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)
 
 
 

Expression of cathepsin L in human tumor cells is under the control of distinct regulatory mechanisms.

Cathepsin L, a cysteine protease, is overexpressed in human tumor cells and plays a major role in melanoma progression. Our aim was herein to identify molecular mechanisms, which contribute to its overexpression. We found that cathepsin L protein expression correlated with mRNA level in tumor cells. Therefore, we focused on mechanisms involved in cathepsin L mRNA regulation. CpG island was localized in the 5' region of cathepsin L gene that encompassed regulatory regions identified as essential for promoter activity. CpG dinucleotides, not methylated in any melanoma cells analysed, were methylated in a B lymphoma cell line, which poorly express cathepsin L. Our data demonstrate that in lymphoma cells, cathepsin L silencing was methylation-dependent. Furthermore, gene amplification was involved in cathepsin L overexpression in one melanoma cell line, while transcriptional mechanisms but not mRNA stability are responsible of cathepsin L overexpression in others melanoma cells. In addition, NF-Y, Sp1, Sp2 and Sp3 transcription factors, essential to basal cathepsin L transcription, are not directly involved in overexpression. Thus, our data provides the first demonstration that cathepsin L expression in tumor cells is under the control of distinct molecular mechanisms.[1]

References

 
WikiGenes - Universities