Impaired expression of integrin alpha-4 subunit in cultured mast cells derived from mutant mice of mi/mi genotype.

Content Provider	Semantic Scholar
Author	Kim, D. Kyle Morii, Eiichi Ogihara, Hideki Hashimoto, Koji Oritani, Kenji Lee, Young Mok Jippo, Tomoko Adachi, Satoko Kanakura, Yuzuru Kitamura, Yukihiko
Copyright Year	1998
Abstract	The mi locus encodes a member of the basic-helix-loop-helix-leucine zipper protein family of transcription factors (hereafter called MITF). We have reported that expression of several genes was impaired in cultured mast cells (CMCs) of mi/mi mice due to a defective transactivation ability of mutant MITF (mi-MITF). Because attachment of mi/mi CMCs to fibroblasts is impaired, we examined the expression of integrin genes in mi/mi CMCs in the present study. Among the integrin genes examined, the expression of integrin alpha4 subunit was barely detectable in mi/mi CMCs, and the alpha4 protein was not detected by flow cytometry either. The specific adhesion to vascular cell adhesion molecule-1 (VCAM-1), the ligand for alpha4 subunit, was observed in +/+ CMCs but not in mi/mi CMCs, indicating that the expression of integrin alpha4 subunit at a functional level did not occur in mi/mi CMCs. In the promoter region of the alpha4 subunit gene, there was a CACTTG motif to which normal MITF (+- MITF) bound. The coexpression of +-MITF but not of mi-MITF transactivated the promoter of the alpha4 subunit gene. The deletion or mutation of the CACTTG motif abolished the transactivation by +-MITF, suggesting that +-MITF directly transactivated the gene encoding alpha4 subunit of integrin.
File Format	PDF HTM / HTML
PubMed reference number	9731055
Journal	Medline
Volume Number	92
Issue Number	6
Alternate Webpage(s)	http://www.bloodjournal.org/content/bloodjournal/92/6/1973.full.pdf?sso-checked=true
Journal	Blood
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article