Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Stanislaw K Jozwiakowski"'
Autor:
Diana C Odermatt, Wei Ting C Lee, Sebastian Wild, Stanislaw K Jozwiakowski, Eli Rothenberg, Kerstin Gari
Publikováno v:
PLoS Genetics, Vol 16, Iss 6, p e1008740 (2020)
FANCJ/BRIP1 is an iron-sulfur (FeS) cluster-binding DNA helicase involved in DNA inter-strand cross-link (ICL) repair and G-quadruplex (G4) metabolism. Mutations in FANCJ are associated with Fanconi anemia and an increased risk for developing breast
Externí odkaz:
https://doaj.org/article/5ba9429496e64078af68f76d1c54c78e
Autor:
Tomasz Skorski, Janusz Blasiak, Michal O. Nowicki, Ewelina Stoczynska, Dariusz Pytel, Kimberly Cramer, Stanislaw K. Jozwiakowski, Tomasz Poplawski, Artur Slupianek
Supplementary Figures 1-4 from BCR/ABL Stimulates WRN to Promote Survival and Genomic Instability
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6087ab740ea7bc1beacd4deb08fdc1e5
https://doi.org/10.1158/0008-5472.22388429
https://doi.org/10.1158/0008-5472.22388429
Autor:
Tomasz Skorski, Janusz Blasiak, Michal O. Nowicki, Ewelina Stoczynska, Dariusz Pytel, Kimberly Cramer, Stanislaw K. Jozwiakowski, Tomasz Poplawski, Artur Slupianek
Supplementary Methods from BCR/ABL Stimulates WRN to Promote Survival and Genomic Instability
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::142bf8dafd6554cbe4cb49a2ab6e669d
https://doi.org/10.1158/0008-5472.22388426.v1
https://doi.org/10.1158/0008-5472.22388426.v1
Autor:
Diana C, Odermatt, Wei Ting C, Lee, Sebastian, Wild, Stanislaw K, Jozwiakowski, Eli, Rothenberg, Kerstin, Gari
Publikováno v:
PLoS Genetics
FANCJ/BRIP1 is an iron-sulfur (FeS) cluster-binding DNA helicase involved in DNA inter-strand cross-link (ICL) repair and G-quadruplex (G4) metabolism. Mutations in FANCJ are associated with Fanconi anemia and an increased risk for developing breast
Publikováno v:
Life Science Alliance
The iron–sulfur cluster in human DNA polymerase delta has an impact on DNA polymerase and exonuclease activities and can hence influence the fidelity of DNA synthesis.
Replication of eukaryotic genomes relies on the family B DNA polymerases Po
Replication of eukaryotic genomes relies on the family B DNA polymerases Po
Autor:
Davide, Schiavone, Stanislaw K, Jozwiakowski, Marina, Romanello, Guillaume, Guilbaud, Thomas A, Guilliam, Laura J, Bailey, Julian E, Sale, Aidan J, Doherty
Publikováno v:
Molecular Cell
Summary G quadruplexes (G4s) can present potent blocks to DNA replication. Accurate and timely replication of G4s in vertebrates requires multiple specialized DNA helicases and polymerases to prevent genetic and epigenetic instability. Here we report
Publikováno v:
Nucleic Acids Research
PrimPol is a primase-polymerase found in humans, and other eukaryotes, involved in bypassing lesions encountered during DNA replication. PrimPol employs both translesion synthesis and repriming mechanisms to facilitate lesion bypass by the replisome.
Publikováno v:
Molecular Cell
Molecular Cell, Elsevier, 2013, 52 (4), pp.554-565. ⟨10.1016/j.molcel.2013.10.034⟩
Molecular Cell, Elsevier, 2013, 52 (4), pp.554-565. ⟨10.1016/j.molcel.2013.10.034⟩
Summary Faithful copying of the genome is essential for life. In eukaryotes, a single archaeo-eukaryotic primase (AEP), DNA primase, is required for the initiation and progression of DNA replication. Here we have identified additional eukaryotic AEP-
Autor:
Howard D. Lindsay, Andrew J. Green, Irena Stevanovic, Aidan J. Doherty, Sean G. Rudd, Elaine M. Taylor, Julie Bianchi, Laura J. Bailey, Stanislaw K. Jozwiakowski, Violetta Soura, Travis H. Stracker
Publikováno v:
Molecular Cell
Summary DNA damage can stall the DNA replication machinery, leading to genomic instability. Thus, numerous mechanisms exist to complete genome duplication in the absence of a pristine DNA template, but identification of the enzymes involved remains i
Autor:
Dariusz Pytel, Tomasz Poplawski, Michał Nowicki, Tomasz Skorski, Kimberly Cramer, Artur Slupianek, Ewelina Stoczyńska, Stanislaw K. Jozwiakowski, Janusz Blasiak
Publikováno v:
Cancer Research. 71:842-851
BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homol