16 activity than the previous cell-specific mouse models that we have used for detailed mechanistic studies of the effect of WNT16 on cortical bone. In these previous studies, we used Runx2-Cre and Dmp1-Cre mouse models to demonstrate that
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Claes Ohlsson, Petra Henning, Karin H Nilsson, Jianyao Wu, Karin L Gustafsson, Klara Sjögren, Anna Törnqvist, Antti Koskela, Fu-Ping Zhang, Marie K Lagerquist, Matti Poutanen, Juha Tuukkanen, Ulf H Lerner, and Sofia Movérare-Skrtic
Bernard Freudenthal, John Logan, Sanger Institute Mouse Pipelines, Peter I Croucher, Graham R Williams, and J H Duncan Bassett
two functions by creating either a reporter-tagged knockout or a conditional mutation if the gene-trap cassette is removed by FLP recombinase, thereby reverting the knockout mutation to wild type, although with addition of loxP sites that flank a
K L Gustafsson, K H Nilsson, H H Farman, A Andersson, V Lionikaite, P Henning, J Wu, S H Windahl, U Islander, S Movérare-Skrtic, K Sjögren, H Carlsten, J-Å Gustafsson, C Ohlsson, and M K Lagerquist
.2015 ) 27807202 10.1152/physrev.00033.2015 Antonson P Omoto Y Humire P Gustafsson JA 2012 Generation of ERalpha-floxed and knockout mice using the Cre/LoxP system . Biochemical and Biophysical Research Communications 424 710 – 716 . ( https
Rachel V Richardson, Emma J Batchen, Adrian J W Thomson, Rowan Darroch, Xinlu Pan, Eva A Rog-Zielinska, Wiktoria Wyrzykowska, Kathleen Scullion, Emad A S Al-Dujaili, Mary E Diaz, Carmel M Moran, Christopher J Kenyon, Gillian A Gray, and Karen E Chapman
reduced (rather than increased) in another GR-knockout model (Meijer et al . 1997). Elevated MR expression has been suggested to drive cardiac fibrosis ( Lother et al . 2011 ), and MR antagonism is protective in murine models of pressure
Zhenguang Zhang, Agnes E Coutinho, Tak Yung Man, Tiina M J Kipari, Patrick W F Hadoke, Donald M Salter, Jonathan R Seckl, and Karen E Chapman
flanked by LoxP sites ( Hsd11b1 f/f mice) (recombination strategy shown in Supplementary Fig. 1). LysM-Cre transgenic mice are reported to efficiently delete LoxP -flanked target genes in granulocytes and mature macrophages, with lower efficiencies
Jethro S Johnson, Monica N Opiyo, Marian Thomson, Karim Gharbi, Jonathan R Seckl, Andreas Heger, and Karen E Chapman
bowel diseases . Molecular and Cellular Endocrinology 301 104 – 108 . ( doi:10.1016/j.mce.2008.10.030 ) Tang SH Silva FJ Tsark WM Mann JR 2002 A Cre/loxP-deleter transgenic line in mouse strain 129S1/SvImJ . Genesis 32 199
Katie J Mylonas, Neil A Turner, Sumia A Bageghni, Christopher J Kenyon, Christopher I White, Kieran McGregor, Robert A Kimmitt, Richard Sulston, Valerie Kelly, Brian R Walker, Karen E Porter, Karen E Chapman, and Gillian A Gray
crossing Sm22α-Cre mice with Hsd11b1 fl/fl mice, homozygous for a ‘floxed’ allele of Hsd11b1 (generated by Artemis Pharmaceuticals, Cologne, Germany), directly onto a C57BL/6J background. LoxP sites flanked exon 3 of the mouse Hsd11b1 gene. Excision
