A novel platform for identifying metabolic gene functions has already revealed interactions between proteins and metabolites that are fundamental to cell metabolism.
New findings describe how the enzyme CST is recruited to the end of the telomere, where it maintains telomere length with the help of subtle chemical changes made to the protein POT1.
Thomas Tuschl has devoted his career to making discoveries that bridge the gap between bench and business—and have resulted in entirely new classes of drugs.
The end replication problem dictates that telomeres shrink unless telomerase intervenes. But the problem is actually twice as complicated, with telomerase providing only part of the solution.
“I believe this is going to be a very fruitful find. Every time people have studied nutrient sensing, we’ve learned a lot about biology, and many drugs have been developed as a result.”
