TY - JOUR
T1 - Generation of a cre recombinase-conditional Nos1ap over-expression transgenic mouse
AU - Auer, Dallas R.
AU - Sysa-Shah, Polina
AU - Bedja, Djahida
AU - Simmers, Jessica L.
AU - Pak, Evgenia
AU - Dutra, Amalia
AU - Cohn, Ronald
AU - Gabrielson, Kathleen L.
AU - Chakravarti, Aravinda
AU - Kapoor, Ashish
N1 - Funding Information:
Acknowledgments We are grateful to Dr. Andras Nagy (Mount Sinai Hospital, Toronto) for providing the pCLIP vector and to Dr. Kenneth Chien (Massachusetts General Hospital, Boston) for providing the Mlc2v-cre mice. We are transgenic founder 333 (Tg?;cre? n = 7, Tg?;cre- n = 5, Tg-;cre- n = 7). Expression of Nos1ap transcript was higher in Tg?;cre? mice as compared to Tg-;cre- mice, t(12) = 5.98, p \ 0.001 and expression of Nos1ap transcript was not significantly different between Tg?;cre- and Tg-;cre- mice, t(10) = 0.07, p = 0.94; c Same as a, mice derived from transgenic founder 314 (Tg?;cre?n = 8, Tg-;cre- n = 7). No significant difference in expression level was observed between the two groups of mice derived from transgenic founder 314, t(13) = 0.22, p = 0.83 thankful to Dr. Gordon Tomaselli, Dr. David Kass and Gary Steel (Johns Hopkins University, Baltimore) for critical discussions. This work was supported in part by funds from the Donald R. Reynolds Foundation and the National Institutes of Health.
PY - 2014/6
Y1 - 2014/6
N2 - Polymorphic non-coding variants at the NOS1AP locus have been associated with the common cardiac, metabolic and neurological traits and diseases. Although, in vitro gene targeting-based cellular and biochemical studies have shed some light on NOS1AP function in cardiac and neuronal tissue, to enhance our understanding of NOS1AP function in mammalian physiology and disease, we report the generation of cre recombinase-conditional Nos1ap over-expression transgenic mice (Nos1ap Tg). Conditional transgenic mice were generated by the pronuclear injection method and three independent, single-site, multiple copies integration event-based founder lines were selected. For heart-restricted over-expression, Nos1ap Tg mice were crossed with Mlc2v-cre and Nos1ap transcript over-expression was observed in left ventricles from Nos1ap Tg; Mlc2v-cre F1 mice. We believe that with the potential of conditional over-expression, Nos1ap Tg mice will be a useful resource in studying NOS1AP function in various tissues under physiological and disease states.
AB - Polymorphic non-coding variants at the NOS1AP locus have been associated with the common cardiac, metabolic and neurological traits and diseases. Although, in vitro gene targeting-based cellular and biochemical studies have shed some light on NOS1AP function in cardiac and neuronal tissue, to enhance our understanding of NOS1AP function in mammalian physiology and disease, we report the generation of cre recombinase-conditional Nos1ap over-expression transgenic mice (Nos1ap Tg). Conditional transgenic mice were generated by the pronuclear injection method and three independent, single-site, multiple copies integration event-based founder lines were selected. For heart-restricted over-expression, Nos1ap Tg mice were crossed with Mlc2v-cre and Nos1ap transcript over-expression was observed in left ventricles from Nos1ap Tg; Mlc2v-cre F1 mice. We believe that with the potential of conditional over-expression, Nos1ap Tg mice will be a useful resource in studying NOS1AP function in various tissues under physiological and disease states.
KW - Cardiac arrhythmia
KW - Conditional over-expression
KW - GENOME-wide association studies
KW - NOS1AP
KW - QT interval
KW - Sudden cardiac death
KW - Transgenic mouse
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U2 - 10.1007/s10529-014-1473-x
DO - 10.1007/s10529-014-1473-x
M3 - Article
C2 - 24563304
AN - SCOPUS:84899911713
SN - 0141-5492
VL - 36
SP - 1179
EP - 1185
JO - Biotechnology Letters
JF - Biotechnology Letters
IS - 6
ER -