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- W2313431637 abstract "KIT tyrosine kinase receptor is essential for several tissue stem cells, especially for hematopoietic stem cells (HSCs). Moderately decreased KIT signaling is well known to cause anemia and defective HSC self-renewal, whereas gain-of-function mutations are infrequently found in leukemias. Thus, maintaining KIT signal strength is critically important for homeostasis. KIT signaling in HSCs involves effectors such as SHP2 and PTPN11. This review summarizes the recent developments on the novel mechanisms regulating or reinforcing KIT signal strength in HSCs and its perturbation in polycythemia vera.Stem cell leukemia (SCL) is a transcription factor that is essential for HSC development. Genetic experiments indicate that Kit, protein tyrosine phosphatase, nonreceptor type 11 (Ptpn11), or Scl control long-term HSC self-renewal, survival, and quiescence in adults. Kit is now shown to be centrally involved in two feedforward loops in HSCs, one with Ptpn11 and the other with Scl.Knowledge of the regulatory mechanisms that favor self-renewal divisions or a lineage determination process is central to the design of strategies to expand HSCs for the purpose of cell therapy. In addition, transcriptome and phosphoproteome analyses of erythroblasts in polycythemia vera identified lower SCL expression and hypophosphorylated KIT, suggesting that the KIT-SCL loop is relevant to the pathophysiology of human blood disorders as well." @default.
- W2313431637 created "2016-06-24" @default.
- W2313431637 creator A5014965154 @default.
- W2313431637 creator A5018570031 @default.
- W2313431637 creator A5076143416 @default.
- W2313431637 date "2014-07-01" @default.
- W2313431637 modified "2023-10-18" @default.
- W2313431637 title "Kit and Scl regulation of hematopoietic stem cells" @default.
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- W2313431637 doi "https://doi.org/10.1097/moh.0000000000000052" @default.
- W2313431637 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24857885" @default.
- W2313431637 hasPublicationYear "2014" @default.
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