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Updated: Jun 23, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
Published on: October 5, 2012
Bax-an emerging role in ectopic cell death
Eleni Dicou1, J Regino Perez-Polo
1Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555-0652, USA. dicoueleni@yahoo.fr
Abstract:
During embryonic and early postnatal development the combination of cell proliferation, migration, survival and cell death is intimately regulated. In the mouse embryo, significant numbers of primordial germ cells, the founder cells of the gametes, fail to migrate correctly to the genital ridges early in histogenesis. Studies in Bcl-2 associated X protein null mice (Bax(-/-)) have shown that the pro-apoptotic Bax gene is required for the programmed cell death of germ cells left in ectopic locations during and after germ cell migration. Independent studies carried out in the central nervous system of Bax(-/-) mice have shown impaired and ectopic neuronal migration in the cerebellum and olfactory bulb during development and in the adult hippocampus. Taken together, these evidences identify Bax as a major mechanism in ectopic cell death and are the subject of this review.
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