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  • 1
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    Stability, precision, and near-24-hour period of the human circadian pacemaker (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Regulation of circadian period in humans was thought to differ from that of other species, with the period of the activity rhythm reported to range from 13 to 65 hours (median 25.2 hours) and the period of the body temperature rhythm reported to average 25 hours in adulthood, and to shorten with age. However, those observations were based on studies of humans exposed to light levels sufficient to confound circadian period estimation. Precise estimation of the periods of the endogenous circadian rhythms of melatonin, core body temperature, and cortisol in healthy young and older individuals living in carefully controlled lighting conditions has now revealed that the intrinsic period of the human circadian pacemaker averages 24.18 hours in both age groups, with a tight distribution consistent with other species. These findings have important implications for understanding the pathophysiology of disrupted sleep in older people.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Duffy, J F -- Shanahan, T L -- Brown, E N -- Mitchell, J F -- Rimmer, D W -- Ronda, J M -- Silva, E J -- Allan, J S -- Emens, J S -- Dijk, D J -- Kronauer, R E -- MO1-RR02635/RR/NCRR NIH HHS/ -- P01-AG09975/AG/NIA NIH HHS/ -- R01-GM53559/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2177-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Circadian, Neuroendocrine, and Sleep Disorders Section, Division of Endocrinology, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381883" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aging/*physiology ; Biological Clocks/genetics/*physiology ; Body Temperature ; Circadian Rhythm/genetics/*physiology ; Darkness ; Female ; Humans ; Hydrocortisone/blood ; Light ; Male ; Melatonin/blood ; Middle Aged ; Sleep
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Is there an intrinsic period of the circadian clock? Response (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Dijk, D J -- Kronauer, R E -- Brown, E N -- Duffy, J F -- Allan, J S -- Shanahan, T L -- Rimmer, D W -- Ronda, J M -- Mitchell, J F -- Silva, E J -- Emens, J S -- New York, N.Y. -- Science. 2000 May 19;288(5469):1174-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Circadian, Neuroendocrine, and Sleep Disorders Section, Division of Endocrinology, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11536927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/genetics/*physiology ; Chronobiology Phenomena ; Circadian Rhythm/genetics/*physiology ; Darkness ; Humans ; Sleep
    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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  • 3
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    A function for kinesin I in the posterior transport of oskar mRNA and Staufen protein (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: The asymmetric localization of messenger RNA (mRNA) and protein determinants plays an important role in the establishment of complex body plans. In Drosophila oocytes, the anterior localization of bicoid mRNA and the posterior localization of oskar mRNA are key events in establishing the anterior-posterior axis. Although the mechanisms that drive bicoid and oskar localization have been elusive, oocyte microtubules are known to be essential. Here we report that the plus end-directed microtubule motor kinesin I is required for the posterior localization of oskar mRNA and an associated protein, Staufen, but not for the anterior-posterior localization of other asymmetric factors. Thus, a complex containing oskar mRNA and Staufen may be transported along microtubules to the posterior pole by kinesin I.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764218/" 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/PMC1764218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brendza, R P -- Serbus, L R -- Duffy, J B -- Saxton, W M -- R01 GM046295-09/GM/NIGMS NIH HHS/ -- R01GM46295/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2120-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Body Patterning ; Drosophila ; *Drosophila Proteins ; Female ; Homeodomain Proteins/genetics ; Insect Proteins/*genetics ; Kinesin/genetics/*metabolism ; Male ; Microtubules/metabolism ; Molecular Motor Proteins/genetics/*metabolism ; Oocytes/*metabolism ; Oogenesis ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/genetics ; Transgenes
    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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    Biomedicine. Turncoat antibodies (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, P E -- Fried, M -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2009-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, WA 98109, USA. pduffy@sbri.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557864" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/immunology ; Cell Adhesion ; Chondroitin Sulfates/metabolism ; Erythrocytes/metabolism/*parasitology ; Female ; Humans ; Hyaluronic Acid/metabolism ; Immunoglobulin G/immunology/*metabolism ; Malaria Vaccines ; Malaria, Falciparum/immunology/*parasitology/prevention & control ; Placenta/metabolism/parasitology ; Placenta Diseases/immunology/parasitology ; Plasmodium falciparum/immunology ; Pregnancy ; Pregnancy Complications, Parasitic/immunology/*parasitology/prevention & control ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/immunology/*metabolism ; Receptors, Fc/*metabolism ; Trophoblasts/immunology/metabolism/parasitology
    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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    Atopic disease and immunologic response (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, D -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):17; author reply 18-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122695" target="_blank"〉PubMed〈/a〉
    Keywords: BCG Vaccine/immunology ; Dermatitis, Atopic/*immunology ; Humans ; Hypersensitivity, Delayed/immunology ; Tuberculin/*immunology ; Tuberculin Test ; Tuberculosis/immunology
    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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  • 6
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    Chemical genetics of Plasmodium falciparum (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-05-21
    Description: Malaria caused by Plasmodium falciparum is a disease that is responsible for 880,000 deaths per year worldwide. Vaccine development has proved difficult and resistance has emerged for most antimalarial drugs. To discover new antimalarial chemotypes, we have used a phenotypic forward chemical genetic approach to assay 309,474 chemicals. Here we disclose structures and biological activity of the entire library-many of which showed potent in vitro activity against drug-resistant P. falciparum strains-and detailed profiling of 172 representative candidates. A reverse chemical genetic study identified 19 new inhibitors of 4 validated drug targets and 15 novel binders among 61 malarial proteins. Phylochemogenetic profiling in several organisms revealed similarities between Toxoplasma gondii and mammalian cell lines and dissimilarities between P. falciparum and related protozoans. One exemplar compound displayed efficacy in a murine model. Our findings provide the scientific community with new starting points for malaria drug discovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874979/" 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/PMC2874979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guiguemde, W Armand -- Shelat, Anang A -- Bouck, David -- Duffy, Sandra -- Crowther, Gregory J -- Davis, Paul H -- Smithson, David C -- Connelly, Michele -- Clark, Julie -- Zhu, Fangyi -- Jimenez-Diaz, Maria B -- Martinez, Maria S -- Wilson, Emily B -- Tripathi, Abhai K -- Gut, Jiri -- Sharlow, Elizabeth R -- Bathurst, Ian -- El Mazouni, Farah -- Fowble, Joseph W -- Forquer, Isaac -- McGinley, Paula L -- Castro, Steve -- Angulo-Barturen, Inigo -- Ferrer, Santiago -- Rosenthal, Philip J -- Derisi, Joseph L -- Sullivan, David J -- Lazo, John S -- Roos, David S -- Riscoe, Michael K -- Phillips, Margaret A -- Rathod, Pradipsinh K -- Van Voorhis, Wesley C -- Avery, Vicky M -- Guy, R Kiplin -- AI045774/AI/NIAID NIH HHS/ -- AI053680/AI/NIAID NIH HHS/ -- AI067921/AI/NIAID NIH HHS/ -- AI075517/AI/NIAID NIH HHS/ -- AI075594/AI/NIAID NIH HHS/ -- AI080625/AI/NIAID NIH HHS/ -- AI082617/AI/NIAID NIH HHS/ -- AI28724/AI/NIAID NIH HHS/ -- AI35707/AI/NIAID NIH HHS/ -- AI53862/AI/NIAID NIH HHS/ -- AI772682/AI/NIAID NIH HHS/ -- CA78039/CA/NCI NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-03/AI/NIAID NIH HHS/ -- P01 AI035707/AI/NIAID NIH HHS/ -- P01 AI035707-140007/AI/NIAID NIH HHS/ -- P01 CA078039-10/CA/NCI NIH HHS/ -- P41 RR001614/RR/NCRR NIH HHS/ -- P41 RR001614-246970/RR/NCRR NIH HHS/ -- R01 AI045774/AI/NIAID NIH HHS/ -- R01 AI045774-09/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- R56 AI082617/AI/NIAID NIH HHS/ -- R56 AI082617-01/AI/NIAID NIH HHS/ -- U01 AI053862/AI/NIAID NIH HHS/ -- U01 AI053862-05/AI/NIAID NIH HHS/ -- U01 AI075594-03/AI/NIAID NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 May 20;465(7296):311-5. doi: 10.1038/nature09099.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Biology and Therapeutics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/*analysis/isolation & purification/*pharmacology ; Cell Line ; *Drug Discovery ; Drug Evaluation, Preclinical ; Drug Resistance/drug effects ; Drug Therapy, Combination ; Erythrocytes/drug effects/parasitology ; Humans ; Malaria, Falciparum/drug therapy/parasitology ; Mice ; Phenotype ; Phylogeny ; Plasmodium falciparum/*drug effects/*genetics/metabolism ; Reproducibility of Results ; Small Molecule Libraries/chemistry/pharmacology
    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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  • 7
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    Activation-induced B cell fates are selected by intracellular stochastic competition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: In response to stimulation, B lymphocytes pursue a large number of distinct fates important for immune regulation. Whether each cell's fate is determined by external direction, internal stochastic processes, or directed asymmetric division is unknown. Measurement of times to isotype switch, to develop into a plasmablast, and to divide or to die for thousands of cells indicated that each fate is pursued autonomously and stochastically. As a consequence of competition between these processes, censorship of alternative outcomes predicts intricate correlations that are observed in the data. Stochastic competition can explain how the allocation of a proportion of B cells to each cell fate is achieved. The B cell may exemplify how other complex cell differentiation systems are controlled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Ken R -- Wellard, Cameron J -- Markham, John F -- Zhou, Jie H S -- Holmberg, Ross -- Hawkins, Edwin D -- Hasbold, Jhagvaral -- Dowling, Mark R -- Hodgkin, Philip D -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):338-41. doi: 10.1126/science.1213230. Epub 2012 Jan 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hamilton Institute, National University of Ireland, Maynooth, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/*immunology ; Cell Death ; Cell Differentiation ; Cell Division ; Female ; Immunoglobulin Class Switching ; *Lymphocyte Activation ; Mice ; Models, Immunological ; Stochastic Processes
    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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  • 8
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    Ecological context influences epidemic size and parasite-driven evolution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: The occurrence and magnitude of disease outbreaks can strongly influence host evolution. In particular, when hosts face a resistance-fecundity trade-off, they might evolve increased resistance to infection during larger epidemics but increased susceptibility during smaller ones. We tested this theoretical prediction by using a zooplankton-yeast host-parasite system in which ecological factors determine epidemic size. Lakes with high productivity and low predation pressure had large yeast epidemics; during these outbreaks, hosts became more resistant to infection. However, with low productivity and high predation, epidemics remained small and hosts evolved increased susceptibility. Thus, by modulating disease outbreaks, ecological context (productivity and predation) shaped host evolution during epidemics. Consequently, anthropogenic alteration of productivity and predation might strongly influence both ecological and evolutionary outcomes of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Meghan A -- Ochs, Jessica Housley -- Penczykowski, Rachel M -- Civitello, David J -- Klausmeier, Christopher A -- Hall, Spencer R -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1636-8. doi: 10.1126/science.1215429.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230, USA. duffy@gatech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Daphnia/*microbiology/*physiology ; *Ecosystem ; Female ; Fishes ; *Host-Pathogen Interactions ; Indiana ; *Lakes ; Male ; Metschnikowia/*pathogenicity ; Models, Biological ; Population Dynamics ; Predatory Behavior ; Reproduction ; Zooplankton/microbiology/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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  • 9
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    Antibodies to PfSEA-1 block parasite egress from RBCs and protect against malaria infection (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-24
    Description: Novel vaccines are urgently needed to reduce the burden of severe malaria. Using a differential whole-proteome screening method, we identified Plasmodium falciparum schizont egress antigen-1 (PfSEA-1), a 244-kilodalton parasite antigen expressed in schizont-infected red blood cells (RBCs). Antibodies to PfSEA-1 decreased parasite replication by arresting schizont rupture, and conditional disruption of PfSEA-1 resulted in a profound parasite replication defect. Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasitemia and delayed mortality after lethal challenge with the Plasmodium berghei strain ANKA. Tanzanian children with antibodies to recombinant PfSEA-1A (rPfSEA-1A) did not experience severe malaria, and Kenyan adolescents and adults with antibodies to rPfSEA-1A had significantly lower parasite densities than individuals without these antibodies. By blocking schizont egress, PfSEA-1 may synergize with other vaccines targeting hepatocyte and RBC invasion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184151/" 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/PMC4184151/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raj, Dipak K -- Nixon, Christian P -- Nixon, Christina E -- Dvorin, Jeffrey D -- DiPetrillo, Christen G -- Pond-Tor, Sunthorn -- Wu, Hai-Wei -- Jolly, Grant -- Pischel, Lauren -- Lu, Ailin -- Michelow, Ian C -- Cheng, Ling -- Conteh, Solomon -- McDonald, Emily A -- Absalon, Sabrina -- Holte, Sarah E -- Friedman, Jennifer F -- Fried, Michal -- Duffy, Patrick E -- Kurtis, Jonathan D -- 1K08AI100997-01A1/AI/NIAID NIH HHS/ -- DP2 AI112219/AI/NIAID NIH HHS/ -- DP2-AI112219/AI/NIAID NIH HHS/ -- K08 AI100997/AI/NIAID NIH HHS/ -- P20GM103421/GM/NIGMS NIH HHS/ -- P30 AI042853/AI/NIAID NIH HHS/ -- P30AI042853/AI/NIAID NIH HHS/ -- R01 AI102907/AI/NIAID NIH HHS/ -- R01-AI076353/AI/NIAID NIH HHS/ -- R01-AI102907/AI/NIAID NIH HHS/ -- R01-AI52059/AI/NIAID NIH HHS/ -- T32-DA013911/DA/NIDA NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 May 23;344(6186):871-7. doi: 10.1126/science.1254417.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Division of Infectious Diseases, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pediatrics, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. ; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA. ; Fred Hutchinson Cancer Research Center Program in Biostatistics and Biomathematics, Department of Biostatistics and Global Health, University of Washington, Seattle, WA 98109, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. jonathan_kurtis@brown.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855263" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies, Protozoan/blood/*immunology ; Antigens, Protozoan/*immunology ; Child ; Erythrocytes/*parasitology ; Hepatocytes/immunology/parasitology ; Humans ; Immunoglobulin G/blood/immunology ; Kenya ; Malaria/prevention & control ; Malaria Vaccines/*immunology ; Malaria, Falciparum/*prevention & control ; Mice ; Plasmodium berghei/immunology ; Plasmodium falciparum/*growth & development/immunology ; Protozoan Proteins/*immunology ; Recombinant Proteins/immunology ; Schizonts/*growth & development ; Young Adult
    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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  • 10
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    A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-15
    Description: So far, two genes associated with familial melanoma have been identified, accounting for a minority of genetic risk in families. Mutations in CDKN2A account for approximately 40% of familial cases, and predisposing mutations in CDK4 have been reported in a very small number of melanoma kindreds. Here we report the whole-genome sequencing of probands from several melanoma families, which we performed in order to identify other genes associated with familial melanoma. We identify one individual carrying a novel germline variant (coding DNA sequence c.G1075A; protein sequence p.E318K; rs149617956) in the melanoma-lineage-specific oncogene microphthalmia-associated transcription factor (MITF). Although the variant co-segregated with melanoma in some but not all cases in the family, linkage analysis of 31 families subsequently identified to carry the variant generated a log of odds (lod) score of 2.7 under a dominant model, indicating E318K as a possible intermediate risk variant. Consistent with this, the E318K variant was significantly associated with melanoma in a large Australian case-control sample. Likewise, it was similarly associated in an independent case-control sample from the United Kingdom. In the Australian sample, the variant allele was significantly over-represented in cases with a family history of melanoma, multiple primary melanomas, or both. The variant allele was also associated with increased naevus count and non-blue eye colour. Functional analysis of E318K showed that MITF encoded by the variant allele had impaired sumoylation and differentially regulated several MITF targets. These data indicate that MITF is a melanoma-predisposition gene and highlight the utility of whole-genome sequencing to identify novel rare variants associated with disease susceptibility.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266855/" 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/PMC3266855/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, Satoru -- Woods, Susan L -- Boyle, Glen M -- Aoude, Lauren G -- MacGregor, Stuart -- Zismann, Victoria -- Gartside, Michael -- Cust, Anne E -- Haq, Rizwan -- Harland, Mark -- Taylor, John C -- Duffy, David L -- Holohan, Kelly -- Dutton-Regester, Ken -- Palmer, Jane M -- Bonazzi, Vanessa -- Stark, Mitchell S -- Symmons, Judith -- Law, Matthew H -- Schmidt, Christopher -- Lanagan, Cathy -- O'Connor, Linda -- Holland, Elizabeth A -- Schmid, Helen -- Maskiell, Judith A -- Jetann, Jodie -- Ferguson, Megan -- Jenkins, Mark A -- Kefford, Richard F -- Giles, Graham G -- Armstrong, Bruce K -- Aitken, Joanne F -- Hopper, John L -- Whiteman, David C -- Pharoah, Paul D -- Easton, Douglas F -- Dunning, Alison M -- Newton-Bishop, Julia A -- Montgomery, Grant W -- Martin, Nicholas G -- Mann, Graham J -- Bishop, D Timothy -- Tsao, Hensin -- Trent, Jeffrey M -- Fisher, David E -- Hayward, Nicholas K -- Brown, Kevin M -- 10118/Cancer Research UK/United Kingdom -- 10589/Cancer Research UK/United Kingdom -- AR043369-14/AR/NIAMS NIH HHS/ -- C490/A11021/Cancer Research UK/United Kingdom -- C588/A10589/Cancer Research UK/United Kingdom -- C588/A4994/Cancer Research UK/United Kingdom -- C8197/A10123/Cancer Research UK/United Kingdom -- C8216/A6129/Cancer Research UK/United Kingdom -- CA88363/CA/NCI NIH HHS/ -- K24CA149202/CA/NCI NIH HHS/ -- P50CA9368/CA/NCI NIH HHS/ -- R01 AR043369/AR/NIAMS NIH HHS/ -- R01 CA-83115-01A2/CA/NCI NIH HHS/ -- R01 CA088363/CA/NCI NIH HHS/ -- R01 CA088363-09/CA/NCI NIH HHS/ -- R01 CA83115/CA/NCI NIH HHS/ -- England -- Nature. 2011 Nov 13;480(7375):99-103. doi: 10.1038/nature10630.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22080950" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Female ; Gene Expression Regulation, Neoplastic ; *Genetic Predisposition to Disease ; Humans ; Male ; Melanoma/*genetics ; Microphthalmia-Associated Transcription Factor/*genetics ; Middle Aged ; *Mutation ; Sumoylation/genetics ; Young Adult
    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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