Daniel Håkansson
Stockholm University
4 Papers
128 Citations
Daniel Håkansson is an academic researcher from Stockholm University. The author has contributed to research in topics: DNA repair & Pyrene. The author has an hindex of 4, co-authored 4 publications. Previous affiliations of Daniel Håkansson include Kerman Medical University.
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Papers
The ERCC1/XPF endonuclease is required for completion of homologous recombination at DNA replication forks stalled by inter-strand cross-links
Ali Z. Al-Minawi,Yin-Fai Lee,Daniel Håkansson,Fredrik Johansson,Cecilia Lundin,Nasrollah Saleh-Gohari,Niklas Schultz,Dag Jenssen,Helen E. Bryant,M Meuth,John M. Hinz,Thomas Helleday +11 more
TL;DR: It is reported that mitomycin C-induced lesions inhibit replication fork elongation and suggested that ERCC1–XPF plays a role in completion of HR in ICL repair, and no additional sensitivity to cisplatin by siRNA co-depletion of XRCC3 and ER CC1 is found, showing that the two proteins act on the same pathway to promote survival.
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Both replication bypass fidelity and repair efficiency influence the yield of mutations per target dose in intact mammalian cells induced by benzo[a]pyrene-diol-epoxide and dibenzo[a,l]pyrene-diol-epoxide.
Anne Lagerqvist,Daniel Håkansson,Gabriela Prochazka,Cecilia Lundin,Kristian Dreij,Dan Segerbäck,Bengt Jernström,Margareta Törnqvist,Albrecht Seidel,Klaus Erixon,Dag Jenssen +10 more
TL;DR: The mutagenicity of PAH is influenced not only by NER, but also by replication bypass fidelity, which is now also being recognized in terms of forward mutations in intact mammalian cells.
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DNA repair and replication influence the number of mutations per adduct of polycyclic aromatic hydrocarbons in mammalian cells.
Anne Lagerqvist,Daniel Håkansson,Cecilia Lundin,Gabriela Prochazka,Kristian Dreij,Dan Segerbäck,Bengt Jernström,Margareta Törnqvist,Heinz Frank,Albrecht Seidel,Klaus Erixon,Dag Jenssen +11 more
TL;DR: The data demonstrate that neither of these pathways seems to be the sole factor determining the mutation frequency of the four PAH-DE and that the differences in the repair efficiency of these compounds could not be related to the presence of a bay or fjord region in the parent PAH.
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Structural requirements for mutation formation from polycyclic aromatic hydrocarbon dihydrodiol epoxides in their interaction with food chemopreventive compounds
TL;DR: A novel and unexpected finding was that the antimutagenic activity could differ as much as by a factor of 7 towards four carcinogenic PAH metabolites being relatively similar in structure and genotoxic activity.
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