This parasite self-destructs: Researcher

Image: Caption of the figure accompanying "Reaction hijacking of tyrosine tRNA synthetase as a new antimalaria strategy throughout the life cycle by Stanley C. Xieetal." Science abn0611. Illustrated target of ML901 (colored structure), a new antimalaria compound that exhibits highly specific and potent inhibition of malaria parasites but is nontoxic to mammalian cells. ML901 breaks through specific gaps in an enzyme called tyrosine tRNA synthetase (painted in pink), which is part of the mechanism used by Plasmodium malaria to produce the proteins needed to replicate itself. find. Parasites can quickly shatter and stop, causing illness or infecting others through mosquitoes (purple). Image generated by Leann Tilley and Riley Metcalfe look more Credits: Images generated by Leann Tilley and Riley Metcalfe As current anti-malaria drugs are weakening, new ways to combat malaria are effective for hundreds of millions of people infected around the world each year, seeing the disease go against itself. May provide a good treatment. A study led by the University of Melbourne was announced today Chemistry Identified the antimalaria compound ML901, which suppresses malaria parasites but does not harm the cells of mammals (humans or other mammals). Co-lead author Professor Lian TillyThe Bio21 Institute at the University of Melbourne stated that the ML901 compound effectively makes the parasite a pathogen of its own demise, supporting its efficacy and selectivity. "The ML901 works by an unusual reaction hijacking mechanism," said Professor Tilley. "Imagine a stealth weapon that you can use to launch a self-destructive attack on your vehicle. Hit the brakes and shut off the engine. The ML901 produces the proteins that Plasmodium needs to breed itself. Find a specific gap in the machine you use for and stop it. "There's a lot to do to tweak what we've discovered, but these results really encourage the search for new anti-malaria drugs." In collaboration with Takeda Pharmaceutical Company, the international peak institution for anti-malaria drug development, malaria drugs, and laboratories on five continents, tests were conducted using molecules provided by Takeda, while identifying ML901 compounds. Did. When the ML901 entered the parasite, it itself attached to amino acids, attacking the protein synthesis mechanism from the inside, and rapidly crushing and stopping the parasite. The molecular structure of human cells means that they are less susceptible to attack by ML901. In tests using both human blood cultures and animal models of malaria, the team found that ML901 is resistant to the drugs currently in use, exhibits rapid and long-term effects, and provides excellent parasite control. I found that I killed an insect. Professor Tilley said the compound has been shown to be effective at all stages of the life cycle and can be used to prevent malaria infections and treat diseases. "It also shows the potential to prevent infected people from transmitting the disease to others, which is important to prevent the spread of malaria." Each year, at least 200 million new malaria infections are diagnosed worldwide, killing more than 600,000 in Africa and Southeast Asia. Over the last 50 years, the ever-increasing levels of resistance to anti-malaria drugs have created an imminent crisis and the urgent need for breakthrough drugs. Based on these findings, Professor Tilley said the team is ready to pursue the development of new anti-malaria drug candidates. "We believe this is just the beginning. Now, like the ML901, we may find drugs that target a variety of deadly infections, including multidrug-resistant bacterial infections. This work opens the way for several new drug discoveries. " Media Inquiries: Stephanie Julef | +61 435 151 096 | sjuleff@unimelb.edu.au Article title Tyrosine tRNA synthetase reaction hijacking as an anti-malaria strategy throughout the new life cycle Article publication date June 2, 2022 Disclaimer: AAAS and Eulek Alert! We are not responsible for the accuracy of news releases posted on Eurek Alert! To use the information by contributing to the institution or through the Eurek Alert system. Sources 1/ https://Google.com/ 2/ https://www.eurekalert.org/news-releases/954690 The mention sources can contact us to remove/changing this article

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