Growth inhibition and DNA damage induced by Cre recombinase in mammalian cells

By Ate Loonstra, M. Vooijs, H. Beverloo, B. Allak, E. van Drunen, Roland Kanaar, A. Berns, J. Jonkers. Proceedings of the National Academy of Sciences of the United States of America, 2001

631 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/71a4aaaad72ae4fd483f438ad8ccc9c6b9bed262

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Manuel Serrano
2. Holger Puchta
3. Jeffrey M. Rosen
4. M. Barbacid
5. Marcos Malumbres

Citations in the corpus

• Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. (2003, background): “These findings suggest that proliferative senescence and senescence induced by primary K-ras / ;CMV-Cre /T and K-ras /V12;CMV-Cre /T MEFs display chromosomal abnormalities despite the presence ofoncogenic stress involve different mechanisms. the CMV-Cre transgene (Loonstra et al., 2001).”
• Modelling breast cancer: one size does not fit all (2007, background): “, inducible Cre recombinase ( Wap -reverse tetracycline transactivator (rtTA))-Cre, Cre-oestrogen receptor tamoxifen-inducible (Cre-ER T ), progesterone receptor (PR)-Cre, PR-bacterial artificial chromosome inducible Cre (PR-BAC iCre )”
• Marker-free transgenic plants (2003, background): “mammalian cells due to Cre expression have been described (Schmidt et al., 2000; Loonstra et al., 2001).”
• Unmodified Cre recombinase crosses the membrane. (2002, methodology): “This method has potential disadvantages: besides the risk of mutagenesis by random integration of the vector DNA into the host genome, the constitutive expression of Cre has been shown to be cytotoxic in many cell types (4,5).”