ALBERT

Description: The high degree of similarity between the mouse and human genomes is demonstrated through analysis of the sequence of mouse chromosome 16 (Mmu 16), which was obtained as part of a whole-genome shotgun assembly of the mouse genome. The mouse genome is about 10% smaller than the human genome, owing to a lower repetitive DNA content. Comparison of the structure and protein-coding potential of Mmu 16 with that of the homologous segments of the human genome identifies regions of conserved synteny with human chromosomes (Hsa) 3, 8, 12, 16, 21, and 22. Gene content and order are highly conserved between Mmu 16 and the syntenic blocks of the human genome. Of the 731 predicted genes on Mmu 16, 509 align with orthologs on the corresponding portions of the human genome, 44 are likely paralogous to these genes, and 164 genes have homologs elsewhere in the human genome; there are 14 genes for which we could find no human counterpart.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mural, Richard J -- Adams, Mark D -- Myers, Eugene W -- Smith, Hamilton O -- Miklos, George L Gabor -- Wides, Ron -- Halpern, Aaron -- Li, Peter W -- Sutton, Granger G -- Nadeau, Joe -- Salzberg, Steven L -- Holt, Robert A -- Kodira, Chinnappa D -- Lu, Fu -- Chen, Lin -- Deng, Zuoming -- Evangelista, Carlos C -- Gan, Weiniu -- Heiman, Thomas J -- Li, Jiayin -- Li, Zhenya -- Merkulov, Gennady V -- Milshina, Natalia V -- Naik, Ashwinikumar K -- Qi, Rong -- Shue, Bixiong Chris -- Wang, Aihui -- Wang, Jian -- Wang, Xin -- Yan, Xianghe -- Ye, Jane -- Yooseph, Shibu -- Zhao, Qi -- Zheng, Liansheng -- Zhu, Shiaoping C -- Biddick, Kendra -- Bolanos, Randall -- Delcher, Arthur L -- Dew, Ian M -- Fasulo, Daniel -- Flanigan, Michael J -- Huson, Daniel H -- Kravitz, Saul A -- Miller, Jason R -- Mobarry, Clark M -- Reinert, Knut -- Remington, Karin A -- Zhang, Qing -- Zheng, Xiangqun H -- Nusskern, Deborah R -- Lai, Zhongwu -- Lei, Yiding -- Zhong, Wenyan -- Yao, Alison -- Guan, Ping -- Ji, Rui-Ru -- Gu, Zhiping -- Wang, Zhen-Yuan -- Zhong, Fei -- Xiao, Chunlin -- Chiang, Chia-Chien -- Yandell, Mark -- Wortman, Jennifer R -- Amanatides, Peter G -- Hladun, Suzanne L -- Pratts, Eric C -- Johnson, Jeffery E -- Dodson, Kristina L -- Woodford, Kerry J -- Evans, Cheryl A -- Gropman, Barry -- Rusch, Douglas B -- Venter, Eli -- Wang, Mei -- Smith, Thomas J -- Houck, Jarrett T -- Tompkins, Donald E -- Haynes, Charles -- Jacob, Debbie -- Chin, Soo H -- Allen, David R -- Dahlke, Carl E -- Sanders, Robert -- Li, Kelvin -- Liu, Xiangjun -- Levitsky, Alexander A -- Majoros, William H -- Chen, Quan -- Xia, Ashley C -- Lopez, John R -- Donnelly, Michael T -- Newman, Matthew H -- Glodek, Anna -- Kraft, Cheryl L -- Nodell, Marc -- Ali, Feroze -- An, Hui-Jin -- Baldwin-Pitts, Danita -- Beeson, Karen Y -- Cai, Shuang -- Carnes, Mark -- Carver, Amy -- Caulk, Parris M -- Center, Angela -- Chen, Yen-Hui -- Cheng, Ming-Lai -- Coyne, My D -- Crowder, Michelle -- Danaher, Steven -- Davenport, Lionel B -- Desilets, Raymond -- Dietz, Susanne M -- Doup, Lisa -- Dullaghan, Patrick -- Ferriera, Steven -- Fosler, Carl R -- Gire, Harold C -- Gluecksmann, Andres -- Gocayne, Jeannine D -- Gray, Jonathan -- Hart, Brit -- Haynes, Jason -- Hoover, Jeffery -- Howland, Tim -- Ibegwam, Chinyere -- Jalali, Mena -- Johns, David -- Kline, Leslie -- Ma, Daniel S -- MacCawley, Steven -- Magoon, Anand -- Mann, Felecia -- May, David -- McIntosh, Tina C -- Mehta, Somil -- Moy, Linda -- Moy, Mee C -- Murphy, Brian J -- Murphy, Sean D -- Nelson, Keith A -- Nuri, Zubeda -- Parker, Kimberly A -- Prudhomme, Alexandre C -- Puri, Vinita N -- Qureshi, Hina -- Raley, John C -- Reardon, Matthew S -- Regier, Megan A -- Rogers, Yu-Hui C -- Romblad, Deanna L -- Schutz, Jakob -- Scott, John L -- Scott, Richard -- Sitter, Cynthia D -- Smallwood, Michella -- Sprague, Arlan C -- Stewart, Erin -- Strong, Renee V -- Suh, Ellen -- Sylvester, Karena -- Thomas, Reginald -- Tint, Ni Ni -- Tsonis, Christopher -- Wang, Gary -- Wang, George -- Williams, Monica S -- Williams, Sherita M -- Windsor, Sandra M -- Wolfe, Keriellen -- Wu, Mitchell M -- Zaveri, Jayshree -- Chaturvedi, Kabir -- Gabrielian, Andrei E -- Ke, Zhaoxi -- Sun, Jingtao -- Subramanian, Gangadharan -- Venter, J Craig -- Pfannkoch, Cynthia M -- Barnstead, Mary -- Stephenson, Lisa D -- New York, N.Y. -- Science. 2002 May 31;296(5573):1661-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, 45 West Gude Drive, Rockville, MD 20850, USA. richard.mural@celera.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040188" target="_blank"〉PubMed〈/a〉

Description: Multidrug resistance (MDR) is a serious complication during treatment of opportunistic fungal infections that frequently afflict immunocompromised individuals, such as transplant recipients and cancer patients undergoing cytotoxic chemotherapy. Improved knowledge of the molecular pathways controlling MDR in pathogenic fungi should facilitate the development of novel therapies to combat these intransigent infections. MDR is often caused by upregulation of drug efflux pumps by members of the fungal zinc-cluster transcription-factor family (for example Pdr1p orthologues). However, the molecular mechanisms are poorly understood. Here we show that Pdr1p family members in Saccharomyces cerevisiae and the human pathogen Candida glabrata directly bind to structurally diverse drugs and xenobiotics, resulting in stimulated expression of drug efflux pumps and induction of MDR. Notably, this is mechanistically similar to regulation of MDR in vertebrates by the PXR nuclear receptor, revealing an unexpected functional analogy of fungal and metazoan regulators of MDR. We have also uncovered a critical and specific role of the Gal11p/MED15 subunit of the Mediator co-activator and its activator-targeted KIX domain in antifungal/xenobiotic-dependent regulation of MDR. This detailed mechanistic understanding of a fungal nuclear receptor-like gene regulatory pathway provides novel therapeutic targets for the treatment of multidrug-resistant fungal infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thakur, Jitendra K -- Arthanari, Haribabu -- Yang, Fajun -- Pan, Shih-Jung -- Fan, Xiaochun -- Breger, Julia -- Frueh, Dominique P -- Gulshan, Kailash -- Li, Darrick K -- Mylonakis, Eleftherios -- Struhl, Kevin -- Moye-Rowley, W Scott -- Cormack, Brendan P -- Wagner, Gerhard -- Naar, Anders M -- A1046223/PHS HHS/ -- CA127990/CA/NCI NIH HHS/ -- EB2026/EB/NIBIB NIH HHS/ -- GM071449/GM/NIGMS NIH HHS/ -- GM30186/GM/NIGMS NIH HHS/ -- GM47467/GM/NIGMS NIH HHS/ -- GM49825/GM/NIGMS NIH HHS/ -- R01 CA127990/CA/NCI NIH HHS/ -- England -- Nature. 2008 Apr 3;452(7187):604-9. doi: 10.1038/nature06836.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Charlestown, Massachusetts 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385733" target="_blank"〉PubMed〈/a〉

Description: As modern humans migrated out of Africa, they encountered many new environmental conditions, including greater temperature extremes, different pathogens and higher altitudes. These diverse environments are likely to have acted as agents of natural selection and to have led to local adaptations. One of the most celebrated examples in humans is the adaptation of Tibetans to the hypoxic environment of the high-altitude Tibetan plateau. A hypoxia pathway gene, EPAS1, was previously identified as having the most extreme signature of positive selection in Tibetans, and was shown to be associated with differences in haemoglobin concentration at high altitude. Re-sequencing the region around EPAS1 in 40 Tibetan and 40 Han individuals, we find that this gene has a highly unusual haplotype structure that can only be convincingly explained by introgression of DNA from Denisovan or Denisovan-related individuals into humans. Scanning a larger set of worldwide populations, we find that the selected haplotype is only found in Denisovans and in Tibetans, and at very low frequency among Han Chinese. Furthermore, the length of the haplotype, and the fact that it is not found in any other populations, makes it unlikely that the haplotype sharing between Tibetans and Denisovans was caused by incomplete ancestral lineage sorting rather than introgression. Our findings illustrate that admixture with other hominin species has provided genetic variation that helped humans to adapt to new environments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134395/" 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/PMC4134395/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huerta-Sanchez, Emilia -- Jin, Xin -- Asan -- Bianba, Zhuoma -- Peter, Benjamin M -- Vinckenbosch, Nicolas -- Liang, Yu -- Yi, Xin -- He, Mingze -- Somel, Mehmet -- Ni, Peixiang -- Wang, Bo -- Ou, Xiaohua -- Huasang -- Luosang, Jiangbai -- Cuo, Zha Xi Ping -- Li, Kui -- Gao, Guoyi -- Yin, Ye -- Wang, Wei -- Zhang, Xiuqing -- Xu, Xun -- Yang, Huanming -- Li, Yingrui -- Wang, Jian -- Wang, Jun -- Nielsen, Rasmus -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01HG003229/HG/NHGRI NIH HHS/ -- R01HG003229-08S2/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Aug 14;512(7513):194-7. doi: 10.1038/nature13408. Epub 2014 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] BGI-Shenzhen, Shenzhen 518083, China [2] Department of Integrative Biology, University of California, Berkeley, California 94720 USA [3] School of Natural Sciences, University of California, Merced, California 95343 USA [4]. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China [3]. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Binhai Genomics Institute, BGI-Tianjin, Tianjin 300308, China [3] Tianjin Translational Genomics Center, BGI-Tianjin, Tianjin 300308, China [4]. ; 1] The People's Hospital of Lhasa, Lhasa 850000, China [2]. ; Department of Integrative Biology, University of California, Berkeley, California 94720 USA. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Binhai Genomics Institute, BGI-Tianjin, Tianjin 300308, China [3] Tianjin Translational Genomics Center, BGI-Tianjin, Tianjin 300308, China. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Bioinformatics and Computational Biology Program, Iowa State University, Ames, Iowa 50011, USA. ; Department of Biological Sciences, Middle East Technical University, 06800 Ankara, Turkey. ; BGI-Shenzhen, Shenzhen 518083, China. ; The Second People's Hospital of Tibet Autonomous Region, Lhasa 850000, China. ; The People's Hospital of the Tibet Autonomous Region, Lhasa 850000, China. ; The hospital of XiShuangBanNa Dai Nationalities, Autonomous Jinghong, 666100 Yunnan, China. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] The Guangdong Enterprise Key Laboratory of Human Disease Genomics, BGI-Shenzhen, 518083 Shenzhen, China [3] Shenzhen Key Laboratory of Transomics Biotechnologies, BGI-Shenzhen, 518083 Shenzhen, China. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia [3] James D. Watson Institute of Genome Science, 310008 Hangzhou, China. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] James D. Watson Institute of Genome Science, 310008 Hangzhou, China. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia [3] Department of Biology, University of Copenhagen, Ole MaaloesVej 5, 2200 Copenhagen, Denmark [4] Macau University of Science and Technology, AvenidaWai long, Taipa, Macau 999078, China [5] Department of Medicine, University of Hong Kong 999077, Hong Kong. ; 1] BGI-Shenzhen, Shenzhen 518083, China [2] Department of Integrative Biology, University of California, Berkeley, California 94720 USA [3] Department of Statistics, University of California, Berkeley, California 94720, USA [4] Department of Biology, University of Copenhagen, 2200 Copenhagen, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043035" target="_blank"〉PubMed〈/a〉

Description: Antibiotics administered in low doses have been widely used as growth promoters in the agricultural industry since the 1950s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we proposed that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy to young mice and evaluated changes in the composition and capabilities of the gut microbiome. Administration of subtherapeutic antibiotic therapy increased adiposity in young mice and increased hormone levels related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids, increases in colonic short-chain fatty acid levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early-life murine metabolic homeostasis through antibiotic manipulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553221/" 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/PMC3553221/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Ilseung -- Yamanishi, Shingo -- Cox, Laura -- Methe, Barbara A -- Zavadil, Jiri -- Li, Kelvin -- Gao, Zhan -- Mahana, Douglas -- Raju, Kartik -- Teitler, Isabel -- Li, Huilin -- Alekseyenko, Alexander V -- Blaser, Martin J -- 1UL1-RR029893/RR/NCRR NIH HHS/ -- R01 DK090989/DK/NIDDK NIH HHS/ -- T-R01-DK090989/DK/NIDDK NIH HHS/ -- UL1 RR029893/RR/NCRR NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- UL1-TR000038/TR/NCATS NIH HHS/ -- England -- Nature. 2012 Aug 30;488(7413):621-6. doi: 10.1038/nature11400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22914093" target="_blank"〉PubMed〈/a〉

Description: The laboratory mouse shares the majority of its protein-coding genes with humans, making it the premier model organism in biomedical research, yet the two mammals differ in significant ways. To gain greater insights into both shared and species-specific transcriptional and cellular regulatory programs in the mouse, the Mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types. By comparing with the human genome, we not only confirm substantial conservation in the newly annotated potential functional sequences, but also find a large degree of divergence of sequences involved in transcriptional regulation, chromatin state and higher order chromatin organization. Our results illuminate the wide range of evolutionary forces acting on genes and their regulatory regions, and provide a general resource for research into mammalian biology and mechanisms of human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266106/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yue, Feng -- Cheng, Yong -- Breschi, Alessandra -- Vierstra, Jeff -- Wu, Weisheng -- Ryba, Tyrone -- Sandstrom, Richard -- Ma, Zhihai -- Davis, Carrie -- Pope, Benjamin D -- Shen, Yin -- Pervouchine, Dmitri D -- Djebali, Sarah -- Thurman, Robert E -- Kaul, Rajinder -- Rynes, Eric -- Kirilusha, Anthony -- Marinov, Georgi K -- Williams, Brian A -- Trout, Diane -- Amrhein, Henry -- Fisher-Aylor, Katherine -- Antoshechkin, Igor -- DeSalvo, Gilberto -- See, Lei-Hoon -- Fastuca, Meagan -- Drenkow, Jorg -- Zaleski, Chris -- Dobin, Alex -- Prieto, Pablo -- Lagarde, Julien -- Bussotti, Giovanni -- Tanzer, Andrea -- Denas, Olgert -- Li, Kanwei -- Bender, M A -- Zhang, Miaohua -- Byron, Rachel -- Groudine, Mark T -- McCleary, David -- Pham, Long -- Ye, Zhen -- Kuan, Samantha -- Edsall, Lee -- Wu, Yi-Chieh -- Rasmussen, Matthew D -- Bansal, Mukul S -- Kellis, Manolis -- Keller, Cheryl A -- Morrissey, Christapher S -- Mishra, Tejaswini -- Jain, Deepti -- Dogan, Nergiz -- Harris, Robert S -- Cayting, Philip -- Kawli, Trupti -- Boyle, Alan P -- Euskirchen, Ghia -- Kundaje, Anshul -- Lin, Shin -- Lin, Yiing -- Jansen, Camden -- Malladi, Venkat S -- Cline, Melissa S -- Erickson, Drew T -- Kirkup, Vanessa M -- Learned, Katrina -- Sloan, Cricket A -- Rosenbloom, Kate R -- Lacerda de Sousa, Beatriz -- Beal, Kathryn -- Pignatelli, Miguel -- Flicek, Paul -- Lian, Jin -- Kahveci, Tamer -- Lee, Dongwon -- Kent, W James -- Ramalho Santos, Miguel -- Herrero, Javier -- Notredame, Cedric -- Johnson, Audra -- Vong, Shinny -- Lee, Kristen -- Bates, Daniel -- Neri, Fidencio -- Diegel, Morgan -- Canfield, Theresa -- Sabo, Peter J -- Wilken, Matthew S -- Reh, Thomas A -- Giste, Erika -- Shafer, Anthony -- Kutyavin, Tanya -- Haugen, Eric -- Dunn, Douglas -- Reynolds, Alex P -- Neph, Shane -- Humbert, Richard -- Hansen, R Scott -- De Bruijn, Marella -- Selleri, Licia -- Rudensky, Alexander -- Josefowicz, Steven -- Samstein, Robert -- Eichler, Evan E -- Orkin, Stuart H -- Levasseur, Dana -- Papayannopoulou, Thalia -- Chang, Kai-Hsin -- Skoultchi, Arthur -- Gosh, Srikanta -- Disteche, Christine -- Treuting, Piper -- Wang, Yanli -- Weiss, Mitchell J -- Blobel, Gerd A -- Cao, Xiaoyi -- Zhong, Sheng -- Wang, Ting -- Good, Peter J -- Lowdon, Rebecca F -- Adams, Leslie B -- Zhou, Xiao-Qiao -- Pazin, Michael J -- Feingold, Elise A -- Wold, Barbara -- Taylor, James -- Mortazavi, Ali -- Weissman, Sherman M -- Stamatoyannopoulos, John A -- Snyder, Michael P -- Guigo, Roderic -- Gingeras, Thomas R -- Gilbert, David M -- Hardison, Ross C -- Beer, Michael A -- Ren, Bing -- Mouse ENCODE Consortium -- 095908/Wellcome Trust/United Kingdom -- 1U54HG007004/HG/NHGRI NIH HHS/ -- 3RC2HG005602/HG/NHGRI NIH HHS/ -- F31CA165863/CA/NCI NIH HHS/ -- F32HL110473/HL/NHLBI NIH HHS/ -- GM083337/GM/NIGMS NIH HHS/ -- GM085354/GM/NIGMS NIH HHS/ -- K99HL119617/HL/NHLBI NIH HHS/ -- P01 GM085354/GM/NIGMS NIH HHS/ -- P01 HL064190/HL/NHLBI NIH HHS/ -- P01 HL110860/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 DK065806/DK/NIDDK NIH HHS/ -- R01 DK096266/DK/NIDDK NIH HHS/ -- R01 ES024992/ES/NIEHS NIH HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R01 GM083337/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG007175/HG/NHGRI NIH HHS/ -- R01 HG007348/HG/NHGRI NIH HHS/ -- R01 HG007354/HG/NHGRI NIH HHS/ -- R01DK065806/DK/NIDDK NIH HHS/ -- R01HD043997-09/HD/NICHD NIH HHS/ -- R01HG003991/HG/NHGRI NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- R56 DK065806/DK/NIDDK NIH HHS/ -- RC2 HG005573/HG/NHGRI NIH HHS/ -- RC2HG005573/HG/NHGRI NIH HHS/ -- T32 GM081739/GM/NIGMS NIH HHS/ -- U01 HL099656/HL/NHLBI NIH HHS/ -- U01 HL099993/HL/NHLBI NIH HHS/ -- U54 HG006997/HG/NHGRI NIH HHS/ -- U54 HG006998/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Nov 20;515(7527):355-64. doi: 10.1038/nature13992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. [2] Department of Biochemistry and Molecular Biology, College of Medicine, The Pennsylvania State University, Hershey, Pennsylvania 17033, USA. ; Department of Genetics, Stanford University, 300 Pasteur Drive, MC-5477 Stanford, California 94305, USA. ; Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Center for Comparative Genomics and Bioinformatics, Huck Institutes of the Life Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Biological Science, 319 Stadium Drive, Florida State University, Tallahassee, Florida 32306-4295, USA. ; Functional Genomics, Cold Spring Harbor Laboratory, Bungtown Road, Cold Spring Harbor, New York 11724, USA. ; Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Division of Biology, California Institute of Technology, Pasadena, California 91125, USA. ; 1] Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. [2] Department of Theoretical Chemistry, Faculty of Chemistry, University of Vienna, Waehringerstrasse 17/3/303, A-1090 Vienna, Austria. ; Departments of Biology and Mathematics and Computer Science, Emory University, O. Wayne Rollins Research Center, 1510 Clifton Road NE, Atlanta, Georgia 30322, USA. ; 1] Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. [2] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. [2] Department of Radiation Oncology, University of Washington, Seattle, Washington 98195, USA. ; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. ; 1] Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. [2] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California 92697, USA. ; Center for Biomolecular Science and Engineering, School of Engineering, University of California Santa Cruz (UCSC), Santa Cruz, California 95064, USA. ; Departments of Obstetrics/Gynecology and Pathology, and Center for Reproductive Sciences, University of California San Francisco, San Francisco, California 94143, USA. ; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Yale University, Department of Genetics, PO Box 208005, 333 Cedar Street, New Haven, Connecticut 06520-8005, USA. ; Computer &Information Sciences &Engineering, University of Florida, Gainesville, Florida 32611, USA. ; McKusick-Nathans Institute of Genetic Medicine and Department of Biomedical Engineering, Johns Hopkins University, 733 N. Broadway, BRB 573 Baltimore, Maryland 21205, USA. ; 1] European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] Bill Lyons Informatics Centre, UCL Cancer Institute, University College London, London WC1E 6DD, UK. ; Department of Biological Structure, University of Washington, HSB I-516, 1959 NE Pacific Street, Seattle, Washington 98195, USA. ; MRC Molecular Haemotology Unit, University of Oxford, Oxford OX3 9DS, UK. ; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, New York 10065, USA. ; HHMI and Ludwig Center at Memorial Sloan Kettering Cancer Center, Immunology Program, Memorial Sloan Kettering Cancer Canter, New York, New York 10065, USA. ; Dana Farber Cancer Institute, Harvard Medical School, Cambridge, Massachusetts 02138, USA. ; University of Iowa Carver College of Medicine, Department of Internal Medicine, Iowa City, Iowa 52242, USA. ; Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pathology, University of Washington, Seattle, Washington 98195, USA. ; Department of Comparative Medicine, University of Washington, Seattle, Washington 98195, USA. ; Bioinformatics and Genomics program, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Hematology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] Division of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA. [2] Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Bioengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, Missouri 63108, USA. ; NHGRI, National Institutes of Health, 5635 Fishers Lane, Bethesda, Maryland 20892-9307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409824" target="_blank"〉PubMed〈/a〉

Description: Regulated transcription controls the diversity, developmental pathways and spatial organization of the hundreds of cell types that make up a mammal. Using single-molecule cDNA sequencing, we mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body. We find that few genes are truly 'housekeeping', whereas many mammalian promoters are composite entities composed of several closely separated TSSs, with independent cell-type-specific expression profiles. TSSs specific to different cell types evolve at different rates, whereas promoters of broadly expressed genes are the most conserved. Promoter-based expression analysis reveals key transcription factors defining cell states and links them to binding-site motifs. The functions of identified novel transcripts can be predicted by coexpression and sample ontology enrichment analyses. The functional annotation of the mammalian genome 5 (FANTOM5) project provides comprehensive expression profiles and functional annotation of mammalian cell-type-specific transcriptomes with wide applications in biomedical research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529748/" 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/PMC4529748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉FANTOM Consortium and the RIKEN PMI and CLST (DGT) -- Forrest, Alistair R R -- Kawaji, Hideya -- Rehli, Michael -- Baillie, J Kenneth -- de Hoon, Michiel J L -- Haberle, Vanja -- Lassmann, Timo -- Kulakovskiy, Ivan V -- Lizio, Marina -- Itoh, Masayoshi -- Andersson, Robin -- Mungall, Christopher J -- Meehan, Terrence F -- Schmeier, Sebastian -- Bertin, Nicolas -- Jorgensen, Mette -- Dimont, Emmanuel -- Arner, Erik -- Schmidl, Christian -- Schaefer, Ulf -- Medvedeva, Yulia A -- Plessy, Charles -- Vitezic, Morana -- Severin, Jessica -- Semple, Colin A -- Ishizu, Yuri -- Young, Robert S -- Francescatto, Margherita -- Alam, Intikhab -- Albanese, Davide -- Altschuler, Gabriel M -- Arakawa, Takahiro -- Archer, John A C -- Arner, Peter -- Babina, Magda -- Rennie, Sarah -- Balwierz, Piotr J -- Beckhouse, Anthony G -- Pradhan-Bhatt, Swati -- Blake, Judith A -- Blumenthal, Antje -- Bodega, Beatrice -- Bonetti, Alessandro -- Briggs, James -- Brombacher, Frank -- Burroughs, A Maxwell -- Califano, Andrea -- Cannistraci, Carlo V -- Carbajo, Daniel -- Chen, Yun -- Chierici, Marco -- Ciani, Yari -- Clevers, Hans C -- Dalla, Emiliano -- Davis, Carrie A -- Detmar, Michael -- Diehl, Alexander D -- Dohi, Taeko -- Drablos, Finn -- Edge, Albert S B -- Edinger, Matthias -- Ekwall, Karl -- Endoh, Mitsuhiro -- Enomoto, Hideki -- Fagiolini, Michela -- Fairbairn, Lynsey -- Fang, Hai -- Farach-Carson, Mary C -- Faulkner, Geoffrey J -- Favorov, Alexander V -- Fisher, Malcolm E -- Frith, Martin C -- Fujita, Rie -- Fukuda, Shiro -- Furlanello, Cesare -- Furino, Masaaki -- Furusawa, Jun-ichi -- Geijtenbeek, Teunis B -- Gibson, Andrew P -- Gingeras, Thomas -- Goldowitz, Daniel -- Gough, Julian -- Guhl, Sven -- Guler, Reto -- Gustincich, Stefano -- Ha, Thomas J -- Hamaguchi, Masahide -- Hara, Mitsuko -- Harbers, Matthias -- Harshbarger, Jayson -- Hasegawa, Akira -- Hasegawa, Yuki -- Hashimoto, Takehiro -- Herlyn, Meenhard -- Hitchens, Kelly J -- Ho Sui, Shannan J -- Hofmann, Oliver M -- Hoof, Ilka -- Hori, Furni -- Huminiecki, Lukasz -- Iida, Kei -- Ikawa, Tomokatsu -- Jankovic, Boris R -- Jia, Hui -- Joshi, Anagha -- Jurman, Giuseppe -- Kaczkowski, Bogumil -- Kai, Chieko -- Kaida, Kaoru -- Kaiho, Ai -- Kajiyama, Kazuhiro -- Kanamori-Katayama, Mutsumi -- Kasianov, Artem S -- Kasukawa, Takeya -- Katayama, Shintaro -- Kato, Sachi -- Kawaguchi, Shuji -- Kawamoto, Hiroshi -- Kawamura, Yuki I -- Kawashima, Tsugumi -- Kempfle, Judith S -- Kenna, Tony J -- Kere, Juha -- Khachigian, Levon M -- Kitamura, Toshio -- Klinken, S Peter -- Knox, Alan J -- Kojima, Miki -- Kojima, Soichi -- Kondo, Naoto -- Koseki, Haruhiko -- Koyasu, Shigeo -- Krampitz, Sarah -- Kubosaki, Atsutaka -- Kwon, Andrew T -- Laros, Jeroen F J -- Lee, Weonju -- Lennartsson, Andreas -- Li, Kang -- Lilje, Berit -- Lipovich, Leonard -- Mackay-Sim, Alan -- Manabe, Ri-ichiroh -- Mar, Jessica C -- Marchand, Benoit -- Mathelier, Anthony -- Mejhert, Niklas -- Meynert, Alison -- Mizuno, Yosuke -- de Lima Morais, David A -- Morikawa, Hiromasa -- Morimoto, Mitsuru -- Moro, Kazuyo -- Motakis, Efthymios -- Motohashi, Hozumi -- Mummery, Christine L -- Murata, Mitsuyoshi -- Nagao-Sato, Sayaka -- Nakachi, Yutaka -- Nakahara, Fumio -- Nakamura, Toshiyuki -- Nakamura, Yukio -- Nakazato, Kenichi -- van Nimwegen, Erik -- Ninomiya, Noriko -- Nishiyori, Hiromi -- Noma, Shohei -- Noazaki, Tadasuke -- Ogishima, Soichi -- Ohkura, Naganari -- Ohimiya, Hiroko -- Ohno, Hiroshi -- Ohshima, Mitsuhiro -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry A -- Pain, Arnab -- Passier, Robert -- Patrikakis, Margaret -- Persson, Helena -- Piazza, Silvano -- Prendergast, James G D -- Rackham, Owen J L -- Ramilowski, Jordan A -- Rashid, Mamoon -- Ravasi, Timothy -- Rizzu, Patrizia -- Roncador, Marco -- Roy, Sugata -- Rye, Morten B -- Saijyo, Eri -- Sajantila, Antti -- Saka, Akiko -- Sakaguchi, Shimon -- Sakai, Mizuho -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schneider, Claudio -- Schultes, Erik A -- Schulze-Tanzil, Gundula G -- Schwegmann, Anita -- Sengstag, Thierry -- Sheng, Guojun -- Shimoji, Hisashi -- Shimoni, Yishai -- Shin, Jay W -- Simon, Christophe -- Sugiyama, Daisuke -- Sugiyama, Takaai -- Suzuki, Masanori -- Suzuki, Naoko -- Swoboda, Rolf K -- 't Hoen, Peter A C -- Tagami, Michihira -- Takahashi, Naoko -- Takai, Jun -- Tanaka, Hiroshi -- Tatsukawa, Hideki -- Tatum, Zuotian -- Thompson, Mark -- Toyodo, Hiroo -- Toyoda, Tetsuro -- Valen, Elvind -- van de Wetering, Marc -- van den Berg, Linda M -- Verado, Roberto -- Vijayan, Dipti -- Vorontsov, Ilya E -- Wasserman, Wyeth W -- Watanabe, Shoko -- Wells, Christine A -- Winteringham, Louise N -- Wolvetang, Ernst -- Wood, Emily J -- Yamaguchi, Yoko -- Yamamoto, Masayuki -- Yoneda, Misako -- Yonekura, Yohei -- Yoshida, Shigehiro -- Zabierowski, Susan E -- Zhang, Peter G -- Zhao, Xiaobei -- Zucchelli, Silvia -- Summers, Kim M -- Suzuki, Harukazu -- Daub, Carsten O -- Kawai, Jun -- Heutink, Peter -- Hide, Winston -- Freeman, Tom C -- Lenhard, Boris -- Bajic, Vladimir B -- Taylor, Martin S -- Makeev, Vsevolod J -- Sandelin, Albin -- Hume, David A -- Carninci, Piero -- Hayashizaki, Yoshihide -- BB/F003722/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G022771/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I001107/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_PC_U127597124/Medical Research Council/United Kingdom -- MC_UP_1102/1/Medical Research Council/United Kingdom -- R01 DE022969/DE/NIDCR NIH HHS/ -- R01 GM084875/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):462-70. doi: 10.1038/nature13182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670764" target="_blank"〉PubMed〈/a〉

Description: The living Laotian rodent Laonastes aenigmamus, first described in early 2005, has been interpreted as the sole member of the new family Laonastidae on the basis of its distinctive morphology and apparent phylogenetic isolation from other living rodents. Here we show that Laonastes is actually a surviving member of the otherwise extinct rodent family Diatomyidae, known from early Oligocene to late Miocene sites in Pakistan, India, Thailand, China, and Japan. Laonastes is a particularly striking example of the "Lazarus effect" in Recent mammals, whereby a taxon that was formerly thought to be extinct is rediscovered in the extant biota, in this case after a temporal gap of roughly 11 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, Mary R -- Marivaux, Laurent -- Li, Chuan-Kui -- Beard, K Christopher -- Metais, Gregoire -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1456-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Vertebrate Paleontology, Carnegie Museum of Natural History, 4400 Forbes Avenue, Pittsburgh, PA 15213, USA. dawsonm@carnegiemnh.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527978" target="_blank"〉PubMed〈/a〉

Description: The lateral habenula (LHb) has recently emerged as a key brain region in the pathophysiology of depression. However, the molecular mechanism by which LHb becomes hyperactive in depression remains unknown. Through a quantitative proteomic screen, we found that expression of the beta form of calcium/calmodulin-dependent protein kinase type II (betaCaMKappaIotaIota) was significantly up-regulated in the LHb of animal models of depression and down-regulated by antidepressants. Increasing beta-, but not alpha-, CaMKII in the LHb strongly enhanced the synaptic efficacy and spike output of LHb neurons and was sufficient to produce profound depressive symptoms, including anhedonia and behavioral despair. Down-regulation of betaCaMKII levels, blocking its activity or its target molecule the glutamate receptor GluR1 reversed the depressive symptoms. These results identify betaCaMKII as a powerful regulator of LHb neuron function and a key molecular determinant of depression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932364/" 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/PMC3932364/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Kun -- Zhou, Tao -- Liao, Lujian -- Yang, Zhongfei -- Wong, Catherine -- Henn, Fritz -- Malinow, Roberto -- Yates, John R 3rd -- Hu, Hailan -- P41 GM103533/GM/NIGMS NIH HHS/ -- R01 MH067880/MH/NIMH NIH HHS/ -- R01 MH091119/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 30;341(6149):1016-20. doi: 10.1126/science.1240729.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, P R China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23990563" target="_blank"〉PubMed〈/a〉

Description: Blood gas and tissue pH regulation depend on the ability of the brain to sense CO2 and/or H(+) and alter breathing appropriately, a homeostatic process called central respiratory chemosensitivity. We show that selective expression of the proton-activated receptor GPR4 in chemosensory neurons of the mouse retrotrapezoid nucleus (RTN) is required for CO2-stimulated breathing. Genetic deletion of GPR4 disrupted acidosis-dependent activation of RTN neurons, increased apnea frequency, and blunted ventilatory responses to CO2. Reintroduction of GPR4 into RTN neurons restored CO2-dependent RTN neuronal activation and rescued the ventilatory phenotype. Additional elimination of TASK-2 (K(2P)5), a pH-sensitive K(+) channel expressed in RTN neurons, essentially abolished the ventilatory response to CO2. The data identify GPR4 and TASK-2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Natasha N -- Velic, Ana -- Soliz, Jorge -- Shi, Yingtang -- Li, Keyong -- Wang, Sheng -- Weaver, Janelle L -- Sen, Josh -- Abbott, Stephen B G -- Lazarenko, Roman M -- Ludwig, Marie-Gabrielle -- Perez-Reyes, Edward -- Mohebbi, Nilufar -- Bettoni, Carla -- Gassmann, Max -- Suply, Thomas -- Seuwen, Klaus -- Guyenet, Patrice G -- Wagner, Carsten A -- Bayliss, Douglas A -- HL074011/HL/NHLBI NIH HHS/ -- HL108609/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 12;348(6240):1255-60. doi: 10.1126/science.aaa0922. Epub 2015 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. ; Institute of Physiology, University of Zurich, Zurich, CH-8057, Switzerland. ; Institute of Veterinary Physiology, University of Zurich, Zurich, CH-8057, Switzerland. Centre de Recherche du CHU de Quebec, Departement de Pediatrie, Faculte de Medecine, Universite Laval, Quebec, QC, Canada. ; Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. Department of Physiology, Hebei Medical University, Shijiazhuang, Hebei, 050017, China. ; Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia. Department of Neurology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA. ; Novartis Institutes for Biomedical Research, Basel, CH-4002, Switzerland. ; Institute of Veterinary Physiology, University of Zurich, Zurich, CH-8057, Switzerland. ; Institute of Physiology, University of Zurich, Zurich, CH-8057, Switzerland. Wagnerca@access.uzh.ch bayliss@virginia.edu. ; Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. Wagnerca@access.uzh.ch bayliss@virginia.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26068853" target="_blank"〉PubMed〈/a〉

Description: An ethanol-preferring line of rats, developed by selective breeding, consumed as much as 9.4 +/- 1.7 grams of ethanol per kilogram of body weight per day through intragastric self-infusions, yielding blood ethanol concentrations of 92 to 415 milligrams per 100 milliliters. By contrast, the ethanol- nonpreferring line self-administered only 0.7 +/- 0.2 gram per kilogram per day. These findings indicate that the reinforcing effect of ethanol is postabsorptive and is not mediated by the drug's smell or taste. Hence the ethanol-preferring line of rats may be suitable animal model of alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waller, M B -- McBride, W J -- Gatto, G J -- Lumeng, L -- Li, T K -- AA-03243/AA/NIAAA NIH HHS/ -- MH-00203/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1984 Jul 6;225(4657):78-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6539502" target="_blank"〉PubMed〈/a〉