ArticleDevelopment (Cambridge, England)2012
p120-catenin is essential for terminal end bud function and mammary morphogenesis.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- The dynamics of tubulogenesis in development and disease.Development (Cambridge, England) · 2025Review
- Functions of p120-catenin in physiology and diseases.Frontiers in molecular biosciences · 2024Review
- A junction-dependent mechanism drives murine mammary cell intercalation for ductal elongation.Developmental cell · 2023Article
- CTNND1 variants cause familial exudative vitreoretinopathy through the Wnt/cadherin axis.JCI insight · 2022Article
- The molecular basis of mammary gland development and epithelial differentiation.Seminars in cell & developmental biology · 2021Review
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- VE-cadherin endocytosis controls vascular integrity and patterning during development.The Journal of cell biology · 2020Article
- p120-catenin regulates WNT signaling and EMT in the mouse embryo.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Differential expression of p120-catenin 1 and 3 isoforms in epithelial tissues.Scientific reports · 2019Article
- Loss of E-Cadherin-Dependent Cell-Cell Adhesion and the Development and Progression of Cancer.Cold Spring Harbor perspectives in biology · 2018Review
- NFkB hyperactivation causes invasion of esophageal squamous cell carcinoma with EGFR overexpression and p120-catenin down-regulation.Oncotarget · 2018Article
- Slug/Pcad pathway controls epithelial cell dynamics in mammary gland and breast carcinoma.Oncogene · 2018Article
- p120-Catenin is an obligate haploinsufficient tumor suppressor in intestinal neoplasia.The Journal of clinical investigation · 2017Article
- β-Catenin haploinsufficiency promotes mammary tumorigenesis in an ErbB2-positive basal breast cancer model.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis.Nature communications · 2016Article
- p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice.Journal of mammary gland biology and neoplasia · 2016Article
- p120 Catenin Suppresses Basal Epithelial Cell Extrusion in Invasive Pancreatic Neoplasia.Cancer research · 2016Article
- Phosphorylation and isoform use in p120-catenin during development and tumorigenesis.Biochimica et biophysica acta · 2016Review
- p120-catenin controls contractility along the vertical axis of epithelial lateral membranes.Journal of cell science · 2016Article
- p120 Catenin is required for normal tubulogenesis but not epithelial integrity in developing mouse pancreas.Developmental biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Although p120-catenin (p120) is crucial for E-cadherin function, ablation experiments in epithelial tissues from different organ systems reveal markedly different effects. Here, we examine for the first time the consequences of p120 knockout during mouse mammary gland development. An MMTV-Cre driver was used to target knockout to the epithelium at the onset of puberty. p120 ablation was detected in approximately one-quarter of the nascent epithelium at the forth week post-partum. However, p120 null cells were essentially nonadherent, excluded from the process of terminal end bud (TEB) morphogenesis and lost altogether by week six. This elimination process caused a delay in TEB outgrowth, after which the gland developed normally from cells that had retained p120. Mechanistic studies in vitro indicate that TEB dysfunction is likely to stem from striking E-cadherin loss, failure of cell-cell adhesion and near total exclusion from the collective migration process. Our findings reveal an essential role for p120 in mammary morphogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.