Turaga works at Georgia State University.
By Dileep Thekkethil
Indian American scientist Ravi Turaga from Georgia State University is among a group of researchers who have designed a new killer protein that can destroy cells that results in the development and progression life threatening diseases such as cancer.
ProAgio, designed from a human protein, targets the cell receptor integrin v3 at a novel site that has not been targeted by other scientists.
The researchers from Georgia State University found ProAgio induces apoptosis, or programmed cell death, of cells that express integrin v3.
This integrin has been a focus for drug development because abnormal expression of v3 is linked to the development and progression of a number of diseases.
“This integrin pair, v3, is not expressed in high levels in normal tissue,” said Zhi-Ren Liu, lead author of the study and professor in the Department of Biology at Georgia State.
“In most cases, it’s associated with a number of different pathological conditions. Therefore, it constitutes a very good target for multiple disease treatment,” said Liu.
Integrins play a critical role in binding together the extracellular matrix of the cells. The integrin family of proteins consists of alpha and beta subtypes, which form transmembrane heterodimers.
Many scientists consider Integrin v3 as a potential target for drugs that prevent inflammation and the growth of new blood vessels.
Turaga and the other researchers did extensive cell and molecular testing which confirmed ProAgio interacts and binds well with integrin v3.
“We took a unique angle,” Lui said. “We designed a protein that binds to a different site. Once the protein binds to the site, it directly triggers cell death. When we’re able to kill pathological cells, then we’re able to kill the disease.”
In addition, tests with mouse models of cancer showed ProAgio strongly inhibits tumor growth. Tissue analyses indicated the protein effectively prevents the growth of tumor blood vessels, while existing blood vessels were not affected.