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Publication : Cell type-specific deficiency of c-kit gene expression in mutant mice of mi/mi genotype.

First Author  Isozaki K Year  1994
Journal  Am J Pathol Volume  145
Issue  4 Pages  827-36
PubMed ID  7524330 Mgi Jnum  J:20877
Mgi Id  MGI:68944 Citation  Isozaki K, et al. (1994) Cell type-specific deficiency of c-kit gene expression in mutant mice of mi/mi genotype. Am J Pathol 145(4):827-36
abstractText  The mi locus of mice encodes a novel member of the basic-helix-loop-helix-leucine zipper protein family of transcription factors (hereafter called mi factor). In addition to microphthalmus, osteopetrosis, and lack of melanocytes, mice of mi/mi genotype are deficient in mast cells. Since the c-kit receptor tyrosine kinase plays an important role in the development of mast cells, and since the c-kit expression by cultured mast cells from mi/mi mice is deficient in both mRNA and protein levels, the mast cell deficiency of mi/mi mice has been attributed at least in part to the deficient expression of c-kit. However, it remained to be examined whether the c-kit expression was also deficient in tissues of mi/mi mice. In the present study, we examined the c-kit expression by mi/mi skin mast cells using in situ hybridization and immunohistochemistry. Moreover, we examined the c-kit expression by various cells other than mast cells in tissues of mi/mi mice. We found that the c-kit expression was deficient in mast cells but not in erythroid precursors, testicular germ cells, and neurons of mi/mi mice. This suggested that the regulation of the c-kit transcription by the mi factor was dependent on cell types. Mice of mi/mi genotype appeared to be a useful model to analyze the function of transcription factors in the whole-animal level.
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