ArticleOncogene2005
p53 mediates a default programme of mammary gland involution in the absence of STAT3.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Fur removal promotes an earlier expression of involution-related genes in mammary gland of lactating mice.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023Article
- Transcriptome Analysis of Goat Mammary Gland Tissue Reveals the Adaptive Strategies and Molecular Mechanisms of Lactation and Involution.International journal of molecular sciences · 2022Article
- Alveolar cells in the mammary gland: lineage commitment and cell death.The Biochemical journal · 2022Review
- The BH3-only protein BIM contributes to late-stage involution in the mouse mammary gland.Cell death and differentiation · 2016Article
- Dispersal of an ancient retroposon in the TP53 promoter of Bovidae: phylogeny, novel mechanisms, and potential implications for cow milk persistency.BMC genomics · 2015Article
- p63 is a prosurvival factor in the adult mammary gland during post-lactational involution, affecting PI-MECs and ErbB2 tumorigenesis.Cell death and differentiation · 2014Article
- Article
- A dual role for oncostatin M signaling in the differentiation and death of mammary epithelial cells in vivo.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Patterns of cell signaling pathway activation that characterize mammary development.Development (Cambridge, England) · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated a proapoptotic role for the transcription factor STAT3 in involuting murine mammary epithelium, resulting in delayed involution and lower levels of apoptosis in the STAT3 null gland relative to wild-type controls. As p53 was implicated in the eventual involution of the STAT3 null gland, we examined the effect of STAT3 loss in the mammary gland in a p53 null background. Combined loss of STAT3 and p53 severely perturbed involution, with hyperdelayed loss of epithelium and reappearance of adipocytes. The early apoptotic response was almost completely abrogated, although elevated levels of delayed apoptosis persisted at days 6, 17 and 4 weeks of involution in STAT3-p53 doubly null mammary glands. A 5.7-fold upregulation of the cyclin-dependent kinase inhibitor p21Waf1 at 3 days of involution in STAT3 null glands was abolished in STAT3-p53 doubly null glands -- suggesting that the critical factor triggering delayed involution in the STAT3 null gland is a p53-dependent rise in p21Waf1 levels around day 3 of involution. Further, STAT3-p53 doubly null glands showed significantly higher levels of proliferation compared to STAT3 or p53 singly null (or wild-type) glands at days 6, 17 and 4 weeks of involution. Combined loss of STAT3 and p53 therefore results in hyperdelayed involution, demonstrating their synergistic physiological roles in normal involution. This inappropriate retention of p53-deficient cells may represent a novel mechanism of tumour predisposition.
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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.