University of Nebraska Medical Center

Kyle J. Hewitt, PhD

Associate Professor, Department of Genetics, Cell Biology, and Anatomy
Co-Director, Molecular Genetics & Cell Biology PhD Program


Headshot of Kyle J. Hewitt, PhD

Dr. Kyle Hewitt is a research scientist with a background in cell, molecular and developmental biology, bioinformatics, genetics, and hematology. Dr. Hewitt's lab uses cutting-edge tools to understand mechanisms of stem cell self-renewal and differentiation, stem cell genesis and maintenance in hematopoiesis, and enhancer and gene enhancers facilitating regeneration in anemia and leukemia. They discovered a GATA transcription factor target gene, Sterile Alpha Motif Domain-14 (Samd14), promoted hematopoietic stem/progenitor cell function, facilitates cell signaling and regeneration via receptor tyrosine kinase signaling, and is required for survival in a model of acute anemia. Using ex vivo assays, mouse models, and computational approaches, they are discovering new pathways and mechanisms of regenerative hematopoiesis and leukemia.

  • Post-doc, University of Wisconsin-Madison
  • PhD, Cell, Molecular, Developmental Biology, Tufts University
  • BA, Biology, Colorado College

Dr. Hewitt's research lab investigates mechanisms that guide physiological and regenerative blood formation. They are especially absorbed with understanding how gene regulation is controlled during the differentiation of all the varied cell types that exist in the blood system, the role of the GATA family of transcription factors in development, and diseases that arise from deregulated transcription factor activities including chronic anemias and leukemias.

Among the ongoing projects in the lab:

  • The Sterile Alpha Motif-14 (SAMD14)locus contains a GATA2-regulated enhancer (Samd14-Enh) that drives its expression in anemia, with relevance to stem cell homeostasis, anemia, hematopoietic/erythropoietic stress, and the cardiovascular system more broadly. We are working towards a general model to describe Samd14 activities and its cognate transcriptional enhancer in hematopoietic stem/progenitor cells.
  • While SAM proteins are involved in many cell processes, no general principles have emerged to explain many SAMs in the human proteome, whether SAM domains can substitute for others, and what features confer functional properties this poorly studied family of protein domains in hematologic disease. We are defining new functions for SAM proteins in transcription and cell signaling.
  • Mutations in coding and noncoding regions of the transcription factor GATA2 cause a diverse range of adverse phenotypes, including myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), primary immunodeficiencies, and aplastic anemia. We use ranked prioritization approaches and CRISPR/Cas9 gene editing to test non-coding DNA element function in cells and animals.