NDLI: NHERF1/EBP50 controls lactation by establishing basal membrane polarity complexes with prolactin receptor.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Morales, F. C. Hayashi, Y. Van Pelt, C. S. Georgescu, M-M
Description	Country affiliation: United States Author Affiliation: Morales FC ( Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.)
Abstract	The development of the lactating mammary gland is a complex multifactorial process occurring in mammals during pregnancy. We show here that this process requires NHERF1/EBP50 (Na/H exchanger regulatory factor 1/ERM-binding phosphoprotein 50) expression and that successful lactation depends on NHERF1 allele copy number, with rates of 50 and 20% in NHERF1(+/-) and (-/-) mice, respectively. The prolactin receptor (PRLR)-STAT5 signaling provides the central axis triggering the differentiation of secretory mammary alveolar cells. In successfully lactating glands, NHERF1 is massively upregulated and forms complexes with PRLR, but also with ß-catenin, E-cadherin and ezrin at the alveolar basal membrane, establishing basal polarity. In NHERF1-deficient glands, the basal polarity is disrupted, the PRLR levels and basal membrane localization are abolished, and the downstream STAT5 activation collapses with consequent reduction of milk protein synthesis. NHERF1/EBP50, a protein deregulated in breast cancer, thus emerges as an important physiological mediator of milk secretion, by engagement of PRLR in multimeric complexes at the alveolar basal membrane with subsequent network activation leading to cell differentiation.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.131
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-09-20
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Cytoskeletal Proteins Research Support, N.i.h., Extramural Cell Polarity Mammary Glands, Animal Sodium-hydrogen Antiporter Lactation Beta Catenin Phosphoproteins Genetics Proto-oncogene Proteins C-akt Stat5 Transcription Factor Signal Transduction Research Support, American Recovery And Reinvestment Act Mice, Inbred C57bl Deficiency Genotype Metabolism Pregnancy Discipline Cell Biology Growth & Development Animals Alleles Up-regulation Cadherins Mice Receptors, Prolactin
Content Type	Text
Resource Type	Article

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