National Yang-Ming University, Institute of Anatomy and Cell Biology describes research in anatomy
2007 NOV 20 -- Fresh data on anatomy are presented in the report 'The CBF1-independent Notch1 signal pathway activates human c-myc expression partially via transcription factor YY1.' According to recent research from Taipei, Taiwan, "Transcription factor Ying Yang 1 (YY1) indirectly regulates the C promoter-binding factor 1 (CBF1)-dependent Notch1 signaling via direct interaction with the Notch1 receptor intracellular domain (N1IC) on CBF1-response elements. To evaluate the possibility that the N1IC might modulate the gene expression of YY1 target genes through associating with YY1 on the YY1-response elements, we herein investigated the effect of Notch1 signaling on the expression of YY1 target genes." "We found that the N1IC bound to the double-stranded oligonucleotides of YY1-response element to activate luciferase activity of the reporter gene with YY1-response elements through a CBF1-independent manner. Furthermore, the N1IC also bound to the promoter of human c-myc oncogene, a YY1 target gene, to elevate c-myc expression via a CBF1-independent pathway. The activation of reporter genes with YY1-response elements or human c-myc promoter by N1IC depended on the formation of N1IC-YY1-associated complex. To delineate the role of the Notch signal pathway in tumorigenesis, K562 cell lines expressing the N1IC were established. Compared with control cells, the proliferation and the tumor growth of N1IC-expressing K562 cells were suppressed. Taken together, these results suggest that the N1IC enhances the human c-myc promoter activity that is partially modulated by YY1 through a CBF1-independent pathway," wrote W.R. Liao and colleagues, National Yang-Ming University, Institute of Anatomy and Cell Biology. The researchers concluded: "However, the enhancement of c-myc expression by N1IC is insufficient to promote the tumor growth of K562 cells." Liao and colleagues published their study in Carcinogenesis (The CBF1-independent Notch1 signal pathway activates human c-myc expression partially via transcription factor YY1. Carcinogenesis, 2007;28(9):1867-76). For additional information, contact W.R. Liao, Institute of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, 155, Section 2, Li-Nong Street, Taipei 112, Taiwan. Publisher contact information for the journal Carcinogenesis is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England. Keywords: Taiwan, Taipei, Anatomy, Biotechnology, Carcinogenesis, Gene Therapy, Genetics, Genomics, Oligonucleotide, Reporter Gene. This article was prepared by Life Science Weekly editors from staff and other reports. Copyright 2007, Life Science Weekly via NewsRx.com.
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