Title of article :
Slug, a highly conserved zinc finger transcriptional repressor, protects hematopoietic progenitor cells from radiation-induced apoptosis in vivo
Author/Authors :
Inoue، نويسنده , , Akira and Seidel، نويسنده , , Markus G. and Wu، نويسنده , , Wenshu and Kamizono، نويسنده , , Shintaro and Ferrando، نويسنده , , Adolfo A. and Bronson، نويسنده , , Roderick T. and Iwasaki، نويسنده , , Hiromi and Akashi، نويسنده , , Koichi and Morimoto، نويسنده , , Akira and Hitzler، نويسنده , , Johann K. and Pestina، نويسنده , , Tamara I. and Jackson، نويسنده , , Carl W. and Tanaka، نويسنده , , Ryuhei and Chong، نويسنده , , Miriam J. and McKinnon، نويسنده , , Peter J. and Inukai، نويسنده , , Takeshi and Grosveld، نويسنده , , Gerard C. and Look، نويسنده , , A.Thomas، نويسنده ,
Abstract :
We show here that a zinc finger transcriptional repressor, Slug, which is aberrantly upregulated by the E2A-HLF oncoprotein in pro-B cell acute leukemia, functions as an antiapoptotic factor in normal hematopoietic progenitor cells. Slug−/− mice were much more radiosensitive than wild-type mice, dying earlier and showing accentuated decreases in peripheral blood cell counts, as well as abundant microhemorrhages and widely disseminated bacterial microabscesses throughout the body. Slug expression was detected in diverse subsets of hematopoietic progenitors, but not in more differentiated B and T lymphoid cells, and there was a significant increase in apoptotic (TUNEL-positive) bone marrow progenitor cells in irradiated Slug−/− mice compared to wild-type controls. These results implicate Slug in a novel survival pathway that protects hematopoietic progenitors from apoptosis after DNA damage.
