mRNA is the bridge between DNA and protein production. When the mRNA brings genetic information of DNA out of the nucleus, it needs to wipe out non-coding fragment and splice the remaining fragments together. The cutting process is critical and at least 15% of human diseases are related to cutting errors, including some cancers and neurodegenerative diseases.
Scientists at University of Chicago found two RNA helicases play a key role in the quality control of cutting. They would give RNA tension in order to avoid cutting at the wrong site. The study, published in the journal Cell has changed people's awareness of the RNA helicase in the past. This enzyme can't only move and unwind along the RNA helicase but also pull the choice of regulatory RNA cleavage site.
"These enzymes may play a role in school reading, by applying pressure at a certain distance, the site is not good enough from the spliceosome it out," senior author of the paper, University of Chicago professor Jonathan Staley said.
Staley and colleagues previously showed that work, RNA helicase Prp16 proofreading and Prp22 can play the role of RNA splicing, and now they finally clarify the mechanism of action of these two enzymes. Studies have shown Prp16 and Prp22 not move along the RNA and the spliceosome directly to squeeze down the wrong position; they do not need to work directly to the wrong location. Both enzymes are actually the wrong site away from the spliceosome.
The researchers also found that, Prp16 and Prp22 help find the spliceosome and splice site selection, and ultimately alternative splicing. "These helicases prevent a cut site, while another led to cutting sites," Staley said. "This is the first discovered helicase like splicing factor, like work, so that a different gene to produce a protein product."
Not long ago, a multinational team of splicing first systematic research on a large scale. They published an article that, with a gene encoding a protein isoforms often bears the distinct role, regardless of the structure of how they are similar in the journal Cell. Dr. Xinping Yang First Affiliated Hospital of Southern Medical University (South Hospital) is a co-first author of this article.
December 2014, a study published in the journal Cell, a tiny fragment microexon affects the nervous system protein interaction. Neurons use microexon by selective cutting, microexon protein splicing to generate some of the nervous system on the mRNA required. In this process, if an exception occurs, the function of the nervous system would be a major impact. This discovery opened up a bit so that people new ways to study the etiology of autism.
In healthy cells, the selective cutting is normal physiological activity which is subject to strict regulation. U2AF, as an important cofactor involved in pre-mRNA splicing, has been a hot topic in related fields. However, with regard U2AF's function in mammalian genomes, there are many fundamental issues to be resolved. In October 2014, a research team from Wuhan University published an article in the journal Nature Structural & Molecular Biology, resolving the mechanism of U2AF in the human genome.
Go through this link to learn more: http://www.cusabio.com/Polyclonal-Antibody/MAGEA10-Antibody-11098208.html
没有评论:
发表评论