Page 21 - Gates-AnnualReport-2018

SELECT MEMBER PUBLICATIONS AND HONORS*
Bruce Appel, Ph.D., Assistant Professor, Department of Pediatrics
Using zebrafish spinal cord as a model, Dr. Appel and his colleagues discovered that gradients in the concentration of signaling molecules instruct neural progenitor cells either to develop as myelinating oligodendrocytes or to persist as oligodendrocyte precursor cells (Ravanelli et al., Developmental Biology, 2018). These findings address a long-standing problem in vertebrate neural development of how apparently similar populations of progenitors produce different kinds of neurons and glia.
Kristin Artinger, Ph.D., Associate Professor, Department of Craniofacial Biology and Lee Niswander, Ph.D., Professor, Department of Molecular, Cellular and Developmental Biology, CU Boulder
In this paper, Drs. Niswander and Artinger identify the epigenetic regulators required for growth and differentiation of craniofacial cartilage and bone in both zebrafish and mice (Sen et al., J Dev Biol, 2018). This study provides insight into how cranial neural crest cells are regulated to give rise to the different shapes and sizes of the bone and cartilage in the craniofacial skeleton and how genetic alterations of these regulators may result in craniofacial defects.
James Bamburg, Ph.D., Professor, Department of Biochemistry and Molecular Biology,
Colorado State University
Following the analysis of four different stroke models in mouse brains, Dr. Bamburg and his colleagues discover that cofilin- actin rod pathology develops around the site ischemic injury in all four models (Won et al., PLoS One, 2018). Therapeutic approaches that prevent the aggregation of cofilin-actin rods may reduce synaptic loss after stroke.
Valeria Canto-Soler, Ph.D., Associate Professor, Department of Ophthalmology
In collaboration with Dr. Redenti, at City University of New York, Dr. Canto-Soler demonstrates that retinal progenitor cells release extracellular vesicles (EV) containing mRNA, miRNA and proteins associated with multipotency and retinal development (Zhou et al, Scientific Reports, 2018). They also confirmed that EV can transfer their cargo to other retinal progenitor cells, thus identifying a novel mechanism involved in differentiation and fate determination during retinal development.
James DeGregori, Ph.D., Professor, Department of Biochemistry and Molecular Genetics
Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are one of the most frequently observed genetic defects in acute myeloid leukemia (AML). Although FLT3 inhibitors have shown impressive anti-leukemic activity in clinical trials, sustained remissions using these inhibitors as a monotherapy have not been achieved. In this study, Dr. DeGregori reports that the combined use of FLT3 inhibitors with a glutaminase inhibitor results in significantly improved survival in a patient-derived xenograft AML mouse model (Gregory et al., Exp Hematol, 2018).
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