Cell proliferation and ku protein expression in ageing humans

Frasca, Daniela; Barattini, Paola; Goso, Cristina; Pucci, Sabina; Rizzo, Giovanni; Bartoloni, Carlo; Costanzo, Mario; Errani, A.R.; Guidi, L.; Antico, L; Tricerri, A.; Doria, Gino

doi:10.1016/s0047-6374(97)00137-1

Cited by 16 publications

(7 citation statements)

References 20 publications

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“…It is interesting to note that, in contrast with that of others, this benign pathology showed the same band density in both types of tissue, and thus can be considered to be an additional control. It is worth noting that the Ku heterodimer shows a cumulative binding to DNA fragments and that this property is correlated with the amount of the protein, as previously demonstrated 32–34. Figure 2b shows the supershift of the bands due to the Ku DNA‐binding activity.…”

Section: Resultssupporting

confidence: 66%

Simple and Efficient Iridium(III)‐Catalyzed Water Oxidations

et al. 2011

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BACKGROUND The Ku protein is a tightly associated heterodimer, comprised of 70‐kilodalton (kD) and 86‐kD subunits, that forms the DNA‐dependent protein kinase (DNA‐PK) complex together with the 470‐kD DNA‐PKcs catalytic subunit, and is involved mainly in DNA double‐strand breaks (DSBs) repair. The objective of the current study was to investigate the expression and DNA‐binding activity of the Ku protein in fresh tissues from patients with bladder carcinoma and to compare it with that in nontumor tissues obtained from the same organ. Moreover, the DNA‐binding activity of Ku was assessed after exposure of the tumor cells to 1 or 2 grays (Gy) of X‐rays. Furthermore, the level of phosphorylated Ku was analyzed in both the nuclear and cytoplasmic compartment of normal tissue after exposure to 2 Gy of X‐rays. METHODS The expression and DNA‐binding activity of Ku protein were assessed in tumor samples from patients who all were diagnosed with transitional cell carcinoma (TCC) of the bladder using Western blot analysis and the electrophoretic mobility shift assay, respectively. RESULTS Enhanced Ku activity and expression were found in tumor tissue compared with normal tissue for each patient. Moreover, variations in Ku activity were found in a dose‐dependent manner after the tumor cells were exposed to 1 or 2 Gy of X‐rays. A decrease in phosphorylated Ku in the cytoplasm and a parallel increase in the nucleus of normal tissue cells were observed after exposure to X‐rays. CONCLUSIONS The results of the current study suggest a possible role of Ku in regulating the DNA‐PK activity of DSBs repair in bladder tumors. Cancer 2001;92:2484–92. © 2001 American Cancer Society.

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Section: Resultssupporting

confidence: 66%

Simple and Efficient Iridium(III)‐Catalyzed Water Oxidations

et al. 2011

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“…It is worth noting that the Ku heterodimer shows a cumulative binding to DNA fragments and that this property is correlated with the amount of the protein, as previously demonstrated. [32][33][34] Figure 2b shows the supershift of the bands due to the Ku DNA-binding activity.…”

Section: Resultsmentioning

confidence: 99%

Expression and DNA binding activity of the Ku heterodimer in bladder carcinoma

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Gensabella

Lamberti

et al. 2001

Cancer

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“…The 56-bp dsDNA (5′-GATCAGTGATGGAGTTGGCCACTCCCTCTCTGCGCGCTCGCTCGCTCACTGAGGCC-3′) was end labeled with using DIG-11-ddUTP (Roche) [45]. DNA end-binding reaction and detection were performed according to the manufacturer's protocol (Roche).…”

Section: Methodsmentioning

confidence: 99%

ATM Modulates the Loading of Recombination Proteins onto a Chromosomal Translocation Breakpoint Hotspot

et al. 2010

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Chromosome translocations induced by DNA damaging agents, such as ionizing radiation and certain chemotherapies, alter genetic information resulting in malignant transformation. Abrogation or loss of the ataxia-telangiectasia mutated (ATM) protein, a DNA damage signaling regulator, increases the incidence of chromosome translocations. However, how ATM protects cells from chromosome translocations is still unclear. Chromosome translocations involving the MLL gene on 11q23 are the most frequent chromosome abnormalities in secondary leukemias associated with chemotherapy employing etoposide, a topoisomerase II poison. Here we show that ATM deficiency results in the excessive binding of the DNA recombination protein RAD51 at the translocation breakpoint hotspot of 11q23 chromosome translocation after etoposide exposure. Binding of Replication protein A (RPA) and the chromatin remodeler INO80, which facilitate RAD51 loading on damaged DNA, to the hotspot were also increased by ATM deficiency. Thus, in addition to activating DNA damage signaling, ATM may avert chromosome translocations by preventing excessive loading of recombinational repair proteins onto translocation breakpoint hotspots.

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Cell proliferation and ku protein expression in ageing humans

Cited by 16 publications

References 20 publications

Simple and Efficient Iridium(III)‐Catalyzed Water Oxidations

Simple and Efficient Iridium(III)‐Catalyzed Water Oxidations

Expression and DNA binding activity of the Ku heterodimer in bladder carcinoma

ATM Modulates the Loading of Recombination Proteins onto a Chromosomal Translocation Breakpoint Hotspot

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