The primary goal of this application is to establish a foundation of basic scientists with translational research projects studying developmental mechanisms underlying children's disease by establishing the Center for Pediatric Research. The origin of many pediatric diseases is from altered developmental programming related to the processes of cell proliferation, morphogenesis, migration, differentiation, and programmed death. These developmental processes are at the root of pediatric disease and are disrupted through genetic disorders, aberrant fetal programming, altered growth &development, and environmental pressures. Our multidisciplinary Center applies genetic, biochemical, cell, and molecular approaches across several model organisms to characterize alterations during development as they pertain to pediatric diseases and disorders. Projects from five outstanding early-stage investigators with the potential to become competitive scientists at the national level have been selected for this application. Center success will be achieved through the following Aims: 1) create a supportive environment for the training and mentorship of basic scientists studying developmental processes related to pediatric disease mechanisms;2) utilize new and existing resources that will enhance pediatric research;3) enhance communication mechanisms to promote and initiate clinical and translational research projects;4) expand training and learning opportunities in the biology of pediatric disease and development;and 5) evaluate success of the Center. Through these Aims, the Center for Pediatric Research will develop a strong foundation in basic and translational research by fostering a collaborative environment for scientists and physicians. Strengthened by our institution's strong commitment to children's medicine, we propose that the Center will enhance pediatric research efforts in South Dakota.
This proposal will establish an multidisciplinary research center focused on understanding the cellular and molecular basis of childhood disease and mentor young scientists investigating treatment strategies aimed at ameliorating these diseases.
|Forred, Benjamin J; Neuharth, Skyla; Kim, Dae In et al. (2016) Identification of Redox and Glucose-Dependent Txnip Protein Interactions. Oxid Med Cell Longev 2016:5829063|
|Rickel, Kirby; Fang, Fang; Tao, Jianning (2016) Molecular genetics of osteosarcoma. Bone :|
|Kim, Dae In; Jensen, Samuel C; Noble, Kyle A et al. (2016) An improved smaller biotin ligase for BioID proximity labeling. Mol Biol Cell 27:1188-96|
|White, Katherine A; Hutton, Scott R; Weimer, Jill M et al. (2016) Diet-induced obesity prolongs neuroinflammation and recruits CCR2(+) monocytes to the brain following herpes simplex virus (HSV)-1 latency in mice. Brain Behav Immun 57:68-78|
|Simpkins, Jessica A; Rickel, Kirby E; Madeo, Marianna et al. (2016) Disruption of a cystine transporter downregulates expression of genes involved in sulfur regulation and cellular respiration. Biol Open 5:689-97|
|Booze, Michelle L; Hansen, Jason M; Vitiello, Peter F (2016) A novel mouse model for the identification of thioredoxin-1 protein interactions. Free Radic Biol Med 99:533-543|
|Yao, Qingqing; Liu, Yangxi; Tao, Jianning et al. (2016) Hypoxia-mimicking nanofibrous scaffolds promote endogenous bone regeneration. ACS Appl Mater Interfaces :|
|Alam, Samer G; Zhang, Qiao; Prasad, Nripesh et al. (2016) The mammalian LINC complex regulates genome transcriptional responses to substrate rigidity. Sci Rep 6:38063|
|Mdaki, Kennedy S; Larsen, Tricia D; Wachal, Angela L et al. (2016) Maternal high-fat diet impairs cardiac function in offspring of diabetic pregnancy through metabolic stress and mitochondrial dysfunction. Am J Physiol Heart Circ Physiol 310:H681-92|
|Baack, Michelle L; Puumala, Susan E; Messier, Stephen E et al. (2016) Daily Enteral DHA Supplementation Alleviates Deficiency in Premature Infants. Lipids 51:423-33|
Showing the most recent 10 out of 30 publications