The Murphy Laboratory focuses on the use of high throughput genomic technologies as a means to understand the immune mechanisms that lead to graft injury and loss, with the aim of identifying gene expression profiles and or genetic variants that may be used to predict those at greatest risk. Data from the laboratory has shown that genetic polymorphisms in key immunoregulatory molecules, specifically chemokines and their receptors, and costimulatory molecules, are associated with altered risk for acute rejection and may influence long-term graft survival in liver and kidney transplant recipients.
We have also initiated a systems biology approach to the identification of genetic drivers of fibrosis in the allograft and the potential application to native kidney. Through this mechanism we have identified several novel mediators of fibrosis which are being investigated further in humans and animal models. SHROOM3 is one such gene. An intronic SNP in SHROOM3 increases expression of SHROOM3 and drives fibrosis in human allograft recipients and murine models of CKD. Read more.