p63-Specific Activation of the BPAG-1e Promoter

Osada, Motonobu; Nagakawa, Yuichi; Park, Hannah Lui; Yamashita, Keishi; Wu, Guojun; Kim, Myoung Sook; Fomenkov, Alexey; Trink, Barry; Sidransky, David

doi:10.1111/j.0022-202x.2005.23801.x

Cited by 41 publications

(48 citation statements)

References 47 publications

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“…5G). Recently several studies have examined the potential p63 DNA binding consensus sites within p63-responsive genes (14,15,17). In these studies, p63 was shown to preferentially bind to DNA elements that are distinct from the p53 DNA binding element.…”

Section: Discussionmentioning

confidence: 99%

“…TAp63g has also been shown to activate the expression of Jagged 1 and Jagged 2, which are involved in Notch signaling, whereas Notch 1 activation has also been shown to suppress DNp63a expression, demonstrating a cross-talk between these pathways (7,8). Additional studies have shown that the biological effects of p63 in development and tumor suppression is exerted through the regulation of multiple signaling pathways (9)(10)(11)(12)(13)(14)(15)(16)(17). p73, another member of the p53 family, was also discovered based on structural similarities to p53 (18).…”

Section: Introductionmentioning

confidence: 99%

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p63 Overexpression Induces the Expression of Sonic Hedgehog

Caserta

Kommagani²,

Yuan

et al. 2006

Molecular Cancer Research

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p63 and p73 are members of the p53 protein family and have been shown to play an important role in cell death, development, and tumorigenesis. In particular, p63 has been shown to be involved in the maintenance of epidermal stem cells and in the stratification of the epidermis. Sonic Hedgehog (Shh) is a morphogen that has also been implicated to play a role in epithelial stem cell proliferation and in the development of organs. Recently, Shh has also been shown to play an important role in the progression of a variety of cancers. In this report, we show that p63 and p73 but not p53 overexpression induces Shh expression. In particular, p63; and p63B (both TA and #N isoforms) and TAp73B isoform induce Shh. Expression of Shh was found to be significantly reduced in mouse embryo fibroblasts obtained from p63À/À mice. The naturally occurring p63 mutant TAp63;(R279H) and the tumor suppressor protein p14 ARF inhibited the TAp63;-mediated transactivation of Shh. The region À228 to À102 bp of Shh promoter was found to be responsive to TAp63;-induced transactivation and TAp63; binds to regions within the Shh promoter in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

p63 Overexpression Induces the Expression of Sonic Hedgehog

Caserta

Kommagani²,

Yuan

et al. 2006

Molecular Cancer Research

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“…Compared with 2 known targets of p63, the p21 and BPAG genes (30,31), ChIP efficiencies expressed as a percentage of input chromatin at peak 229 and peak 58 regions were higher than, or at least similar to, those of the known binding sites ( Figure 5C). Use of 2 different p63 antibodies confirmed that the observed binding was specific for p63 ( Figure 5C).…”

Section: Irf6 Expression Is Dependent Upon Functional P63 Having Estab-mentioning

confidence: 91%

Cooperation between the transcription factors p63 and IRF6 is essential to prevent cleft palate in mice

Thomason¹,

Zhou²,

Kouwenhoven³

et al. 2010

J. Clin. Invest.

135

191

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Cleft palate is a common congenital disorder that affects up to 1 in 2,500 live human births and results in considerable morbidity to affected individuals and their families. The etiology of cleft palate is complex, with both genetic and environmental factors implicated. Mutations in the transcription factor-encoding genes p63 and interferon regulatory factor 6 (IRF6) have individually been identified as causes of cleft palate; however, a relationship between the key transcription factors p63 and IRF6 has not been determined. Here, we used both mouse models and human primary keratinocytes from patients with cleft palate to demonstrate that IRF6 and p63 interact epistatically during development of the secondary palate. Mice simultaneously carrying a heterozygous deletion of p63 and the Irf6 knockin mutation R84C, which causes cleft palate in humans, displayed ectodermal abnormalities that led to cleft palate. Furthermore, we showed that p63 transactivated IRF6 by binding to an upstream enhancer element; genetic variation within this enhancer element is associated with increased susceptibility to cleft lip. Our findings therefore identify p63 as a key regulatory molecule during palate development and provide a mechanism for the cooperative role of p63 and IRF6 in orofacial development in mice and humans.

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“…7C) perp, 91 envoplakin, 69 and BPAG-1. 92 Fig. 8 shows a simplified scheme of the actions of p63 in epidermal development, with particular emphasis on IKKα and K14, although the table does not aim at undermining the importance of other targets.…”

Section: Transcriptional Regulation By P63mentioning

confidence: 99%