Evidence map›Paper›PMID 11739413›Full record

ArticleThe Journal of cell biology2001

Impaired mammary gland and lymphoid development caused by inducible expression of Axin in transgenic mice.

W Hsu, R Shakya, F Costantini

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 123 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Endothelial Wnt/β-catenin signaling reduces immune cell infiltration in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  6. Review
  7. Review
  8. Deregulation of the Hippo pathway in mouse mammary stem cells promotes mammary tumorigenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Mechanistic insight into Myc stabilization in breast cancer involving aberrant Axin1 expression.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Article
  19. Article
  20. Wnt and mammary stem cells: hormones cannot fly wingless.Current opinion in pharmacology · 2010
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

W HsuDepartment of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
R Shakya
F Costantini
Columbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axin is a component of the canonical Wnt pathway that negatively regulates signal transduction by promoting degradation of beta-catenin. To study the role of Axin in development, we developed strains of transgenic mice in which its expression can be manipulated by the administration of doxycycline (Dox). Animals carrying both mouse mammary tumor virus (MMTV)-reverse tetracycline transactivator and tetracycline response element (TRE)2-Axin-green fluorescent protein (GFP) transgenes exhibited Dox-dependent Axin expression and, when induced from birth, displayed abnormalities in the development of mammary glands and lymphoid tissues, both sites in which the MMTV promoter is active. The transgenic mammary glands underwent normal ductal elongation and side branching during sexual maturation and early pregnancy, but failed to develop lobulo-alveoli, resulting in a defect in lactation. Axin attenuated the expression of cyclin D1, a Wnt target that promotes the growth and differentiation of mammary lobulo-alveoli. Increased apoptosis occurred in the mammary epithelia, consistent with the inhibition of a Wnt/cyclin D1 survival signal by Axin. High levels of programmed cell death also occurred in the thymus and spleen. Immature thymocytes underwent massive apoptosis, indicating that the overexpression of Axin blocks the normal development of T lymphocytes. Our data imply that the Axin tumor suppressor controls cell survival, growth, and differentiation through the regulation of an apoptotic signaling pathway.

Indexed as

Repressor ProteinsAnimalsAnti-Bacterial AgentsApoptosisAxin ProteinDoxycyclineFemaleGene Expression Regulation, DevelopmentalIn Situ Nick-End LabelingLactationLymphoid TissueMammary Glands, AnimalMiceMice, TransgenicPregnancyProteinsAnti-Bacterial AgentsAxin ProteinDoxycyclineProteinsRepressor Proteins

Identifiers

PMID11739413
PMCPMC2150907
OpenAlexW1985095911

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.