Journal ArticleDOI
p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development
Annie Yang,Ronen Schweitzer,Deqin Sun,Mourad Kaghad,Nancy Walker,Roderick T. Bronson,Clifford J. Tabin,Arlene H. Sharpe,Daniel Caput,Christopher P. Crum,Frank McKeon +10 more
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TLDR
It is reported that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development, and results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelialDevelopment and morphogenesis.Abstract:
The p63 gene, a homologue of the tumour-suppressor p53, is highly expressed in the basal or progenitor layers of many epithelial tissues. Here we report that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development. p63 is expressed in the ectodermal surfaces of the limb buds, branchial arches and epidermal appendages, which are all sites of reciprocal signalling that direct morphogenetic patterning of the underlying mesoderm. The limb truncations are due to a failure to maintain the apical ectodermal ridge, a stratified epithelium, essential for limb development. The embryonic epidermis of p63-/- mice undergoes an unusual process of non-regenerative differentiation, culminating in a striking absence of all squamous epithelia and their derivatives, including mammary, lacrymal and salivary glands. Taken together, our results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelial development and morphogenesis.read more
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Classification of human lung carcinomas by mRNA expression profiling reveals distinct adenocarcinoma subclasses
Arindam Bhattacharjee,William G. Richards,Jane Staunton,Cheng Li,Stefano Monti,Priya Vasa,Christine Ladd,Javad Beheshti,Raphael Bueno,Michael A. Gillette,Massimo Loda,Griffin M. Weber,Eugene J. Mark,Eric S. Lander,Wing Hung Wong,Bruce E. Johnson,Todd R. Golub,Todd R. Golub,David J. Sugarbaker,Matthew Meyerson +19 more
TL;DR: A molecular taxonomy of lung carcinoma is generated and results suggest that integration of expression profile data with clinical parameters could aid in diagnosis of lung cancer patients.
Journal ArticleDOI
The single-cell transcriptional landscape of mammalian organogenesis
Junyue Cao,Malte Spielmann,Xiaojie Qiu,Xingfan Huang,Daniel M. Ibrahim,Daniel M. Ibrahim,Andrew J. Hill,Fan Zhang,Stefan Mundlos,Stefan Mundlos,Lena Christiansen,Frank J. Steemers,Cole Trapnell,Jay Shendure +13 more
TL;DR: A cell atlas of mouse organogenesis provides a global view of developmental processes occurring during this critical period, including focused analyses of the apical ectodermal ridge, limb mesenchyme and skeletal muscle.
Journal ArticleDOI
The first 30 years of p53: growing ever more complex
Arnold J. Levine,Moshe Oren +1 more
TL;DR: Thirty years ago p53 was discovered as a cellular partner of simian virus 40 large T-antigen, the oncoprotein of this tumour virus, and new functions of this protein were revealed, including the regulation of metabolic pathways and cytokines that are required for embryo implantation.
Journal ArticleDOI
p63 identifies keratinocyte stem cells
Graziella Pellegrini,Elena Dellambra,Osvaldo Golisano,Enrica Martinelli,Ivana Fantozzi,Sergio Bondanza,Diego Ponzin,Frank McKeon,Michele De Luca +8 more
TL;DR: It is shown by clonal analysis that p63 is abundantly expressed by epidermal and limbal holoclones, but is undetectable in paraclones, and will be of practical importance for the clinical application of epithelial cultures in cell therapy as well as for studies on epithelial tumorigenesis.
Journal ArticleDOI
Control of apoptosis by p53.
Jordan S. Fridman,Scott W. Lowe +1 more
TL;DR: The current understanding of p53 illustrates how apoptosis can be integrated into a larger tumor suppressor network controlled by different signals, environmental factors, and cell type.
References
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Journal ArticleDOI
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Lawrence A. Donehower,Michele Harvey,Betty L. Slagle,Mark J. McArthur,Charles A. Montgomery,Janet S. Butel,Allan Bradley +6 more
TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
Journal ArticleDOI
Serial cultivation of strains of human epidermal keratinocytes: the formation of keratinizing colonies from single cells.
James G. Rheinwatd,Howard Green +1 more
TL;DR: Human diploid epidermis epidermal cells have been successfully grown in serial culture and it is possible to isolate keratinocyte clones free of viable fibroblasts, and human diploids keratinocytes appear to have a finite culture lifetime.
Journal ArticleDOI
p53: puzzle and paradigm.
Linda J. Ko,Carol Prives +1 more
TL;DR: Some of the key developments leading to the current state of knowledge in p53 research are presented and how they either shed light on or add to the complexities of p53 are discussed.
Journal ArticleDOI
p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities.
Annie Yang,Mourad Kaghad,Yunmei Wang,Emily Gillett,Mark D. Fleming,Mark D. Fleming,Mark D. Fleming,Volker Dötsch,Nancy C. Andrews,Nancy C. Andrews,Daniel Caput,Frank McKeon +11 more
TL;DR: The cloning of p63, a gene at chromosome 3q27-29 that bears strong homology to the tumor suppressor p53 and to the related gene, p73, is described and the possibility of physiological interactions among members of the p53 family is suggested.
Journal ArticleDOI
Tumor spectrum analysis in p53-mutant mice.
Tyler Jacks,Lee Remington,Bart O. Williams,Earlene M. Schmitt,Shlomit Halachmi,Roderick T. Bronson,Robert A. Weinberg +6 more
TL;DR: It is reaffirm that p53 function is not required for normal mouse development and conclude that p 53 status can strongly influence tumor latency and tissue distribution.
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Heterozygous germline mutations in the p53 homolog p63 are the cause of EEC syndrome.
Jacopo Celli,Pascal H.G. Duijf,Ben C.J. Hamel,Michael J. Bamshad,Bridget Kramer,Arie P. T. Smits,Ruth Newbury-Ecob,Raoul C.M. Hennekam,Griet Van Buggenhout,Arie van Haeringen,C. Geoffrey Woods,Anthonie J. van Essen,Robert M.W. de Waal,Gert Vriend,Daniel A. Haber,Annie Yang,Frank McKeon,Han G. Brunner,Hans van Bokhoven +18 more