www.eurekalert.org/pub_releases/2008-10/wuso-sss102008. -
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Published on: 10/20/2008
Last Visited: 10/21/2008
"It's also interesting to note that the cell sees the genetic material of some invaders, such as DNA viruses, as damaged DNA," says senior author Barry Sleckman, M.D., Ph.D, director of the Division of Laboratory and Genomic Medicine and an expert in DNA repair.
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"This explains why the lymphocyte counts in these patients drop so sharply," Sleckman says.
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Sleckman wanted to examine the implications of DNA breaks in lymphocytes.
In a cell line developed in his lab, researchers induced double-stranded breaks in lymphocyte DNA using the same enzymes the cells normally use to create the breaks.
They then analyzed the genes activated as a result.
As expected, the breaks turned on two groups of genes: one, headed by the p53 protein, pushes the cell toward self-destruction; the other, headed by the NFKappa-B proteins, pushes for survival of the cell and repair of the damaged DNA.
These groups of genes are normally activated in any cell that experiences DNA damage.
But Sleckman and his colleagues also found several lymphocyte-specific genes activated by the breaks.
"Several of these genes are involved in the migration and homing of lymphocytes," says Sleckman.
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"It's entirely possible that some of these breaks are activating genetic mechanisms that are unrelated to DNA repair or cell survival, like the mechanisms we identified in lymphocytes," says Sleckman.