Robert A. McKnight, PhD, MS
- Departments: Pediatrics - Research Assistant Professor
- Divisions: Neonatology
Academic Office Information
295 Chipeta Way, Room: 2S010
Salt Lake City, UT 84108
Robert A McKnight, PhD. My current research focuses on the affects of antenatal betamethasone and mechanical ventilation on expression of genes critical to lung and brain development and function. We use the high throughput sequencing method ATAC-seq to identify changes in assess to DNA regulatory sites. RNA-seq is then used to determine whether a change in DNA access altered transcription. Our results show that mechanical ventilation is far more disruptive to creating gene-specific DNA access than noninvasive ventilation. We use the same high throughput methods to study the effects of antenatal betamethasone on preterm lamb brain and lung gene expression. The overall goal of our betamethasone studies is to optimize the dose of betamethasone to use based on maternal BMI and fetal gestation age.
Research StatementDr. McKnight's current research interest focuses on the effects of DNA methylation induced by prenatal stress. In vivo animal models of uteroplacental insufficiency as well as in vitro cell culture systems are used to test the effects of DNA methylation on gene expression. In particular the IGF-1 and eEF2K genes are used to evaluate the effects of in utero -induced DNA methylation on gene accessibility including promoter sequences and developmentally regulated enhancers.
|Fellowship||National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases
|Postdoctoral Fellowship||National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases
|Doctoral Training||University of California - Davis
|Graduate Training||University of Louisiana at Lafayette
|Undergraduate||Iowa State University
- Zinkhan EK, Yu B, Callaway CW, McKnight RA (2018). Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring. J Dev Orig Health Dis, 9(3), 315-328.
- Habibian JS, Jefic M, Bagchi RA, Lane RH, McKnight RA, McKinsey TA, Morrison RF, Ferguson BS (2017). DUSP5 functions as a feedback regulator of TNFα-induced ERK1/2 dephosphorylation and inflammatory gene expression in adipocytes. Sci Rep, 7(1), 12879.