SCF (KITL) is a hematopoietic growth factor, and it can synergize with a number of other cytokines to stimulate growth of hemopoietic progenitors in vitro and stimulates blood cell production in vivo. SCF is encoded by Sl ('steel'), a gene critical to the development of several distinct cell lineages during embryonic life. KITL was identified as a soluble protein; nevertheless, the predicted amino acid sequence indicates that it is an integral transmembrane protein. KITL is generated by proteolytic cleavage from a transmembrane precursor. Two splice variants have been descrived for KITL, and proteolytic processing of both transmembrane protein products occurs on the cell surface. The binding of KITL, induces the dimerization of the KIT molecule, followed by a change in the configuration of the intracellular domain and the autophosphorylation of the receptor, opening several docking sites for signal transduction molecules. Dysregulation of SCF–KI signaling and gain-of-function KIT mutations contribute to the genesis of many cancers, like acute myeloid leukemia, gastrointestinal stromal tumors, and mastocytosis.
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Description:
SCF (KITL) is a hematopoietic growth factor, and it can synergize with a number of other cytokines to stimulate growth of hemopoietic progenitors in vitro and stimulates blood cell production in vivo. SCF is encoded by Sl ('steel'), a gene critical to the development of several distinct cell lineages during embryonic life. KITL was identified as a soluble protein; nevertheless, the predicted amino acid sequence indicates that it is an integral transmembrane protein. KITL is generated by proteolytic cleavage from a transmembrane precursor. Two splice variants have been descrived for KITL, and proteolytic processing of both transmembrane protein products occurs on the cell surface. The binding of KITL, induces the dimerization of the KIT molecule, followed by a change in the configuration of the intracellular domain and the autophosphorylation of the receptor, opening several docking sites for signal transduction molecules. Dysregulation of SCF–KI signaling and gain-of-function KIT mutations contribute to the genesis of many cancers, like acute myeloid leukemia, gastrointestinal stromal tumors, and mastocytosis.
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