Experts and Doctors on endodeoxyribonucleases in Italy


Locale: Italy
Topic: endodeoxyribonucleases

Top Publications

  1. Pascucci B, Maga G, Hubscher U, Bjoras M, Seeberg E, Hickson I, et al. Reconstitution of the base excision repair pathway for 7,8-dihydro-8-oxoguanine with purified human proteins. Nucleic Acids Res. 2002;30:2124-30 pubmed
    ..Thus, the assembly of all the core proteins for 8-oxoG repair catalyses one major pathway that involves single nucleotide repair patches. ..
  2. Antonioli P, Bachi A, Fasoli E, Righetti P. Efficient removal of DNA from proteomic samples prior to two-dimensional map analysis. J Chromatogr A. 2009;1216:3606-12 pubmed publisher
    ..It is hypothesized that the alkaline pH values adopted in the two-phase extraction help to fully disrupt any residual DNA-protein complexes, due to strong Coulombic repulsion. ..
  3. Mayes M, Bossini Castillo L, Gorlova O, Martin J, Zhou X, Chen W, et al. Immunochip analysis identifies multiple susceptibility loci for systemic sclerosis. Am J Hum Genet. 2014;94:47-61 pubmed publisher
  4. De Gregorio L, Gallinari P, Gariboldi M, Manenti G, Pierotti M, Jiricny J, et al. Genetic mapping of thymine DNA glycosylase (Tdg) gene and of one pseudogene in the mouse. Mamm Genome. 1996;7:909-10 pubmed
  5. Costa M, Ochem A, Staub A, Falaschi A. Human DNA helicase VIII: a DNA and RNA helicase corresponding to the G3BP protein, an element of the ras transduction pathway. Nucleic Acids Res. 1999;27:817-21 pubmed
    ..HDH VIII/G3BP is analogous to the heterogeneous nuclear ribonucleoproteins and contains a sequence rich in RGG boxes similar to the C-terminal domain of HDH IV/nucleolin, another DNA and RNA helicase. ..
  6. Puglisi F, Barbone F, Tell G, Aprile G, Pertoldi B, Raiti C, et al. Prognostic role of Ape/Ref-1 subcellular expression in stage I-III breast carcinomas. Oncol Rep. 2002;9:11-7 pubmed
    ..014) and Cox proportional hazard model analysis identified APE/Ref-1 as an independent prognostic factor. The results suggest that subcellular localisation of APE/Ref-1 may influence the aggressiveness of breast carcinomas. ..
  7. Clerici M, Mantiero D, Guerini I, Lucchini G, Longhese M. The Yku70-Yku80 complex contributes to regulate double-strand break processing and checkpoint activation during the cell cycle. EMBO Rep. 2008;9:810-8 pubmed publisher
    ..Moreover, DSB resection in ykuDelta cells occurs independently of CDK activity, suggesting that it might be promoted by CDK-dependent inhibition of Yku. ..
  8. Doksani Y, Bermejo R, Fiorani S, Haber J, Foiani M. Replicon dynamics, dormant origin firing, and terminal fork integrity after double-strand break formation. Cell. 2009;137:247-58 pubmed publisher
    ..Our findings have implications for those genome instability syndromes that accumulate DNA breaks during S phase and for forks encountering eroding telomeres. ..
  9. Manfrini N, Guerini I, Citterio A, Lucchini G, Longhese M. Processing of meiotic DNA double strand breaks requires cyclin-dependent kinase and multiple nucleases. J Biol Chem. 2010;285:11628-37 pubmed publisher
    ..Furthermore, the helicase Sgs1 and the nucleases Exo1 and Dna2 participate in lengthening the 5'-3' resection tracts during meiosis by controlling a step subsequent to Spo11 removal. ..

More Information


  1. Robert T, Vanoli F, Chiolo I, Shubassi G, Bernstein K, Rothstein R, et al. HDACs link the DNA damage response, processing of double-strand breaks and autophagy. Nature. 2011;471:74-79 pubmed publisher
    ..We propose that Rpd3, Hda1 and Gcn5 control chromosome stability by coordinating the ATR checkpoint and double-strand-break processing with autophagy. ..
  2. Tricarico R, Cortellino S, Riccio A, Jagmohan Changur S, van der Klift H, Wijnen J, et al. Involvement of MBD4 inactivation in mismatch repair-deficient tumorigenesis. Oncotarget. 2015;6:42892-904 pubmed publisher
    ..Mbd4-deficient mice showed reduced survival when combined with Mlh1-/- genotype. Taken together, these data suggest that MBD4 inactivation may contribute to tumorigenesis, acting as a modifier of MMR-deficient cancer phenotype. ..
  3. Kolinjivadi A, Sannino V, De Antoni A, Zadorozhny K, Kilkenny M, Técher H, et al. Smarcal1-Mediated Fork Reversal Triggers Mre11-Dependent Degradation of Nascent DNA in the Absence of Brca2 and Stable Rad51 Nucleofilaments. Mol Cell. 2017;67:867-881.e7 pubmed publisher
    ..These results indicate that Brca2 and Rad51 prevent formation of abnormal DNA replication intermediates, whose processing by Smarcal1 and Mre11 predisposes to genome instability. ..