Evidence map›Paper›PMID 18765787›Full record

ReviewGenes & development2008

Deciphering the function of canonical Wnt signals in development and disease: conditional loss- and gain-of-function mutations of beta-catenin in mice.

Tamara Grigoryan, Peter Wend, Alexandra Klaus, Walter Birchmeier

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 321 papers.

0numbers the graph read from it
0cells of the map it votes in
321citing papers in PubMed
–field-weighted citation impact
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

321 citing papers in PubMed, 556 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. The development of hair follicles and nail.Developmental biology · 2024
    Review
  10. Article
  11. Review
  12. The Molecular Landscape of Thymic Epithelial Tumors: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Exploring the dynamics of adultFrontiers in neuroscience · 2024
    Article
  17. Review
  18. Review
  19. Article
  20. Review

261 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Tamara GrigoryanMax-Delbück Center for Molecular Medicine, 13125 Berlin, Germany.
Peter Wend
Alexandra Klaus
Walter Birchmeier
Max Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt signaling is one of a handful of powerful signaling pathways that play crucial roles in the animal life by controlling the genetic programs of embryonic development and adult homeostasis. When disrupted, these signaling pathways cause developmental defects, or diseases, among them cancer. The gateway of the canonical Wnt pathway, which contains >100 genes, is an essential molecule called beta-catenin (Armadillo in Drosophila). Conditional loss- and gain-of-function mutations of beta-catenin in mice provided powerful tools for the functional analysis of canonical Wnt signaling in many tissues and organs. Such studies revealed roles of Wnt signaling that were previously not accessible to genetic analysis due to the early embryonic lethality of conventional beta-catenin knockout mice, as well as the redundancy of Wnt ligands, receptors, and transcription factors. Analysis of conditional beta-catenin loss- and gain-of-function mutant mice demonstrated that canonical Wnt signals control progenitor cell expansion and lineage decisions both in the early embryo and in many organs. Canonical Wnt signaling also plays important roles in the maintenance of various embryonic or adult stem cells, and as recent findings demonstrated, in cancer stem cell types. This has opened new opportunities to model numerous human diseases, which have been associated with deregulated Wnt signaling. Our review summarizes what has been learned from genetic studies of the Wnt pathway by the analysis of conditional beta-catenin loss- and gain-of-function mice.

Indexed as

Animalsbeta CateninBone and BonesCentral Nervous SystemExtremitiesGastrointestinal TractHeartHematopoiesisHumansMiceMice, Mutant StrainsModels, AnimalMutationNeural CrestOrgan SpecificitySense Organsbeta CateninWnt Proteins

Identifiers

PMID18765787
PMCPMC2749675
OpenAlexW2110838173

What OpenQuestion holds

Textmetadata
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.