ArticleBreast cancer research : BCR2002
Prolactin signaling and Stat5: going their own separate ways?
Article in Breast cancer research : BCR, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Shaping Cell Identity: Global Transcriptome and Pathway Shifts during Mouse Mammary Epithelial Cell Differentiation.Computational and structural biotechnology journal · 2026Article
- Reciprocal fine-tuning of progesterone and prolactin-regulated gene expression in breast cancer cells.Molecular and cellular endocrinology · 2020Article
- Hormone signaling requirements for the conversion of non-mammary mouse cells to mammary cell fate(s) in vivo.Journal of mammary gland biology and neoplasia · 2015Review
- Image-based evaluation of the molecular events underlying HC11 mammary epithelial cell differentiation.Analytical biochemistry · 2008Article
- Transcriptome analysis identifies pathways associated with enhanced maternal performance in QSi5 mice.BMC genomics · 2008Article
- Alveolar and lactogenic differentiation.Journal of mammary gland biology and neoplasia · 2006Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.