Publications by authors named "Young I Yeom"

2 Publications

  • Page 1 of 1

Planning the human variome project: the Spain report.

Hum Mutat 2009 Apr;30(4):496-510

Division of Personalised Nutrition and Medicine, FDA/National Center for Toxicological Research, Jefferson, Arkansas 72079, USA.

The remarkable progress in characterizing the human genome sequence, exemplified by the Human Genome Project and the HapMap Consortium, has led to the perception that knowledge and the tools (e.g., microarrays) are sufficient for many if not most biomedical research efforts. A large amount of data from diverse studies proves this perception inaccurate at best, and at worst, an impediment for further efforts to characterize the variation in the human genome. Because variation in genotype and environment are the fundamental basis to understand phenotypic variability and heritability at the population level, identifying the range of human genetic variation is crucial to the development of personalized nutrition and medicine. The Human Variome Project (HVP; http://www.humanvariomeproject.org/) was proposed initially to systematically collect mutations that cause human disease and create a cyber infrastructure to link locus specific databases (LSDB). We report here the discussions and recommendations from the 2008 HVP planning meeting held in San Feliu de Guixols, Spain, in May 2008.
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http://dx.doi.org/10.1002/humu.20972DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5879779PMC
April 2009

HPV E6 antisense induces apoptosis in CaSki cells via suppression of E6 splicing.

Exp Mol Med 2002 May;34(2):159-66

Division of Life Sciences, Korea Research Institute of Bioscience and Biotechnology, Yuseong, Taejon.

Cervical cancer is known to be highly associated with viral oncogene E6 and E7 of human papilloma virus. Down-regulation of oncogene expression by antisense-based gene therapy has been extensively studied. To investigate the effect of HPV 16 E6 antisense nucleic acid (AS) on cervical cancer cells, human cervical cancer cell lines, CaSki and SiHa cells harboring HPV 16 genome were transfected with plasmid containing E6(AS). The decreased viability and the apoptotic morphology were observed in E6(AS)-transfected cervical cancer cell lines. By 6 h after transfection, inhibition of E6 splicing, rapid upregulations of p53 and a p53-responsive protein, GADD45, were displayed in E6(AS)-transfected CaSki cells. Furthermore, E6(AS) induced loss of mitochondrial transmembrane potential, release of mitochondrial cytochrome c into the cytoplasm, and subsequent activation of caspase-9 and caspase-3. These results indicate that HPV 16 E6(AS) induces apoptosis in CaSki cells via upregulation of p53 and release of cytochrome c into cytoplasm, consequently activating procaspase-9 and procaspase-3.
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http://dx.doi.org/10.1038/emm.2002.23DOI Listing
May 2002
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