Cell Death and Differentiation - p73 is critical for the persistence of memory

Editorial
Cell Death and Differentiation (2011) 18, 381–382; doi:10.1038/cdd.2010.178

p73 is critical for the persistence of memory
E R Flores1

1Department of Molecular and Cellular Oncology, Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, USA

Correspondence: ER Flores, Department of Molecular and Cellular Oncology, Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Tel: +713 792 0413; Fax: +713 794 0209; E-mail: elsaflores@mdanderson.org

Over a decade ago, the phenotype of the p73 knockout mouse clearly indicated that p73 is essential for appropriate brain development. p73-deficient mice display ex vacuo hydrocephalus and dysgenesis and hypoplasia of the hippocampus and caudal cortex.1, 2 p73 has been implicated in diseases of neurodegeneration, including Alzheimer's disease.3 The prevailing view regarding the function of p73 in the brain was that the pro-survival mechanism of ΔNp73 was the key to maintaining neural stem cells in the developing and adult brain.3, 4 Four independent groups have now demonstrated that TAp73, the full-length isoform of p73, is critical to maintain neural stem cells and that an appropriate balance of both TAp73 and ΔNp73 is critical to maintain neural stem cells.1, 5, 6, 7

full-text:
Cell Death and Differentiation - p73 is critical for the persistence of memory