New Study Reports Drug Molecules to Regulate Medically Important Protein

New Study Reports Drug Molecules to Regulate Medically Important-Protein

Study carried out by The Scripps Research Institute (TSRI) suggests that various pharmaceutical drugs can regulate signaling and protein expression linked to asthma, obesity, and type 2 diabetes.

The study was published in journal of National Academy of Sciences on December 2017. “The long-term goal is to use this knowledge to help discover new drugs,” said TSRI Professor David Millar, senior author of the study. The was focused on the β2 adrenergic receptor (β2AR), which a protein present on the cell membrane, where it binds external molecules and sends signals to the inside of the cell. β2AR belongs to a class of proteins called G protein-coupled receptors (GPCRs). There are more than 800 known human GPCRs associated with cardiovascular disorders, Parkinson’s disease, and Huntington’s. In fact, GPCRs are so crucial to disease that more than 35% of pharmaceuticals target these receptors.

As a part of the study, scientists incorporated β2AR in nanodiscs, which are small particles that mimic the native cell membrane but contain only a single receptor molecule. A section of the receptor was tagged with a fluorescent probe. The fluorescence intensity was monitored using microscope system. The probe lit up when the receptor was inactive and went dim when active giving the researchers a way to track activation in real time.

According to Cell Free Protein Expression Market report published by Coherent Market Insights, cell free protein expression uses translation machineries to extract the desired cells. It was found that the receptor naturally fluctuates between its active and inactive states in the absence of any drug. Tracking the behavior of an individual receptor molecules revealed these fluctuations for the first time. The findings explain role of β2AR exhibit signaling activity in the absence of any drug molecules and how different drugs can either stimulate or inhibit signaling.

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