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  • 1
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    A comparison of whole-genome shotgun-derived mouse chromosome 16 and the human genome (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    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〉
    Keywords: Animals ; Base Composition ; Chromosomes/*genetics ; Chromosomes, Human/genetics ; Computational Biology ; Conserved Sequence ; Databases, Nucleic Acid ; Evolution, Molecular ; Genes ; Genetic Markers ; *Genome ; *Genome, Human ; Genomics ; Humans ; Mice ; Mice, Inbred A/genetics ; Mice, Inbred DBA/genetics ; Mice, Inbred Strains/*genetics ; Molecular Sequence Data ; Physical Chromosome Mapping ; Proteins/chemistry/genetics ; Sequence Alignment ; *Sequence Analysis, DNA ; Species Specificity ; *Synteny
    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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  • 2
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    The kinetics of two-dimensional TCR and pMHC interactions determine T-cell responsiveness (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-02
    Description: The T-cell receptor (TCR) interacts with peptide-major histocompatibility complexes (pMHC) to discriminate pathogens from self-antigens and trigger adaptive immune responses. Direct physical contact is required between the T cell and the antigen-presenting cell for cross-junctional binding where the TCR and pMHC are anchored on two-dimensional (2D) membranes of the apposing cells. Despite their 2D nature, TCR-pMHC binding kinetics have only been analysed three-dimensionally (3D) with a varying degree of correlation with the T-cell responsiveness. Here we use two mechanical assays to show high 2D affinities between a TCR and its antigenic pMHC driven by rapid on-rates. Compared to their 3D counterparts, 2D affinities and on-rates of the TCR for a panel of pMHC ligands possess far broader dynamic ranges that match that of their corresponding T-cell responses. The best 3D predictor of response is the off-rate, with agonist pMHC dissociating the slowest. In contrast, 2D off-rates are up to 8,300-fold faster, with the agonist pMHC dissociating the fastest. Our 2D data suggest rapid antigen sampling by T cells and serial engagement of a few agonist pMHCs by TCRs in a large self pMHC background. Thus, the cellular environment amplifies the intrinsic TCR-pMHC binding to generate broad affinities and rapid kinetics that determine T-cell responsiveness.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925443/" 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/PMC2925443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jun -- Zarnitsyna, Veronika I -- Liu, Baoyu -- Edwards, Lindsay J -- Jiang, Ning -- Evavold, Brian D -- Zhu, Cheng -- AI060799/AI/NIAID NIH HHS/ -- AI38282/AI/NIAID NIH HHS/ -- NS062358/NS/NINDS NIH HHS/ -- R01 NS062358/NS/NINDS NIH HHS/ -- R01 NS062358-01A1/NS/NINDS NIH HHS/ -- R01 NS071518/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Apr 8;464(7290):932-6. doi: 10.1038/nature08944. Epub 2010 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20357766" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; H-2 Antigens/*immunology/metabolism ; HLA Antigens/*immunology/metabolism ; Humans ; Imaging, Three-Dimensional ; Kinetics ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Immunological ; Receptors, Antigen, T-Cell/agonists/antagonists & ; inhibitors/*immunology/metabolism ; T-Lymphocytes/cytology/*immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Chen Zhu interview. China's modern medical minister. Interview by Richard Stone (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Chen -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1748-9. doi: 10.1126/science.319.5871.1748a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369113" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; China/epidemiology ; Disease Outbreaks ; Humans ; *Medicine, Chinese Traditional ; *Public Health ; Public Health Administration ; Severe Acute Respiratory Syndrome/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    The genome sequence of the malaria mosquito Anopheles gambiae (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-05
    Description: Anopheles gambiae is the principal vector of malaria, a disease that afflicts more than 500 million people and causes more than 1 million deaths each year. Tenfold shotgun sequence coverage was obtained from the PEST strain of A. gambiae and assembled into scaffolds that span 278 million base pairs. A total of 91% of the genome was organized in 303 scaffolds; the largest scaffold was 23.1 million base pairs. There was substantial genetic variation within this strain, and the apparent existence of two haplotypes of approximately equal frequency ("dual haplotypes") in a substantial fraction of the genome likely reflects the outbred nature of the PEST strain. The sequence produced a conservative inference of more than 400,000 single-nucleotide polymorphisms that showed a markedly bimodal density distribution. Analysis of the genome sequence revealed strong evidence for about 14,000 protein-encoding transcripts. Prominent expansions in specific families of proteins likely involved in cell adhesion and immunity were noted. An expressed sequence tag analysis of genes regulated by blood feeding provided insights into the physiological adaptations of a hematophagous insect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holt, Robert A -- Subramanian, G Mani -- Halpern, Aaron -- Sutton, Granger G -- Charlab, Rosane -- Nusskern, Deborah R -- Wincker, Patrick -- Clark, Andrew G -- Ribeiro, Jose M C -- Wides, Ron -- Salzberg, Steven L -- Loftus, Brendan -- Yandell, Mark -- Majoros, William H -- Rusch, Douglas B -- Lai, Zhongwu -- Kraft, Cheryl L -- Abril, Josep F -- Anthouard, Veronique -- Arensburger, Peter -- Atkinson, Peter W -- Baden, Holly -- de Berardinis, Veronique -- Baldwin, Danita -- Benes, Vladimir -- Biedler, Jim -- Blass, Claudia -- Bolanos, Randall -- Boscus, Didier -- Barnstead, Mary -- Cai, Shuang -- Center, Angela -- Chaturverdi, Kabir -- Christophides, George K -- Chrystal, Mathew A -- Clamp, Michele -- Cravchik, Anibal -- Curwen, Val -- Dana, Ali -- Delcher, Art -- Dew, Ian -- Evans, Cheryl A -- Flanigan, Michael -- Grundschober-Freimoser, Anne -- Friedli, Lisa -- Gu, Zhiping -- Guan, Ping -- Guigo, Roderic -- Hillenmeyer, Maureen E -- Hladun, Susanne L -- Hogan, James R -- Hong, Young S -- Hoover, Jeffrey -- Jaillon, Olivier -- Ke, Zhaoxi -- Kodira, Chinnappa -- Kokoza, Elena -- Koutsos, Anastasios -- Letunic, Ivica -- Levitsky, Alex -- Liang, Yong -- Lin, Jhy-Jhu -- Lobo, Neil F -- Lopez, John R -- Malek, Joel A -- McIntosh, Tina C -- Meister, Stephan -- Miller, Jason -- Mobarry, Clark -- Mongin, Emmanuel -- Murphy, Sean D -- O'Brochta, David A -- Pfannkoch, Cynthia -- Qi, Rong -- Regier, Megan A -- Remington, Karin -- Shao, Hongguang -- Sharakhova, Maria V -- Sitter, Cynthia D -- Shetty, Jyoti -- Smith, Thomas J -- Strong, Renee -- Sun, Jingtao -- Thomasova, Dana -- Ton, Lucas Q -- Topalis, Pantelis -- Tu, Zhijian -- Unger, Maria F -- Walenz, Brian -- Wang, Aihui -- Wang, Jian -- Wang, Mei -- Wang, Xuelan -- Woodford, Kerry J -- Wortman, Jennifer R -- Wu, Martin -- Yao, Alison -- Zdobnov, Evgeny M -- Zhang, Hongyu -- Zhao, Qi -- Zhao, Shaying -- Zhu, Shiaoping C -- Zhimulev, Igor -- Coluzzi, Mario -- della Torre, Alessandra -- Roth, Charles W -- Louis, Christos -- Kalush, Francis -- Mural, Richard J -- Myers, Eugene W -- Adams, Mark D -- Smith, Hamilton O -- Broder, Samuel -- Gardner, Malcolm J -- Fraser, Claire M -- Birney, Ewan -- Bork, Peer -- Brey, Paul T -- Venter, J Craig -- Weissenbach, Jean -- Kafatos, Fotis C -- Collins, Frank H -- Hoffman, Stephen L -- R01AI44273/AI/NIAID NIH HHS/ -- U01AI48846/AI/NIAID NIH HHS/ -- U01AI50687/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 4;298(5591):129-49.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, 45 West Gude Drive, Rockville, MD 20850, USA. robert.holt@celera.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12364791" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/classification/*genetics/parasitology/physiology ; Biological Evolution ; Blood ; Chromosome Inversion ; Chromosomes, Artificial, Bacterial ; Computational Biology ; DNA Transposable Elements ; Digestion ; Drosophila melanogaster/genetics ; Enzymes/chemistry/genetics/metabolism ; Expressed Sequence Tags ; Feeding Behavior ; Gene Expression Regulation ; *Genes, Insect ; Genetic Variation ; *Genome ; Haplotypes ; Humans ; Insect Proteins/chemistry/genetics/physiology ; Insect Vectors/genetics/parasitology/physiology ; Malaria, Falciparum/transmission ; Molecular Sequence Data ; Mosquito Control ; Physical Chromosome Mapping ; Plasmodium falciparum/growth & development ; Polymorphism, Single Nucleotide ; Proteome ; *Sequence Analysis, DNA ; Species Specificity ; Transcription Factors/chemistry/genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-08
    Description: TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na(+) transport and salt (NaCl) homeostasis in other cells. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na(+)-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637879/" 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/PMC3637879/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Chuan -- Yosef, Nir -- Thalhamer, Theresa -- Zhu, Chen -- Xiao, Sheng -- Kishi, Yasuhiro -- Regev, Aviv -- Kuchroo, Vijay K -- 1P01HG005062-01/HG/NHGRI NIH HHS/ -- 1P50HG006193-01/HG/NHGRI NIH HHS/ -- AI045757/AI/NIAID NIH HHS/ -- AI073748/AI/NIAID NIH HHS/ -- DP1 CA174427/CA/NCI NIH HHS/ -- DP1 OD003958/OD/NIH HHS/ -- DP1-OD003958-01/OD/NIH HHS/ -- K01 DK090105/DK/NIDDK NIH HHS/ -- K01DK090105/DK/NIDDK NIH HHS/ -- NS030843/NS/NINDS NIH HHS/ -- NS045937/NS/NINDS NIH HHS/ -- P01 AI045757/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P50 HG006193/HG/NHGRI NIH HHS/ -- R01 NS030843/NS/NINDS NIH HHS/ -- R01 NS045937/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 25;496(7446):513-7. doi: 10.1038/nature11984. Epub 2013 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23467085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*drug effects ; Encephalomyelitis, Autoimmune, Experimental/chemically ; induced/immunology/metabolism/pathology ; Forkhead Transcription Factors/metabolism ; HEK293 Cells ; Humans ; Immediate-Early Proteins/deficiency/genetics/*metabolism ; Interferon-gamma/biosynthesis/immunology ; Interleukin-17/biosynthesis/immunology/*metabolism ; Mice ; Phenotype ; Phosphorylation/drug effects ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Receptors, Interleukin/biosynthesis/immunology ; Sodium Chloride/*pharmacology ; Sodium Chloride, Dietary/pharmacology ; Th17 Cells/*drug effects/enzymology/immunology/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    CEACAM1 regulates TIM-3-mediated tolerance and exhaustion (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-11-05
    Description: T-cell immunoglobulin domain and mucin domain-3 (TIM-3, also known as HAVCR2) is an activation-induced inhibitory molecule involved in tolerance and shown to induce T-cell exhaustion in chronic viral infection and cancers. Under some conditions, TIM-3 expression has also been shown to be stimulatory. Considering that TIM-3, like cytotoxic T lymphocyte antigen 4 (CTLA-4) and programmed death 1 (PD-1), is being targeted for cancer immunotherapy, it is important to identify the circumstances under which TIM-3 can inhibit and activate T-cell responses. Here we show that TIM-3 is co-expressed and forms a heterodimer with carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1), another well-known molecule expressed on activated T cells and involved in T-cell inhibition. Biochemical, biophysical and X-ray crystallography studies show that the membrane-distal immunoglobulin-variable (IgV)-like amino-terminal domain of each is crucial to these interactions. The presence of CEACAM1 endows TIM-3 with inhibitory function. CEACAM1 facilitates the maturation and cell surface expression of TIM-3 by forming a heterodimeric interaction in cis through the highly related membrane-distal N-terminal domains of each molecule. CEACAM1 and TIM-3 also bind in trans through their N-terminal domains. Both cis and trans interactions between CEACAM1 and TIM-3 determine the tolerance-inducing function of TIM-3. In a mouse adoptive transfer colitis model, CEACAM1-deficient T cells are hyper-inflammatory with reduced cell surface expression of TIM-3 and regulatory cytokines, and this is restored by T-cell-specific CEACAM1 expression. During chronic viral infection and in a tumour environment, CEACAM1 and TIM-3 mark exhausted T cells. Co-blockade of CEACAM1 and TIM-3 leads to enhancement of anti-tumour immune responses with improved elimination of tumours in mouse colorectal cancer models. Thus, CEACAM1 serves as a heterophilic ligand for TIM-3 that is required for its ability to mediate T-cell inhibition, and this interaction has a crucial role in regulating autoimmunity and anti-tumour immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297519/" 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/PMC4297519/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yu-Hwa -- Zhu, Chen -- Kondo, Yasuyuki -- Anderson, Ana C -- Gandhi, Amit -- Russell, Andrew -- Dougan, Stephanie K -- Petersen, Britt-Sabina -- Melum, Espen -- Pertel, Thomas -- Clayton, Kiera L -- Raab, Monika -- Chen, Qiang -- Beauchemin, Nicole -- Yazaki, Paul J -- Pyzik, Michal -- Ostrowski, Mario A -- Glickman, Jonathan N -- Rudd, Christopher E -- Ploegh, Hidde L -- Franke, Andre -- Petsko, Gregory A -- Kuchroo, Vijay K -- Blumberg, Richard S -- AI039671/AI/NIAID NIH HHS/ -- AI056299/AI/NIAID NIH HHS/ -- AI073748/AI/NIAID NIH HHS/ -- DK0034854/DK/NIDDK NIH HHS/ -- DK044319/DK/NIDDK NIH HHS/ -- DK051362/DK/NIDDK NIH HHS/ -- DK053056/DK/NIDDK NIH HHS/ -- DK088199/DK/NIDDK NIH HHS/ -- GM32415/GM/NIGMS NIH HHS/ -- MOP-93787/Canadian Institutes of Health Research/Canada -- NS045937/NS/NINDS NIH HHS/ -- P01 AI039671/AI/NIAID NIH HHS/ -- P01 AI056299/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- P41 GM111244/GM/NIGMS NIH HHS/ -- R01 DK051362/DK/NIDDK NIH HHS/ -- R01 GM026788/GM/NIGMS NIH HHS/ -- R01 NS045937/NS/NINDS NIH HHS/ -- T32 GM007122/GM/NIGMS NIH HHS/ -- UL1 TR001102/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Jan 15;517(7534):386-90. doi: 10.1038/nature13848. Epub 2014 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA. ; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. ; Rosenstiel Basic Medical Sciences Research Center, Brandeis University, 415 South Street, Waltham, Massachusetts 02454, USA. ; Whitehead Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA. ; Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel 24105, Germany. ; 1] Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA [2] Norwegian PSC Research Center, Division of Cancer Medicine, Surgery and Transplantation, Oslo University Hospital, Oslo 0424, Norway. ; Department of Immunology, University of Toronto, Toronto, Ontario M5S1A8, Canada. ; Cell Signalling Section, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. ; State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. ; Goodman Cancer Research Centre, McGill University, Montreal H3G 1Y6, Canada. ; Beckman Institute, City of Hope, Duarte, California 91010, USA. ; 1] Department of Immunology, University of Toronto, Toronto, Ontario M5S1A8, Canada [2] Keenan Research Centre of St. Michael's Hospital, Toronto, Ontario M5S1A8, Canada. ; GI Pathology, Miraca Life Sciences, Newton, Massachusetts 02464, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/chemistry/immunology/*metabolism ; Autoimmunity/immunology ; Cell Adhesion Molecules/chemistry/immunology/*metabolism ; Cell Line ; Colorectal Neoplasms/immunology ; Disease Models, Animal ; Female ; Humans ; Immune Tolerance/*immunology ; Inflammation/immunology/pathology ; Ligands ; Male ; Membrane Proteins/chemistry/immunology/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Molecular ; Mucous Membrane/immunology/pathology ; Protein Conformation ; Protein Multimerization ; Receptors, Virus/chemistry/immunology/*metabolism ; T-Lymphocytes/*immunology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    OTUD7B controls non-canonical NF-kappaB activation through deubiquitination of TRAF3 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-01-22
    Description: The non-canonical NF-kappaB pathway forms a major arm of NF-kappaB signalling that mediates important biological functions, including lymphoid organogenesis, B-lymphocyte function, and cell growth and survival. Activation of the non-canonical NF-kappaB pathway involves degradation of an inhibitory protein, TNF receptor-associated factor 3 (TRAF3), but how this signalling event is controlled is still unknown. Here we have identified the deubiquitinase OTUD7B as a pivotal regulator of the non-canonical NF-kappaB pathway. OTUD7B deficiency in mice has no appreciable effect on canonical NF-kappaB activation but causes hyperactivation of non-canonical NF-kappaB. In response to non-canonical NF-kappaB stimuli, OTUD7B binds and deubiquitinates TRAF3, thereby inhibiting TRAF3 proteolysis and preventing aberrant non-canonical NF-kappaB activation. Consequently, the OTUD7B deficiency results in B-cell hyper-responsiveness to antigens, lymphoid follicular hyperplasia in the intestinal mucosa, and elevated host-defence ability against an intestinal bacterial pathogen, Citrobacter rodentium. These findings establish OTUD7B as a crucial regulator of signal-induced non-canonical NF-kappaB activation and indicate a mechanism of immune regulation that involves OTUD7B-mediated deubiquitination and stabilization of TRAF3.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578967/" 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/PMC3578967/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Hongbo -- Brittain, George C -- Chang, Jae-Hoon -- Puebla-Osorio, Nahum -- Jin, Jin -- Zal, Anna -- Xiao, Yichuan -- Cheng, Xuhong -- Chang, Mikyoung -- Fu, Yang-Xin -- Zal, Tomasz -- Zhu, Chengming -- Sun, Shao-Cong -- AI057555/AI/NIAID NIH HHS/ -- AI064639/AI/NIAID NIH HHS/ -- CA137059/CA/NCI NIH HHS/ -- GM84459/GM/NIGMS NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA137059/CA/NCI NIH HHS/ -- R01 GM084459/GM/NIGMS NIH HHS/ -- T32 CA009598/CA/NCI NIH HHS/ -- T32CA009598/CA/NCI NIH HHS/ -- England -- Nature. 2013 Feb 21;494(7437):371-4. doi: 10.1038/nature11831. Epub 2013 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/metabolism ; Bacteria/immunology ; Cells, Cultured ; Endopeptidases/deficiency/genetics/*metabolism ; Female ; Fibroblasts ; HEK293 Cells ; Homeostasis ; Humans ; Intestines/immunology ; Male ; Mice ; NF-kappa B/*metabolism ; Proteolysis ; Receptors, Cell Surface/metabolism ; TNF Receptor-Associated Factor 3/*metabolism ; *Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Science-based health care (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Chen -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1429. doi: 10.1126/science.1188965.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299553" target="_blank"〉PubMed〈/a〉
    Keywords: China ; *Delivery of Health Care ; *Evidence-Based Practice ; *Health Care Reform ; Humans
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Reassortment of pandemic H1N1/2009 influenza A virus in swine (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: The emergence of pandemic H1N1/2009 influenza demonstrated that pandemic viruses could be generated in swine. Subsequent reintroduction of H1N1/2009 to swine has occurred in multiple countries. Through systematic surveillance of influenza viruses in swine from a Hong Kong abattoir, we characterize a reassortant progeny of H1N1/2009 with swine viruses. Swine experimentally infected with this reassortant developed mild illness and transmitted infection to contact animals. Continued reassortment of H1N1/2009 with swine influenza viruses could produce variants with transmissibility and altered virulence for humans. Global systematic surveillance of influenza viruses in swine is warranted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569847/" 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/PMC3569847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vijaykrishna, D -- Poon, L L M -- Zhu, H C -- Ma, S K -- Li, O T W -- Cheung, C L -- Smith, G J D -- Peiris, J S M -- Guan, Y -- HHSN266200700005C/AI/NIAID NIH HHS/ -- HHSN266200700005C/PHS HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1529. doi: 10.1126/science.1189132.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Emerging Infectious Diseases and Department of Microbiology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong Special Administrative Region, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558710" target="_blank"〉PubMed〈/a〉
    Keywords: Abattoirs ; Animals ; Disease Outbreaks ; Genes, Viral ; Genotype ; Hemagglutinin Glycoproteins, Influenza Virus/genetics ; Hong Kong ; Humans ; Influenza A Virus, H1N1 Subtype/classification/*genetics/isolation & ; purification/pathogenicity ; Influenza A Virus, H1N2 Subtype/classification/genetics/isolation & purification ; Influenza, Human/epidemiology/virology ; Molecular Sequence Data ; Neuraminidase/genetics ; Orthomyxoviridae Infections/epidemiology/transmission/*veterinary/virology ; Phylogeny ; Population Surveillance ; Reassortant Viruses/classification/*genetics/isolation & purification ; Swine/*virology ; Swine Diseases/epidemiology/transmission/*virology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Transcription factors LRF and BCL11A independently repress expression of fetal hemoglobin (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-01-28
    Description: Genes encoding human beta-type globin undergo a developmental switch from embryonic to fetal to adult-type expression. Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle cell disease and thalassemia. Some experimental results have suggested that these diseases could be treated by induction of fetal-type hemoglobin (HbF). However, the mechanisms that repress HbF in adults remain unclear. We found that the LRF/ZBTB7A transcription factor occupies fetal gamma-globin genes and maintains the nucleosome density necessary for gamma-globin gene silencing in adults, and that LRF confers its repressive activity through a NuRD repressor complex independent of the fetal globin repressor BCL11A. Our study may provide additional opportunities for therapeutic targeting in the treatment of hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" 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/PMC4778394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masuda, Takeshi -- Wang, Xin -- Maeda, Manami -- Canver, Matthew C -- Sher, Falak -- Funnell, Alister P W -- Fisher, Chris -- Suciu, Maria -- Martyn, Gabriella E -- Norton, Laura J -- Zhu, Catherine -- Kurita, Ryo -- Nakamura, Yukio -- Xu, Jian -- Higgs, Douglas R -- Crossley, Merlin -- Bauer, Daniel E -- Orkin, Stuart H -- Kharchenko, Peter V -- Maeda, Takahiro -- R01 AI084905/AI/NIAID NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R56 DK105001/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):285-9. doi: 10.1126/science.aad3312.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia. ; Medical Research Council, Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, UK. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Children's Research Institute, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org. ; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816381" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Erythroblasts/cytology ; Erythropoiesis/genetics ; Fetal Hemoglobin/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Sequence Deletion ; Thalassemia/genetics ; Transcription Factors/genetics/*metabolism ; gamma-Globins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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