Human Molecular Genetics recently published a paper co-authored by Laxman Gangwani, MTech, PhD, of Texas Tech University Health Sciences Center (TTUHSC) in El Paso. The research addresses zinc finger protein 1 (ZPR1), which appears to be a 'protective modifier' of spinal muscular atrophy (SMA), making it a potential target for the development of therapies for the treatment of SMA.
SMA is caused by mutation of the Survival Motor Neurons 1 (SMN1) gene and characterized by degeneration of spinal motor neurons caused by low levels of SMN protein. One of the hallmarks of SMA pathogenesis is the biochemical defect in accumulation of SMN in the nucleus. Dr. Gangwani made a breakthrough discovery in the field of muscular atrophy by indentifying ZPR1 as protein required for the nuclear accumulation of SMN. The present study published finds that ZPR1 corrects the defect in nuclear accumulation of SMN in SMA patient cells and rescues axonal growth defects in spinal motor neurons from SMA mouse model.
Gangwani is an associate professor at the TTUhSC Paul L. Foster School of Medicine in the Department of Biomedical Sciences, Center of Excellence in Neurosciences. His research interests include understanding of the molecular mechanisms of neuron degeneration associated with neurodegenerative disorders, including spinal muscular atrophy.
TTUHSC El Paso Center of Excellence in Neurosciences
Gangwani’s research was also highlighted in Quest, the research and health magazine of the Muscular Dystrophy Association; as well as on the official website of Families of SMA.
Quest (MDA’s Research & Health Magazine)
Comments (1)
PrailiLic
May 21st, 2013
9:34 am