p63 and FGFR: when development meets proliferation
- PMID: 22331572
- PMCID: PMC3376846
- DOI: 10.1002/emmm.201200202
p63 and FGFR: when development meets proliferation
Figures
ΔNp63α functions as a positive determinant of FGFR2 and FGFR3 expression. Mutations found in AEC syndrome are sufficient to suppress, in a heterozygous state, FGFR2 and FGFR3 expression. This causes an impairment of proliferation in embryonic ectodermal cells.
p63 is interconnected with several pathways that are required for one or more steps of secondary palate development as recently reviewed (Dixon et al, 2011).
Comment on
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Mutant p63 causes defective expansion of ectodermal progenitor cells and impaired FGF signalling in AEC syndrome.EMBO Mol Med. 2012 Mar;4(3):192-205. doi: 10.1002/emmm.201100199. Epub 2012 Jan 13. EMBO Mol Med. 2012. PMID: 22247000 Free PMC article.
References
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- Antonini D, Russo MT, De Rosa L, Gorrese M, Del Vecchio L, Missero C. Transcriptional repression of miR-34 family contributes to p63-mediated cell cycle progression in epidermal cells. J Invest Dermatol. 2010;130:1249–1257. - PubMed
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- Crum CP, McKeon FD. p63 in epithelial survival, germ cell surveillance, and neoplasia. Annu Rev Pathol. 2010;5:349–371. - PubMed
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- Ferone G, Thomason HA, Antonini D, De Rosa L, Hu B, Gemei M, Zhou H, Ambrosio R, Rice DP, Acampora D, et al. Mutant p63 causes defective expansion of ectodermal progenitor cells and impaired FGF signaling in AEC syndrome. EMBO Mol Med. 2012 DOI: 10.1002/emmm.201100199. - DOI - PMC - PubMed
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