Northerner
Admin (Retired)
- Relationship to Diabetes
- Type 1
It's known that genetics, or an inherited genome, is a major determinant of one's risk for autoimmune diseases, like Type 1 diabetes. In human cells, a person's genome -- about six feet of DNA -- is compressed into the micrometer space of the nucleus via a three-dimensional folding process. Specialized proteins decode the genetic information, reading instruction from our genome in a sequence-specific manner. But what happens when a sequence variation leads to the misinterpretation of instruction, causing pathogenic misfolding of DNA inside the nucleus? Can the different folding patterns make us more susceptible to autoimmune diseases?
Now, in a first-of-its-kind study, researchers at Penn Medicine found, in mice, that changes in DNA sequence can trigger the chromosomes to misfold in a way that puts one at a heightened risk for Type 1 diabetes. The study, published today in Immunity, revealed that differences in DNA sequences dramatically changed how the DNA was folded inside the nucleus, ultimately affecting the regulation -- the induction or repression -- of genes linked to the development Type 1 diabetes.
https://www.sciencedaily.com/releases/2020/02/200211121506.htm
Now, in a first-of-its-kind study, researchers at Penn Medicine found, in mice, that changes in DNA sequence can trigger the chromosomes to misfold in a way that puts one at a heightened risk for Type 1 diabetes. The study, published today in Immunity, revealed that differences in DNA sequences dramatically changed how the DNA was folded inside the nucleus, ultimately affecting the regulation -- the induction or repression -- of genes linked to the development Type 1 diabetes.
https://www.sciencedaily.com/releases/2020/02/200211121506.htm