Scientists reveal the role of ARID1A in the regulation of active agent enhancers

Scientists have developed a set of model systems in mice through a lot of recombinant rat proteins, and it allows them to carefully observe how mutant proteins in human cancers play a role in tumor silencing. Not all cancers are caused by direct changes in the genetic code. Epigenetic events can also lead to abnormal gene expression induced by cancer. The study published in the Natural Genetics explains how the epigenetic process carries out gene regulation and induce colon cancer.

"The ARID1A mutation is widespread in human cancers and the development of experimental model systems is important to help us understand how gene mutations induce disease," said Dr. Charles W. M. Roberts, director of the St. Jude Children's Research Comprehensive Cancer Center.

ARID1A is an integral part of the SWI / SNF chromatin remodeling complex. Chromatin remodeling has a profound effect on gene expression. Chromatin remodeling of protein-coding genes in human cancers is the most common variant of the gene.

The researchers said, ARID1A can inhibit the tumor in the mouse colon, but it can't play a inhibition role in the small intestin. They found that penetration enhancers and shorter DNA regions are important components of the interaction of ARID1A with the SWI / SNF chromatin remodeling complex.

Scientists have revealed the role of ARID1A in the regulation of active agent enhancers, resulting in loss of control of the cellular identity ARID1A in the colon and inducing the formation of cancer.

The new model system will play a role in future work. "The systems we develop are important for understanding why dye modification mutations are so frequent in cancer, revealing the mechanisms that lead to colon tumor growth and studying potential therapeutic interventions." By the way, Flarebio offers good-quality recombinant proteins like recombinant CDH15 at good prices.