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  • 1
    Electronic Resource
    Electronic Resource
    Expression of different p63 variants in healing skin wounds suggests a role of p63 in reepithelialization and muscle repair (2005)
    Oxford, UK; Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 13 (2005), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Healing of skin wounds in mammals involves partial reconstruction of the dermis and coverage of the injured site by keratinocytes. The latter process is achieved by extensive migration and hyperproliferation of keratinocytes at the wound rim. Because the p53 protein family member p63 is expressed in human hyperproliferative epidermis, this study determined whether enhanced keratinocyte proliferation correlates with the expression of p63. Therefore, we investigated the temporal and spatial distribution of four major variants of the p63 transcription factor—TAp63α, TAp63γ, ΔNp63α and ΔNp63γ—during normal skin wound healing in mice. Transcripts encoding amino-terminally truncated ΔNp63 variants were found at high levels in basal and suprabasal keratinocytes of the hyperproliferative wound epithelium. Interestingly, TAp63 variants, which include the conserved transactivation domain TA at their amino-terminus, were also expressed in wound keratinocytes as well as at the edge of the injured subcutaneous muscle panniculus carnosus. These findings suggest splice-variant specific functions of p63 in reepithelialization and muscle repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2005.130106.x
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  • 2
    Electronic Resource
    Electronic Resource
    p63 protects the female germ line during meiotic arrest (2006)
    [s.l.] : Nature Publishing Group
    Nature 444 (2006), S. 624-628 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Meiosis in the female germ line of mammals is distinguished by a prolonged arrest in prophase of meiosis I between homologous chromosome recombination and ovulation. How DNA damage is detected in these arrested oocytes is poorly understood, but it is variably thought to involve p53, a central ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature05337
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Cloning and chromosomal mapping of the human p53-related KET gene to Chromosome 3q27 and its murine homolog Ket to mouse Chromosome 16 (1998)
    Springer
    Mammalian genome 9 (1998), S. 899-902 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. KET is a member of the newly discovered family of proteins that is related to the tumor suppressor p53. Here we describe the molecular cloning of a human cDNA of 4846 bp encoding a protein of 680 amino acids. The human KET protein shares 98% identity with the previously characterized rat homolog. The remarkably high degree of conservation lends support to the notion that KET proteins have important basic functions in development and differentiation. Using the GeneBridge 4 radiation hybrid panel, we have mapped KET to human Chromosome (Chr) 3q27. KET is located between the somatostatin gene SST (proximal) and the apolipoprotein D gene APOD (distal) in a region of conserved synteny to mouse Chr 16. This chromosomal region is deleted in early stages of tumorigenesis of mouse islet cell carcinomas and contains the hitherto unidentified Loh2 gene, a putative suppressor of angiogenesis. The murine homolog Ket was mapped in an interspecific backcross panel and falls into this region of loss of heterozygosity. From our mapping data we infer that KET might act as a tumor suppressor and is considered as a candidate for Loh2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900891
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    Paper (German National Licenses)
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