Kyle Hewitt
University of Nebraska Medical Center, NE·Genetics
When the body loses red blood cells, as in anemia, it ramps up production to replace them, a process called stress erythropoiesis. Researchers do not yet know which gene switches drive this emergency response, or why the response fails in chronic anemias.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
erythropoiesis
red blood cells
anemia
- Grants
- 2 known grants, through Jun 2028
What they work on
- Define how Samd14, a gene switched on during anemia, supports c-Kit signaling and survival of red blood cell precursors, using primary human and mouse cells.
- Compare mice lacking the GATA2-bound Samd14 enhancer with gene-knockout mice to separate mechanisms needed for regeneration after anemia from those used in normal red-cell production.
- Map a network of GATA2 and regeneration-activated (G2R) enhancers, DNA switches resembling the Samd14 enhancer, that govern responses to anemia.
- Test whether other SAM domain-containing proteins act in c-Kit signaling and red blood cell regeneration, using mouse genetic models.
- Provide low-cost single-cell RNA sequencing with Seq-Well and spatial transcriptomics with MERSCOPE, plus training and computational analysis support for investigators.
More about the research
This project traces a gene circuit that the lab discovered is turned on during anemia. In addition, the lab runs a shared facility that gives researchers affordable access to tools that read gene activity in single cells and in intact tissue.
Why it matters
Anemia is a common blood disorder, and in chronic anemias the body can lose its ability to rebuild red blood cells. Identifying Samd14 as a new player in c-Kit signaling during red-cell regeneration could reveal stress-specific mechanisms with possible therapeutic value for anemias and other blood diseases. The transcriptomics core helps investigators find disease-specific markers and drug targets by making single-cell tools affordable.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Emery H. Bresnick
University of Wisconsin-Madison, WI·Genetics
Test whether GATA2 and C/EBPε, a factor that drives granulocyte formation, work together and separately to set up progenitor gene activity, using GATA2 activation of a Cebpe enhancer as the entry point.
Krystalyn Hudson
University of Virginia, VA·Microbiology & Immunology
Test whether red blood cell units rich in reticulocytes, young red cells that still contain mitochondria, raise alloantibody rates after transfusion, using mouse models that mimic repeat blood donation.
Elizabeth Leibold
University of Utah, UT·Biochemistry
Determine whether loss of Irp2 serine 157 phosphorylation disrupts red blood cell production from within blood-forming cells, using bone marrow transplantation and flow cytometry of cell cycle, proliferation and iron.
The school
University of Nebraska Medical Center: 20 labs on PI Pages, $657M a year on research, 82 research doctorates a year.
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