ReviewJournal of biomedicine & biotechnology2011
A symphony of regulations centered on p63 to control development of ectoderm-derived structures.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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
14 citing papers in PubMed, 27 citations in OpenAlex.
- Molecular mechanisms of thalidomide effectiveness on COVID-19 patients explained: ACE2 is a new ΔNp63α target gene.Journal of molecular medicine (Berlin, Germany) · 2024Article
- A complex structural variant nearHGG advances · 2023Article
- C(3)1-TAg in C57BL/6 J background as a model to study mammary tumor development.Histochemistry and cell biology · 2021Article
- Molecular Mechanisms of the Teratogenic Effects of Thalidomide.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Bhlha9 regulates apical ectodermal ridge formation during limb development.Journal of bone and mineral metabolism · 2018Article
- Limb development: a paradigm of gene regulation.Nature reviews. Genetics · 2017Review
- The apical ectodermal ridge of the mouse model of ectrodactyly Dlx5;Dlx6-/- shows altered stratification and cell polarity, which are restored by exogenous Wnt5a ligand.Human molecular genetics · 2016Article
- FGF8, c-Abl and p300 participate in a pathway that controls stability and function of the ΔNp63α protein.Human molecular genetics · 2015Article
- A novel c.1037C > G (p.Ala346Gly) mutation in TP63 as cause of the ectrodactyly-ectodermal dysplasia and cleft lip/palate (EEC) syndrome.Genetics and molecular biology · 2015Article
- Sp6 and Sp8 transcription factors control AER formation and dorsal-ventral patterning in limb development.PLoS genetics · 2014Article
- DLX5, FGF8 and the Pin1 isomerase control ΔNp63α protein stability during limb development: a regulatory loop at the basis of the SHFM and EEC congenital malformations.Human molecular genetics · 2014Article
- Insights from human genetic studies into the pathways involved in osteoarthritis.Nature reviews. Rheumatology · 2013Review
- BMP-mediated functional cooperation between Dlx5;Dlx6 and Msx1;Msx2 during mammalian limb development.PloS one · 2013Article
- Mechanisms of tissue fusion during development.Development (Cambridge, England) · 2012Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
The p53-related transcription factor p63 is critically important for basic cellular functions during development of the ectoderm and derived structure and tissues, including skin, limb, palate, and hair. On the one side, p63 is required to sustain the proliferation of keratinocyte progenitors, while on the other side it is required for cell stratification, commitment to differentiate, cell adhesion, and epithelial-mesenchymal signaling. Molecules that are components or regulators of the p63 pathway(s) are rapidly being identified, and it comes with no surprise that alterations in the p63 pathway lead to congenital conditions in which the skin and other ectoderm-derived structures are affected. In this paper, we summarize the current knowledge of the molecular and cellular regulations centered on p63, derived from the comprehension of p63-linked human diseases and the corresponding animal models, as well as from cellular models and high-throughput molecular approaches. We point out common themes and features, that allow to speculate on the possible role of p63 downstream events and their potential exploitation in future attempts to correct the congenital defect in preclinical studies.
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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.