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Eva Petermann

Showing results (21-30 of 45) with videos related to

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Molecular Cancer Research : MCR|February 1, 2013
Diminished origin-licensing capacity specifically sensitizes tumor cells to replication stressKristin M Zimmerman, Rebecca M Jones, Eva Petermann, et al.
Molecular Cell|March 2, 2010
Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repairEva Petermann, Manuel Luís Orta, Natalia Issaeva, et al.
Molecular Cancer Therapeutics|July 24, 2014
BRCA2 and RAD51 promote double-strand break formation and cell death in response to gemcitabineRebecca M Jones, Panagiotis Kotsantis, Grant S Stewart, et al.
Molecular Cancer Therapeutics|November 16, 2011
Targeted mutations in the ATR pathway define agent-specific requirements for cancer cell growth and survivalDeborah Wilsker, Jon H Chung, Ivan Pradilla, et al.
Oncotarget|November 1, 2014
Human PIF1 helicase supports DNA replication and cell growth under oncogenic-stressMary E Gagou, Anil Ganesh, Geraldine Phear, et al.
The EMBO Journal|May 12, 2007
Chk1 regulates the density of active replication origins during the vertebrate S phaseApolinar Maya-Mendoza, Eva Petermann, David A F Gillespie, et al.
Journal of Molecular Biology|July 21, 2010
Methylated DNA causes a physical block to replication forks independently of damage signalling, O(6)-methylguanine or DNA single-strand breaks and results in DNA damagePetra Groth, Simon Ausländer, Muntasir Mamun Majumder, et al.
Nature Communications|October 12, 2016
Increased global transcription activity as a mechanism of replication stress in cancerPanagiotis Kotsantis, Lara Marques Silva, Sarah Irmscher, et al.
Methods in Enzymology|June 24, 2006
Measurement of chromosomal DNA single-strand breaks and replication fork progression ratesClaire Breslin, Paula M Clements, Sherif F El-Khamisy, et al.
Molecular and Cellular Biology|April 4, 2006
Chk1 requirement for high global rates of replication fork progression during normal vertebrate S phaseEva Petermann, Apolinar Maya-Mendoza, George Zachos, et al.
Pageof 5

Showing results (21-30 of 45) with videos related to

Sort By:
Pageof 5
Molecular Cancer Research : MCR|February 1, 2013
Diminished origin-licensing capacity specifically sensitizes tumor cells to replication stressKristin M Zimmerman, Rebecca M Jones, Eva Petermann, et al.
Molecular Cell|March 2, 2010
Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repairEva Petermann, Manuel Luís Orta, Natalia Issaeva, et al.
Molecular Cancer Therapeutics|July 24, 2014
BRCA2 and RAD51 promote double-strand break formation and cell death in response to gemcitabineRebecca M Jones, Panagiotis Kotsantis, Grant S Stewart, et al.
Molecular Cancer Therapeutics|November 16, 2011
Targeted mutations in the ATR pathway define agent-specific requirements for cancer cell growth and survivalDeborah Wilsker, Jon H Chung, Ivan Pradilla, et al.
Oncotarget|November 1, 2014
Human PIF1 helicase supports DNA replication and cell growth under oncogenic-stressMary E Gagou, Anil Ganesh, Geraldine Phear, et al.
The EMBO Journal|May 12, 2007
Chk1 regulates the density of active replication origins during the vertebrate S phaseApolinar Maya-Mendoza, Eva Petermann, David A F Gillespie, et al.
Journal of Molecular Biology|July 21, 2010
Methylated DNA causes a physical block to replication forks independently of damage signalling, O(6)-methylguanine or DNA single-strand breaks and results in DNA damagePetra Groth, Simon Ausländer, Muntasir Mamun Majumder, et al.
Nature Communications|October 12, 2016
Increased global transcription activity as a mechanism of replication stress in cancerPanagiotis Kotsantis, Lara Marques Silva, Sarah Irmscher, et al.
Methods in Enzymology|June 24, 2006
Measurement of chromosomal DNA single-strand breaks and replication fork progression ratesClaire Breslin, Paula M Clements, Sherif F El-Khamisy, et al.
Molecular and Cellular Biology|April 4, 2006
Chk1 requirement for high global rates of replication fork progression during normal vertebrate S phaseEva Petermann, Apolinar Maya-Mendoza, George Zachos, et al.
Pageof 5