Ligands are protein molecules that transmit signals between or within cellsLigands work by binding to a cell protein called a receptorAfter binding to the ligand, the receptor can send additional signals to other parts of the cell to regulate our biological processesHowever, if this information is confused, it can cause us to suffer from a range of different diseases
The team, led by Jennifer Cochran, a professor of bioengineering and a professor of bioengineering at Stanford University, has changed a ligand to produce two very different resultsOne group of changes regenerates neuronal cells, while the other group inhibits the growth of lung tumors
The findings, published June 9 in the Proceedings of the National Academy of Sciences, were conducted in mice that simulated actual diseaseThese findings offer hope for the ultimate treatment of neurodegenerative diseases and cancer
A particular ligand will have a specific receptor that usually binds only to the ligand, just like a lock and a keyThe researchers were able to change the arrangement of amino acids in the ligand, and they were able to make millions of keys and let them screen to determine which key might open the matching receptorA more fit, more effective lock key is called super agonistBioengineering can also be used to convert ligands into antagonists, which are equally suitable for receptor locks, but to some extent block signals
"I've always been fascinated by how proteins work as natural molecular machines, and how engineering tools allow us to shape the structure and function of proteins with the creativity of artists, in which case we use amino acids as our palette," Cochran explainsIn 2019, Cochrane teamed up with Alejandro Sweet-Cordero, an associate professor of pediatrics at the University of California, San Francisco, to neutralise a protein that slows the spread of non-small cell lung cancer in miceThe new study builds on the research, led by a team led by graduate student Jun Kim, who designed the ligand CLCF1, which is combined with CNTFR receptors
By changing a set of amino acids in CLCF1, Jin Jun turned the ligand into an superagomiant When they added the superagotic to the tissue petri dish of the damaged neuronal cells, engineering CLCF1 added information signals that promote axon growth, suggesting that the modified ligand was promoting the regeneration of damaged neurons, and by altering the amino acids of CLCF1, Jin Jun and his team were able to turn the ligand into an antagonist that inhibited the growth of lung tumors in mice These proteins may be used in the future to treat neurodegenerative diseases and cancer
Reference: Source: Translational Medicine.com
