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In-depth analysis of the cellular and molecular mechanisms regulating human HSC function will require a surrogate host that supports robust maintenance of transplanted human HSCs in vivo, but the currently available options are problematic. Previously we showed that mutations in the Kit receptor enhance engraftment of transplanted HSCs in the mouse. To generate an improved model for human HSC transplantation and analysis, we developed immune-deficient mouse strains containing Kit mutations. We found that mutation of the Kit receptor enables robust, uniform, sustained, and serially transplantable engraftment of human HSCs in adult mice without a requirement for irradiation conditioning. Using this model, we also showed that differential KIT expression identifies two functionally distinct subpopulations of human HSCs. Thus, we have found that the capacity of this Kit mutation to open up stem cell niches across species barriers has significant potential and broad applicability in human HSC research.

Original publication

DOI

10.1016/j.stem.2014.06.001

Type

Journal article

Journal

Cell Stem Cell

Publication Date

07/08/2014

Volume

15

Pages

227 - 238

Keywords

Animals, Cell Lineage, Crosses, Genetic, Enzyme-Linked Immunosorbent Assay, Fetal Blood, Gene Expression Regulation, Hematopoietic Stem Cell Transplantation, Hematopoietic Stem Cells, Humans, Lymphocytes, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mutation, RNA, Messenger, Species Specificity, Stem Cell Factor, Thymocytes, Time Factors