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Judith Campisi
ANNUAL REVIEW OF PHYSIOLOGY, VOL 75 (2013)
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High resolution imaging of changes in the structure and spatial organization of chromatin, γ-H2A.X and the MRN complex within etoposide-induced DNA repair foci
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Delayed kinetics of DNA double-strand break processing in normal and pathological aging
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DNA damage response activation in mouse embryonic fibroblasts undergoing replicative senescence and following spontaneous immortalization
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ATR signaling can drive cells into senescence in the absence of DNA breaks
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ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin
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PML enhances the regulation of p53 by CK1 in response to DNA damage
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Regulation of apoptosis by PML and the PML-NBs
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Promyelocytic leukemia nuclear bodies behave as DNA damage sensors whose response to DNA double-strand breaks is regulated by NBS1 and the kinases ATM, Chk2, and ATR
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Fixation-induced redistribution of hyperphosphorylated RNA polymerase II in the nucleus of human cells
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PML is a direct p53 target that modulates p53 effector functions
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Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks
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Human fibroblasts require the Rb family of tumor suppressors, but not p53, for PML-induced senescence
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PML regulates p53 stability by sequestering Mdm2 to the nucleolus
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ATR kinase activity regulates the intranuclear translocation of ATR and RPA following ionizing radiation
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PML colocalizes with and stabilizes the DNA damage response protein TopBP1
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PML NBs associate with the hMre11 complex and p53 at sites of irradiation induced DNA damage
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