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  • Humans  (15)
  • Genetic Predisposition to Disease/*genetics  (4)
  • *Genome-Wide Association Study  (2)
  • 11
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    KAI1, a metastasis suppressor gene for prostate cancer on human chromosome 11p11.2 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-12
    Description: A gene from human chromosome 11p11.2 was isolated and was shown to suppress metastasis when introduced into rat AT6.1 prostate cancer cells. Expression of this gene, designated KAI1, was reduced in human cell lines derived from metastatic prostate tumors. KAI1 specifies a protein of 267 amino acids, with four hydrophobic and presumably transmembrane domains and one large extracellular hydrophilic domain with three potential N-glycosylation sites. KAI1 is evolutionarily conserved, is expressed in many human tissues, and encodes a member of a structurally distinct family of leukocyte surface glycoproteins. Decreased expression of this gene may be involved in the malignant progression of prostate and other cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, J T -- Lamb, P W -- Rinker-Schaeffer, C W -- Vukanovic, J -- Ichikawa, T -- Isaacs, J T -- Barrett, J C -- CA 58236/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 May 12;268(5212):884-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754374" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/chemistry/*genetics/physiology ; Antigens, CD82 ; Base Sequence ; Biological Evolution ; *Chromosomes, Human, Pair 11 ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Male ; Membrane Glycoproteins/chemistry/*genetics/physiology ; Mice ; Mice, SCID ; Molecular Sequence Data ; Neoplasm Metastasis/*genetics ; Prostatic Neoplasms/*genetics/pathology ; *Proto-Oncogene Proteins ; Rats ; Transfection ; Tumor Cells, Cultured
    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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  • 12
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    Methylene chloride (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huff, J -- Bucher, J -- Barrett, J C -- New York, N.Y. -- Science. 1996 May 24;272(5265):1083-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Carcinogens/*toxicity ; Female ; Humans ; Liver Neoplasms, Experimental/chemically induced ; Lung Neoplasms/chemically induced ; Male ; Methylene Chloride/*toxicity ; Mice ; Mutagens/*toxicity ; Neoplasms/*chemically induced ; Rats
    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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  • 13
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    The UK10K project identifies rare variants in health and disease (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-09-15
    Description: The contribution of rare and low-frequency variants to human traits is largely unexplored. Here we describe insights from sequencing whole genomes (low read depth, 7x) or exomes (high read depth, 80x) of nearly 10,000 individuals from population-based and disease collections. In extensively phenotyped cohorts we characterize over 24 million novel sequence variants, generate a highly accurate imputation reference panel and identify novel alleles associated with levels of triglycerides (APOB), adiponectin (ADIPOQ) and low-density lipoprotein cholesterol (LDLR and RGAG1) from single-marker and rare variant aggregation tests. We describe population structure and functional annotation of rare and low-frequency variants, use the data to estimate the benefits of sequencing for association studies, and summarize lessons from disease-specific collections. Finally, we make available an extensive resource, including individual-level genetic and phenotypic data and web-based tools to facilitate the exploration of association results.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773891/" 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/PMC4773891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉UK10K Consortium -- Walter, Klaudia -- Min, Josine L -- Huang, Jie -- Crooks, Lucy -- Memari, Yasin -- McCarthy, Shane -- Perry, John R B -- Xu, ChangJiang -- Futema, Marta -- Lawson, Daniel -- Iotchkova, Valentina -- Schiffels, Stephan -- Hendricks, Audrey E -- Danecek, Petr -- Li, Rui -- Floyd, James -- Wain, Louise V -- Barroso, Ines -- Humphries, Steve E -- Hurles, Matthew E -- Zeggini, Eleftheria -- Barrett, Jeffrey C -- Plagnol, Vincent -- Richards, J Brent -- Greenwood, Celia M T -- Timpson, Nicholas J -- Durbin, Richard -- Soranzo, Nicole -- 091551/Wellcome Trust/United Kingdom -- 095515/Wellcome Trust/United Kingdom -- 095564/Wellcome Trust/United Kingdom -- 098498/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- 104036/Wellcome Trust/United Kingdom -- CZD/16/6/4/Chief Scientist Office/United Kingdom -- MC_UU_12013/3/Medical Research Council/United Kingdom -- RG/10/13/28570/British Heart Foundation/United Kingdom -- WT091310/Wellcome Trust/United Kingdom -- England -- Nature. 2015 Oct 1;526(7571):82-90. doi: 10.1038/nature14962. Epub 2015 Sep 14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26367797" target="_blank"〉PubMed〈/a〉
    Keywords: Adiponectin/blood ; Alleles ; Cohort Studies ; Disease/*genetics ; Exome/genetics ; Female ; Genetic Predisposition to Disease/genetics ; Genetic Variation/*genetics ; Genetics, Medical ; Genetics, Population ; Genome, Human/*genetics ; Genome-Wide Association Study ; Genomics ; Great Britain ; *Health ; Humans ; Lipid Metabolism/genetics ; Male ; Molecular Sequence Annotation ; Receptors, LDL/genetics ; Reference Standards ; Sequence Analysis, DNA ; Triglycerides/blood
    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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  • 14
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    Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set out to detect replicated diabetes association signals through analysis of 3757 additional cases and 5346 controls and by integration of our findings with equivalent data from other international consortia. We detected diabetes susceptibility loci in and around the genes CDKAL1, CDKN2A/CDKN2B, and IGF2BP2 and confirmed the recently described associations at HHEX/IDE and SLC30A8. Our findings provide insight into the genetic architecture of type 2 diabetes, emphasizing the contribution of multiple variants of modest effect. The regions identified underscore the importance of pathways influencing pancreatic beta cell development and function in the etiology of type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772310/" 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/PMC3772310/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeggini, Eleftheria -- Weedon, Michael N -- Lindgren, Cecilia M -- Frayling, Timothy M -- Elliott, Katherine S -- Lango, Hana -- Timpson, Nicholas J -- Perry, John R B -- Rayner, Nigel W -- Freathy, Rachel M -- Barrett, Jeffrey C -- Shields, Beverley -- Morris, Andrew P -- Ellard, Sian -- Groves, Christopher J -- Harries, Lorna W -- Marchini, Jonathan L -- Owen, Katharine R -- Knight, Beatrice -- Cardon, Lon R -- Walker, Mark -- Hitman, Graham A -- Morris, Andrew D -- Doney, Alex S F -- Wellcome Trust Case Control Consortium (WTCCC) -- McCarthy, Mark I -- Hattersley, Andrew T -- 083948/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- G0000934/Medical Research Council/United Kingdom -- G0500070/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1336-41. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463249" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Case-Control Studies ; Chromosome Mapping ; Diabetes Mellitus, Type 2/*genetics ; Female ; Genes, p16 ; *Genetic Predisposition to Disease ; *Genome, Human ; Great Britain ; Homeodomain Proteins/genetics ; Humans ; Insulin-Like Growth Factor Binding Proteins/genetics ; Introns ; Male ; Meta-Analysis as Topic ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, Single Nucleotide ; Transcription Factors/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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  • 15
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    Induction of gene amplification by arsenic (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-01
    Description: Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene. The ability of arsenic to induce gene amplification may relate to its carcinogenic effects in humans since amplification of oncogenes is observed in many human tumors. The inability of arsenic to induce gene mutations may relate to the negative results of arsenic in long-term animal studies and suggests that these experiments may not detect some environmental agents that act late in the carcinogenic process in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, T C -- Tanaka, N -- Lamb, P W -- Gilmer, T M -- Barrett, J C -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):79-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arsenates/*pharmacology ; Arsenic/*pharmacology ; *Arsenites ; Cell Line ; DNA/genetics ; Drug Resistance ; Gene Amplification/*drug effects ; Humans ; Methotrexate ; Mice ; Neoplasms, Experimental/chemically induced/genetics ; Nucleic Acid Hybridization ; Oncogenes ; *Sodium Compounds ; Tetrahydrofolate Dehydrogenase/*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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