The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Editor

Share

Personal info

View

Links

About

Terms

 

 
 
 
 
 

Transcriptional regulation of human beta-galactoside alpha2,6-sialyltransferase (hST6Gal I) gene in colon adenocarcinoma cell line.

Previous studies have shown that hST6Gal I mRNA is overexpressed in colorectal cancer tissues compared with non-malignant or benign tissue. Moreover, Form 1 (hepatic form) mRNA isoform had a marked tendency to accumulate in colon cancer [Int. J. Cancer 88 (2000) 58-65]. These findings suggest that the transcriptional regulation of Form 1 is altered during malignant transformation. We report here transcriptional regulation of the hST6Gal I gene in colon adenocarcinoma cell lines. We characterized P1 promoter region, which regulates Form 1 mRNA expression, using luciferase assays. The result indicates that the nt-156 to -1 region is important for transcriptional activity of hST6Gal I gene in colon adenocarcinoma cell lines. The nt-156 to -1 region contains HNF1 recognition element. Mutation of the HNF1 site reduced luciferase activity by about 80% compared with the wild-type construct, suggesting that HNF1 site is involved in the transcription of Form 1 mRNA in colon cancer cells.[1]

References

  1. Transcriptional regulation of human beta-galactoside alpha2,6-sialyltransferase (hST6Gal I) gene in colon adenocarcinoma cell line. Xu, L., Kurusu, Y., Takizawa, K., Tanaka, J., Matsumoto, K., Taniguchi, A. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
 
WikiGenes - Universities