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c‐Myb function in fibroblasts
Author(s) -
Bein Kiflai,
Husain Mansoor,
Ware J. Anthony,
Mucenski Michael L.,
Rosenberg Robert D.,
Simons Michael
Publication year - 1997
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199712)173:3<319::aid-jcp3>3.0.co;2-q
Subject(s) - function (biology) , myb , microbiology and biotechnology , biology , chemistry , computational biology , biochemistry , transcription factor , gene
The protooncogene c‐myb is a nuclear transcription factor that shares significant sequence homology with two other myb family members, A‐myb and B‐myb. Recent studies have suggested that c‐myb is involved in regulation of the cell cycle via control of intracellular calcium [Ca 2+ ] 1 concentration. Given the limited cell type expression of the c‐myb gene, we set out to investigate whether myb‐dependent cell cycle regulation occurs in cells not known to express the c‐myb protein. NIH 3T3 fibroblasts were stably transfected with an inducible c‐myb dominant negative construct composed of a myb DNA binding domain linked to the Drosophila engrailed transcription suppresser (pGREMEn) and a full‐length murine c‐myb cDNA sequence. Induced expression of the dominant negative construct was associated with a G 1 cell cycle arrest and a failure to increase late G 1 intracellular calcium levels. Similar expression studies in mouse embryonic fibroblasts derived from the c‐myb knockout mouse have demonstrated lower baseline [Ca 2+ ] 1 levels than in normal mice fibroblasts that were not further lowered by MEn expression. We conclude that regulation of calcium homeostasis and cell cycle progression via myb‐dependent transcription may play an important role in cells not possessing detectable levels of c‐myb protein. J. Cell. Physiol. 173:319–326, 1997. © 1997 Wiley‐Liss, Inc.