Unifying the p73 knockout phenotypes: TAp73 orchestrates multiciliogenesis.
Multiciliogenesis is essential for the function of different epithelia, and its failure results in brain defects, respiratory diseases, and infertility. In this issue of Genes & Development, Nemajerova and colleagues (pp. 1300-1312) reveal the p53 family member and p73 isoform TAp73 as a transcription factor dictating the differentiation of multiciliated cells. Their findings provide the long-awaited unifying explanation for the diverse phenotypes of the p73 knockout mice.
Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Marco
M
Napoli
Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Elsa R
ER
Flores
D000818:Animals; D002454:Cell Differentiation; D004268:DNA-Binding Proteins / Q000235:genetics; D009687:Nuclear Proteins / Q000235:genetics*; D010641:Phenotype; D014157:Transcription Factors / Q000235:genetics; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D014157:Transcription Factors; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins
TAp73; TP73; airways; central transcriptional regulator; motile multiciliogenesis; p73