Search Results - (Author, Cooperation:L. D. Attardi)

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  1. 1
    Staff View
    Publication Date:
    2014-08-15
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Abnormalities, Multiple/genetics/*metabolism ; Alleles ; Animals ; Apoptosis/genetics ; CHARGE Syndrome/*genetics/*metabolism ; Cell Cycle Checkpoints/genetics ; Craniofacial Abnormalities/genetics/metabolism ; DNA-Binding Proteins/deficiency/genetics/metabolism ; Ear/abnormalities ; Embryo, Mammalian/abnormalities/metabolism ; Female ; Fibroblasts ; Gene Deletion ; Heterozygote ; Humans ; Male ; Mice ; Mutant Proteins/metabolism ; *Phenotype ; Promoter Regions, Genetic/genetics ; Tumor Suppressor Protein p53/*genetics/*metabolism
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    K. T. Bieging ; L. D. Attardi
    Nature Publishing Group (NPG)
    Published 2015
    Staff View
    Publication Date:
    2015-03-25
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; Cystine/*metabolism ; Humans ; Iron/*metabolism ; Neoplasms/*metabolism/*pathology ; Reactive Oxygen Species/*metabolism ; Tumor Suppressor Protein p53/*metabolism
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  3. 3
    Attardi, L. D. ; Jacks, T.
    Springer
    Published 1999
    Staff View
    ISSN:
    1420-9071
    Keywords:
    Key words. p53; mouse model; tumour suppressor gene; cancer; apoptosis; cell-cycle arrest.
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Biology
    Medicine
    Notes:
    Abstract. The use of mouse models has greatly contributed to our understanding of the role of p53 in tumour suppression. Mice homozygous for a deletion in the p53 gene develop tumours at high frequency, providing essential evidence for the importance of p53 as a tumour suppressor. Additionally, crossing these knockout mice or transgenic expression p53 dominant negative alleles with other tumour-prone mouse strains has allowed the effect of p53 loss on tumour development to be examined further. In a variety of mouse models, absence of p53 facilitates tumorigenesis, thus providing a means to study how the lack of p53 enhances tumour development and to define genetic pathways of p53 action. Depending on the particular model system, loss of p53 either results in deregulated cell-cylce entry or aberrant apoptosis (programmed cell death), confirming results found in cell culture systems and providing insight into in vitro function of p53. Finally, as p53 null mice rapidly develop tumours, they are useful for evaluating agents for either chemopreventative or therapeutic activities.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s000180050269

    Articles: DFG German National Licenses