Prolactin signaling and Stat5: going their own separate ways?
AUTOR(ES)
Brisken, Cathrin
FONTE
BioMed Central
RESUMO
Miyoshi et al. compared the role of the prolactin receptor (PrlR) and its downstream mediator, the signal transducer and activator of transcription 5 (Stat5), in mammary epithelial cells in vivo by studying PrlR-/- and Stat5ab-/- mouse mammary epithelial transplants during pregnancy. At first glance, the two mutant epithelia appear to have similar defects in the differentiation of the alveolar epithelium. However, a closer examination by Miyoshi et al. revealed defects in the epithelial architecture of the smallest ducts of Stat5ab-/- transplants not apparent in the PrlR-/- transplants, suggesting that Stat5 is more than a simple mediator of PrlR action.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=137942Documentos Relacionados
- Suppression of interleukin-3-induced gene expression by a C-terminal truncated Stat5: role of Stat5 in proliferation.
- Publications in pneumology: old or new ways?
- Prolactin regulates ZNT2 expression through the JAK2/STAT5 signaling pathway in mammary cells
- Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
- Characterization of Stat5a and Stat5b Homodimers and Heterodimers and Their Association with the Glucocortiocoid Receptor in Mammary Cells
