作者: T Tsujimura , E Morii , M Nozaki , K Hashimoto , Y Moriyama
DOI: 10.1182/BLOOD.V88.4.1225.BLOODJOURNAL8841225
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摘要: The mi locus of mice encodes a member the basic-helix-loop-helix- leucine zipper (bHLH-Zip) protein family transcription factors (hereafter called MITF). Cultured mast cells mi/mi genotype (mi/mi CMCs) did not normally respond to stem cell factor (SCF), ligand for c-kit receptor tyrosine kinase. poor response CMCs SCF was attributed deficient expression both mRNA and levels. purpose present study is investigate effect MITF on gene. First, we introduced cDNA encoding normal (+) or mutant (mi) into using retroviral vector. Overexpression (+)-MITF but mi- normalized SCF, indicating involvement in gene transactivation. Second, analyzed promoter Three CANNTG motifs recognized by bHLH-Zip-type were conserved between mouse human promoters. Among these three motifs, only CACCTG motif (nt -356 - 351) specifically bound (+)-MITF. When luciferase under control contransfected NIH/3T3 fibroblasts with mi-MITF, activity significantly increased when cotransfected. deletion region containing mutation CTCCAG abolished transactivation (+)-MITF, that transactivated through motif. FMA3 mastocytoma FEC-P1 myeloid lines, remarkable observed cells. Thus, appeared be specific lineage.