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Frank McKeon

Researcher at University of Houston

Publications -  154
Citations -  31678

Frank McKeon is an academic researcher from University of Houston. The author has contributed to research in topics: Stem cell & Calcineurin. The author has an hindex of 74, co-authored 151 publications receiving 30024 citations. Previous affiliations of Frank McKeon include Harvard University & National University of Singapore.

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p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development

TL;DR: 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.
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p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities.

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.
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Monoallelically expressed gene related to p53 at 1p36, a region frequently deleted in neuroblastoma and other human cancers.

TL;DR: The demonstration that p73 is monoallelically expressed supports the notion that it is a candidate gene in neuroblastoma and proposes that the disregulation of p73 contributes to tumorigenesis and that p53-related proteins operate in a network of developmental and cell cycle controls.
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p63 identifies keratinocyte stem cells

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.
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Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD.

TL;DR: In hippocampal neurons, L-glutamate triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase.