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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia
Three participants are identified (AT gene(s), p53, and GADD45) in a signal transduction pathway that controls cell cycle arrest following DNA damage; abnormalities in this pathway probably contribute to tumor development. Expand
Phosphorylation of human p53 by p38 kinase coordinates N‐terminal phosphorylation and apoptosis in response to UV radiation
Results suggest that p38 kinase plays a prominent role in an integrated regulation of N‐terminal phosphorylation that regulates p53‐mediated apoptosis after UV radiation. Expand
DNA Repair Pathway Stimulated by the Forkhead Transcription Factor FOXO3a Through the Gadd45 Protein
Findings indicate that in mammals FOXO3a regulates the resistance of cells to stress by inducing DNA repair and thereby may also affect organismal life-span. Expand
Initiation of a G2/M checkpoint after ultraviolet radiation requires p38 kinase
It is reported that p38 kinase has a critical role in the initiation of a G2 delay after ultraviolet radiation, and regulation of Cdc25B phosphorylation by p38 is a critical event for initiating the G2/M checkpoint after ultraviolet Radiation. Expand
p53-Mediated DNA Repair Responses to UV Radiation: Studies of Mouse Cells Lacking p53, p21, and/orgadd45 Genes
  • Martin L. Smith, J. Ford, +6 authors A. Fornace
  • Medicine, Biology
  • Molecular and Cellular Biology
  • 15 May 2000
Evidence is provided that Gadd45 affects chromatin remodelling of templates concurrent with DNA repair, thus indicating that gadd45 may participate in the coupling between chromatin assembly and DNA repair. Expand
Interaction of the p53-regulated protein Gadd45 with proliferating cell nuclear antigen.
Gadd45 was found to bind to PCNA, a normal component of Cdk complexes and a protein involved in DNA replication and repair, establishing GADD45 as a link between the p53-dependent cell cycle checkpoint and DNA repair. Expand
Characterization of the p53 tumor suppressor pathway in cell lines of the National Cancer Institute anticancer drug screen and correlations with the growth-inhibitory potency of 123 anticancer agents.
The analysis revealed that cells with mutant p53 sequence tended to exhibit less growth inhibition in this screen than the wild-type p53 cell lines when treated with the majority of clinically used anticancer agents: including DNA cross-linking agents, antimetabolites, and topoisomerase I and II inhibitors. Expand
Wip1 phosphatase modulates ATM-dependent signaling pathways.
It is proposed that the Wip1 phosphatase is an integral component of an ATM-dependent signaling pathway and was critical for resetting ATM phosphorylation as cells repaired damaged DNA. Expand
Alternative p38 activation pathway mediated by T cell receptor–proximal tyrosine kinases
It is shown that T cells stimulated through the T cell receptor (TCR) used an alternative mechanism in which p38 was phosphorylated on Tyr323 and subsequently autophosphorylated residues Thr180 and Tyr182, serving as an important mechanism for TCR activation of p38 in T cells. Expand
Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents.
Five of the gadd cDNA clones encode transcripts that are increased by other growth cessation signals: growth arrest by serum reduction, medium depletion, contact inhibition, or a 24-h exposure to hydroxyurea, suggesting that these genes may represent part of a novel regulatory pathway involved in the negative control of mammalian cell growth. Expand