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Perspectives
BRIT1/MCPH1: A Guardian of Genome and an Enemy of Tumors
Michael Chaplet, Rekha Rai, Deborah Jackson-Bernitsas, Kaiyi Li and Shiaw-Yih Lin
volume 5 | issue 22
15 november 2006Pages: 2579 - 2583
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The DNA of every cell is constantly exposed to insult mediated by endogenous and environmental factors that induced damage in its structure. To react to these attacks and maintain the integrity of the genome, eukaryotic cells are equipped with sophisticated mechanisms to detect, signal the presence of and repair DNA damage. The cellular response to DNA damage is a critical event for maintaining genomic stability and limiting neoplastic transformation. BRIT1, a newly identified protein, forms specific irradiation-induced nuclear foci. Our recent investigation demonstrates that BRIT1 functions as a proximal factor in the DNA damage checkpoints that control multiple damage sensors and early mediators. BRIT1 is also implicated in cell cycle checkpoints, controlling and regulating other important molecules and thus affecting the timing of mitosis. Depletion of BRIT1 abolishes the DNA damage response and results in centrosomal abnormalities and chromosomal aberrations. Moreover, aberrantly reduced expression of BRIT1 in human carcinomas implicates this protein in cancer initiation and progression. Together, the findings identify BRIT1 as a potential tumor suppressor. Fully elucidating the function of this intriguing protein may lead to new therapeutic approaches for the improved cancer treatment.
Authors
Michael Chaplet
Anderson Cancer Center, Houston, TX
Rekha Rai
Anderson Cancer Center, Houston, TX
Deborah Jackson-Bernitsas
Anderson Cancer Center, Houston, TX
Kaiyi Li
Baylor College of Medicine, Houston, Texas
Shiaw-Yih Lin
Anderson Cancer Center, Houston, TX
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.