Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development

By Yijie Gao, D. Ferguson, W. Xie, J. Manis, J. Sekiguchi, Karen M. Frank, J. Chaudhuri, J. Horner, R. DePinho, F. Alt. Nature, 2000

603 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/9339035b70500ab27b8107865fbc537309ef758f

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Citations in the corpus

Applications of genome editing technology in the targeted therapy of human diseases: mechanisms, advances and prospects (2020, background): “The identification of novel small molecule inhibitors against other NHEJ proteins, such as artemis and XRCC4, may further advance current strategies.(307,308) An improved CRISPR system, called CRISPR/Cpf1 or CRISPR/Cas12a, that employs a smaller and simpler RNA-guided DNA nuclease, Applications of g”
DNA double-strand breaks: signaling, repair and the cancer connection (2001, background): “Notably, loss of Xrcc4 or DNA ligase IV in mice results in embryonic lethality that is associated with widespread apoptosis of newly generated neuron”
Chromosomal stability and the DNA double-stranded break connection (2001, background): “The inactivation of these genes allows the animals to develop past birth, but does not rescue normal V(D)J recombination or the development of their immune syste”
Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, background): “The partial rescue by Trp53 mutation is similar to that observed with Rad51, Brca1, and Brca2 mutants (Moynahan 2002) but is unlike NHEJ mutants, in which the late embryonic lethality is rescued to give rise to viable (although feeble) mice (Frank et al. 2000; Gao et al. 2000).”
p53 in the DNA damage repair process (2016, background): “Mice deficient for p53 and NHEJ were reported to develop a number of pathologies including progenitor B-cell lymphomas (Guidos et al. 1996; Nacht et al. 1996; Vanasse et al. 1999; Frank et al. 2000; Gao et al. 2000; Difilippanto- nio et al. 2002; Gladdyet al. 2003).”
The signals and pathways activating cellular senescence. (2005, background): “This type of premature senescence, bo he tissue culture and in the living mouse, can usu e prevented by p53 inactivation (Frank et al., 2000 ao et al., 2000; Ongusaha et al., 2003).”