-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Splicing of the noncoding portion of the mRNA (indicated by scissors) enhances its export from the nucleus to the cytoplasm, thereby promoting the expression of oncogenes in tumor cel.
Scientists at KAUST have developed an interactive portal that provides cancer researchers with a platform to study how RNA splicing in noncoding parts of genes promotes the growth of different types of tumo.
The new resource, called SpUR (short for Splicing in Untranslated Regions), which is freely available online, details more than 1,000 splicing events commonly found in noncoding regions of mRNAs downstream of protein-coding stop signa.
With this tool, independent research teams can now further explore the role of individual splicing events in cancer development and progressi.
Computer scientist Gao, postdoctoral fellow Bin Zhang and research engineer Adil Salley created the SpUR database with researchers from the Singapore Institute of Cancer Scienc.
Studies have shown that splicing in a sequence downstream of a gene (called the 3' untranslated region, or 3' utr) is prevalent in cancer, particularly in genes associated with tumor aggressivene.
As a proof of principle, the researchers designed splicing exchangers called antisense oligonucleotides (ASOs) that block this splicing process at 3' U.
One potential target: CTNNB1, a gene that provides instructions for making a protein called beta-caten.
In a mouse model of liver cancer, blocking this splicing resulted in complete tumor regressi.
article title
Pan-cancer, pervasive upregulation of 3'UTR splicing drives tumorigenes.
