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BARA/LIN‐9 is required for B‐myb dependent transcriptional activation of cyclin B
Author(s) -
Pilkinton Mark,
Sandoval Raudel,
Song Julie,
Colamonici Oscar
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a462-a
Subject(s) - cyclin a , cyclin b , cyclin d , cyclin a2 , cyclin , microbiology and biotechnology , cyclin e , cell cycle , biology , cytokinesis , cyclin b1 , cyclin dependent kinase complex , cyclin dependent kinase 1 , cyclin dependent kinase , cell division , cell , genetics
Orderly cell cycle progression is determined in part by the sequential expression of cyclins and their positive regulation of specific cyclin dependent kinases. Cyclin B‐CDK1 is the dominant cyclin complex in G2/M and plays an essential role in the last stages of cell division. Cyclin B is transcriptionally regulated along the cell cycle with peak expression in G2/M. Just prior to cytokinesis cyclin B is degraded, allowing the cell to divide and cell cycle to repeat itself. The positive role of B‐myb in transcriptional activation of cyclin B has recently been described. Here we identify a novel protein, BARA/LIN‐9, as a B‐myb interacting protein that is a necessary cofactor for expression of cyclin B. We have found that the presence of BARA/LIN‐9 is critical for cyclin B expression as antisense knock down results in chronically low levels of cyclin B. When co‐expressed with B‐myb the transcriptional activity of a cyclin B promoter increases several fold over control. This report describes a critical component necessary for normal induction of cyclin B in mitotically active cells. Supported by NIH Grant GM‐54709