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1.  The mammalian gene function resource: the international knockout mouse consortium 
Bradley, Allan | Anastassiadis, Konstantinos | Ayadi, Abdelkader | Battey, James F. | Bell, Cindy | Birling, Marie-Christine | Bottomley, Joanna | Brown, Steve D. | Bürger, Antje | Bult, Carol J. | Bushell, Wendy | Collins, Francis S. | Desaintes, Christian | Doe, Brendan | Economides, Aris | Eppig, Janan T. | Finnell, Richard H. | Fletcher, Colin | Fray, Martin | Frendewey, David | Friedel, Roland H. | Grosveld, Frank G. | Hansen, Jens | Hérault, Yann | Hicks, Geoffrey | Hörlein, Andreas | Houghton, Richard | Hrabé de Angelis, Martin | Huylebroeck, Danny | Iyer, Vivek | de Jong, Pieter J. | Kadin, James A. | Kaloff, Cornelia | Kennedy, Karen | Koutsourakis, Manousos | Kent Lloyd, K. C. | Marschall, Susan | Mason, Jeremy | McKerlie, Colin | McLeod, Michael P. | von Melchner, Harald | Moore, Mark | Mujica, Alejandro O. | Nagy, Andras | Nefedov, Mikhail | Nutter, Lauryl M. | Pavlovic, Guillaume | Peterson, Jane L. | Pollock, Jonathan | Ramirez-Solis, Ramiro | Rancourt, Derrick E. | Raspa, Marcello | Remacle, Jacques E. | Ringwald, Martin | Rosen, Barry | Rosenthal, Nadia | Rossant, Janet | Ruiz Noppinger, Patricia | Ryder, Ed | Schick, Joel Zupicich | Schnütgen, Frank | Schofield, Paul | Seisenberger, Claudia | Selloum, Mohammed | Simpson, Elizabeth M. | Skarnes, William C. | Smedley, Damian | Stanford, William L. | Francis Stewart, A. | Stone, Kevin | Swan, Kate | Tadepally, Hamsa | Teboul, Lydia | Tocchini-Valentini, Glauco P. | Valenzuela, David | West, Anthony P. | Yamamura, Ken-ichi | Yoshinaga, Yuko | Wurst, Wolfgang
Mammalian Genome  2012;23(9-10):580-586.
In 2007, the International Knockout Mouse Consortium (IKMC) made the ambitious promise to generate mutations in virtually every protein-coding gene of the mouse genome in a concerted worldwide action. Now, 5 years later, the IKMC members have developed high-throughput gene trapping and, in particular, gene-targeting pipelines and generated more than 17,400 mutant murine embryonic stem (ES) cell clones and more than 1,700 mutant mouse strains, most of them conditional. A common IKMC web portal (www.knockoutmouse.org) has been established, allowing easy access to this unparalleled biological resource. The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research.
doi:10.1007/s00335-012-9422-2
PMCID: PMC3463800  PMID: 22968824
2.  Murine Prkdc Polymorphisms Impact DNA-PKcs Function 
Radiation research  2011;175(4):493-500.
Polymorphic variants of DNA repair genes can increase the carcinogenic potential of exposure to ionizing radiation. Two single nucleotide polymorphisms (SNPs) in Prkdc, the gene encoding the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), have been identified in BALB/c mice and linked to reduced DNA-PKcs activity and mammary cancer susceptibility. We examined three additional mouse strains to better define the roles of the BALB/c Prkdc SNPs (R2140C and M3844V). One is a congenic strain (C.B6) that has the C57BL/6 Prkdc allele on a BALB/c background, and the other is a congenic strain (B6.C) that has the BALB/c variant Prkdc allele on a C57BL/6 background. We also examined the LEWES mouse strain, which possesses only one of the BALB/c Prkdc SNPs (M3844V). Our results demonstrate that both Prkdc SNPs are responsible for deficient DNA-PKcs protein expression, DNA repair and telomere function, while the LEWES SNP affects only DNA-PKcs expression and repair capacity. These studies provide insight into the separation of function between the two BALB/c SNPs as well as direct evidence that SNPs positioned within Prkdc can significantly influence DNA-PKcs function involving DNA repair capacity, telomere end-capping, and potentially cancer susceptibility.
doi:10.1667/RR2431.1
PMCID: PMC3102216  PMID: 21265624
3.  3rd US-EU Workshop Systems level understanding of DNA damage responses 
Mutation research  2010;692(1-2):53-60.
The 3rd US-EU Workshop on Systems level understanding of DNA damage responses was held from March 30 - April 1, 2009 in Egmond aan Zee, The Netherlands. Objectives of the workshop were (1) to assess the current science of the DDR, in particular network level responses to chemotherapeutic and environmentally induced DNA damage; and (2) to establish the basis for a reciprocal scientific exchange program between the EU and US in the relevant areas of DDR research. Here we report the highlights of the meeting program and conclude that this third meeting in 2009 refined the role of DDR networks in human disease.
doi:10.1016/j.mrfmmm.2010.07.012
PMCID: PMC2948618  PMID: 20727903
4.  A New E6/P63 Pathway, Together with a Strong E7/E2F Mitotic Pathway, Modulates the Transcriptome in Cervical Cancer Cells▿  
Journal of Virology  2007;81(17):9368-9376.
Cervical carcinoma is associated with certain types of human papillomaviruses expressing the E6 and E7 oncogenes, which are involved in carcinogenesis through their interactions with the p53 and pRB pathways, respectively. A critical event on the path to malignant transformation is often manifested by the loss of expression of the viral E2 transcription factor due to the integration into the host genome of the viral DNA. Using microarrays, we have previously shown that reintroduction of a functional E2 in the HeLa cervical carcinoma cell line activates a cluster of p53 target genes while at the same time severely repressing a group of E2F target genes. In the present study, using new high-density microarrays containing more than 22,000 human cDNA sequences, we identified a novel p63 pathway among E2-activated genes and 38 new mitotic genes repressed by E2. We then sought to determine the pathways through which these genes were modulated and used an approach that relies on small interfering RNA to demonstrate that the p63 target genes were activated through silencing of the E6/E6AP pathway while the mitotic genes were mainly repressed through E7 silencing. Importantly, a subset of the mitotic genes was shown to be significantly induced in biopsies of stage IV cervical cancers, which points to a prominent E7 pathway in cervical carcinoma.
doi:10.1128/JVI.00427-07
PMCID: PMC1951466  PMID: 17582001

Results 1-4 (4)