Regional loss of imprinting and growth deficiency in mice with a targeted deletion of KvDMR1
Author:
Publisher
Springer Science and Business Media LLC
Subject
Genetics
Link
http://www.nature.com/articles/ng988z.pdf
Reference29 articles.
1. Lee, M.P. et al. Loss of imprinting of a paternally expressed transcript, with antisense orientation to KVLQT1, occurs frequently in Beckwith–Wiedemann syndrome and is independent of insulin-like growth factor II imprinting. Proc. Natl Acad. Sci. USA 96, 5203–5208 (1999).
2. Smilinich, N.J. et al. A maternally methylated CpG island in KvLQT1 is associated with an antisense paternal transcript and loss of imprinting in Beckwith–Wiedemann syndrome. Proc. Natl Acad. Sci. USA 96, 8064–8069 (1999).
3. Engel, J.R. et al. Epigenotype-phenotype correlations in Beckwith–Wiedemann syndrome. J. Med. Genet. 37, 921–926 (2000).
4. Maher, E.R. & Reik, W. Beckwith–Wiedemann syndrome: imprinting in clusters revisited. J. Clin. Invest. 105, 247–252 (2000).
5. Leighton, P.A., Ingram, R.S., Eggenschwiler, J., Efstratiadis, A. & Tilghman, S.M. Disruption of imprinting caused by deletion of the H19 gene region in mice. Nature 375, 34–39 (1995).
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