Cui, Jie -- Zhou, Qi -- Xu, Luohao -- Pan, Hailin -- Wang, Zongji -- Jin, Lijun -- Zhang, Pei -- Hu, Haofu -- Yang, Wei -- Hu, Jiang -- Xiao, Jin -- Yang, Zhikai -- Liu, Yang -- Xie, Qiaolin -- Yu, Hao -- Lian, Jinmin -- Wen, Ping -- Zhang, Fang -- Li, Hui -- Zeng, Yongli -- Xiong, Zijun -- Liu, Shiping -- Zhou, Long -- Huang, Zhiyong -- An, Na -- Wang, Jie -- Zheng, Qiumei -- Xiong, Yingqi -- Wang, Guangbiao -- Wang, Bo -- Wang, Jingjing -- Fan, Yu -- da Fonseca, Rute R -- Alfaro-Nunez, Alonzo -- Schubert, Mikkel -- Orlando, Ludovic -- Mourier, Tobias -- Howard, Jason T -- Ganapathy, Ganeshkumar -- Pfenning, Andreas -- Whitney, Osceola -- Rivas, Miriam V -- Hara, Erina -- Smith, Julia -- Farre, Marta -- Narayan, Jitendra -- Slavov, Gancho -- Romanov, Michael N -- Borges, Rui -- Machado, Joao Paulo -- Khan, Imran -- Springer, Mark S -- Gatesy, John -- Hoffmann, Federico G -- Opazo, Juan C -- Hastad, Olle -- Sawyer, Roger H -- Kim, Heebal -- Kim, Kyu-Won -- Kim, Hyeon Jeong -- Cho, Seoae -- Li, Ning -- Huang, Yinhua -- Bruford, Michael W -- Zhan, Xiangjiang -- Dixon, Andrew -- Bertelsen, Mads F -- Derryberry, Elizabeth -- Warren, Wesley -- Wilson, Richard K -- Li, Shengbin -- Ray, David A -- Green, Richard E -- O'Brien, Stephen J -- Griffin, Darren -- Johnson, Warren E -- Haussler, David -- Ryder, Oliver A -- Willerslev, Eske -- Graves, Gary R -- Alstrom, Per -- Fjeldsa, Jon -- Mindell, David P -- Edwards, Scott V -- Braun, Edward L -- Rahbek, Carsten -- Burt, David W -- Houde, Peter -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Avian Genome Consortium -- Jarvis, Erich D -- Gilbert, M Thomas P -- Wang, Jun -- DP1 OD000448/OD/NIH HHS/ -- DP1OD000448/OD/NIH HHS/ -- R01 HL087216/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1311-20. doi: 10.1126/science.1251385. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. ; Royal Veterinary College, University of London, London, UK. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Departamento de Biologia, Faculdade de Ciencias, Universidade do Porto, Rua do Campo Alegre, 4169-007 Porto, Portugal. ; Department of Biological Sciences, University of South Carolina, Columbia, SC, USA. ; Department of Biology and Molecular Biology, Montclair State University, Montclair, NJ 07043, USA. ; Department of Animal Ecology, Uppsala University, Norbyvagen 18D, S-752 36 Uppsala, Sweden. ; Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Biological Sciences and Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia. Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore 169857, Singapore. ; Department of Integrative Biology University of California, Berkeley, CA 94720, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. College of Life Sciences, Wuhan University, Wuhan 430072, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. BGI Education Center,University of Chinese Academy of Sciences,Shenzhen, 518083, China. ; Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, UK. ; School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Instituto de Ciencias Biomedicas Abel Salazar (ICBAS), Universidade do Porto, Portugal. ; Department of Biology, University of California Riverside, Riverside, CA 92521, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. ; Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, Post Office Box 7011, S-750 07, Uppsala, Sweden. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 151-742, Republic of Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. ; Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. College of Animal Science and Technology, China Agricultural University, Beijing 100094, China. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. Key Lab of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101 China. ; International Wildlife Consultants, Carmarthen SA33 5YL, Wales, UK. ; Centre for Zoo and Wild Animal Health, Copenhagen Zoo, Roskildevej 38, DK-2000 Frederiksberg, Denmark. ; Department of Ecology and Evolutionary Biology, Tulane University, New Orleans, LA, USA. Museum of Natural Science, Louisiana State University, Baton Rouge, LA 70803, USA. ; The Genome Institute at Washington University, St. Louis, MO 63108, USA. ; College of Medicine and Forensics, Xi'an Jiaotong University, Xi'an, 710061, China. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ; Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, Russia. Nova Southeastern University Oceanographic Center 8000 N Ocean Drive, Dania, FL 33004, USA. ; Smithsonian Conservation Biology Institute, National Zoological Park, 1500 Remount Road, Front Royal, VA 22630, USA. ; Genetics Division, San Diego Zoo Institute for Conservation Research, 15600 San Pasqual Valley Road, Escondido, CA 92027, USA. ; Department of Vertebrate Zoology, MRC-116, National Museum of Natural History, Smithsonian Institution, Post Office Box 37012, Washington, DC 20013-7012, USA. Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China. Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, SE-750 07 Uppsala, Sweden. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Department of Biochemistry & Biophysics, University of California, San Francisco, CA 94158, USA. ; Department of Organismic and Evolutionary Biology and Museum of Comparative Zoology, Harvard University, 26 Oxford Street, Cambridge, MA 02138, USA. ; Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. Imperial College London, Grand Challenges in Ecosystems and the Environment Initiative, Silwood Park Campus, Ascot, Berkshire SL5 7PY, UK. ; Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Roslin Institute Building, University of Edinburgh, Easter Bush Campus, Midlothian EH25 9RG, UK. ; Department of Biology, New Mexico State University, Box 30001 MSC 3AF, Las Cruces, NM 88003, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA Laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia, 6102, Australia. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. Department of Biology, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Medicine, University of Hong Kong, Hong Kong. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504712" target="_blank"〉PubMed〈/a〉

Description: The Escherichia coli catabolite activator protein (CAP) activates transcription at P(lac), P(gal), and other promoters through interactions with the RNA polymerase alpha subunit carboxyl-terminal domain (alphaCTD). We determined the crystal structure of the CAP-alphaCTD-DNA complex at a resolution of 3.1 angstroms. CAP makes direct protein-protein interactions with alphaCTD, and alphaCTD makes direct protein-DNA interactions with the DNA segment adjacent to the DNA site for CAP. There are no large-scale conformational changes in CAP and alphaCTD, and the interface between CAP and alphaCTD is small. These findings are consistent with the proposal that activation involves a simple "recruitment" mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benoff, Brian -- Yang, Huanwang -- Lawson, Catherine L -- Parkinson, Gary -- Liu, Jinsong -- Blatter, Erich -- Ebright, Yon W -- Berman, Helen M -- Ebright, Richard H -- GM21589/GM/NIGMS NIH HHS/ -- GM41376/GM/NIGMS NIH HHS/ -- GM64375/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 30;297(5586):1562-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute and Department of Chemistry, Howard Hughes Medical Institute, Rutgers University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12202833" target="_blank"〉PubMed〈/a〉