Whole exome sequencing reveals a functional mutation in the GAIN domain of the Bai2 receptor underlying a forward mutagenesis hyperactivity QTL
Author:
Funder
U.S. Department of Defense
University of California, Davis
NIH Office of the Director
Publisher
Springer Science and Business Media LLC
Subject
Genetics
Link
http://link.springer.com/article/10.1007/s00335-017-9716-5/fulltext.html
Reference32 articles.
1. Andrews TD et al (2012) Massively parallel sequencing of the mouse exome to accurately identify rare, induced mutations: an immediate source for thousands of new mouse models. Open Biol 2:120061. doi: 10.1098/rsob.120061
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3. Bolliger MF, Martinelli DC, Sudhof TC (2011) The cell-adhesion G protein-coupled receptor BAI3 is a high-affinity receptor for C1q-like proteins. Proc Natl Acad Sci USA 108:2534–2539. doi: 10.1073/pnas.1019577108
4. DuBridge RB, Tang P, Hsia HC, Leong PM, Miller JH, Calos MP (1987) Analysis of mutation in human cells by using an Epstein-Barr virus shuttle system. Mol Cell Biol 7:379–387
5. Duman JG, Tzeng CP, Tu YK, Munjal T, Schwechter B, Ho TS, Tolias KF (2013) The adhesion-GPCR BAI1 regulates synaptogenesis by controlling the recruitment of the Par3/Tiam1 polarity complex to synaptic sites. J Neurosci 33:6964–6978. doi: 10.1523/JNEUROSCI.3978-12.2013
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