|Former Common name||No Data|
|H-2 Haplotype||No Data|
|Genotype||a/a B/B C/C|
|Strain development||Developed by Dr. Nobuhiko Kojima, National Institute for Physiological Sciences, Japan at 1994. The FynB fragment mutated from TAT to TTT at codon 531 by site-directed mutagenesis under the control of the CaMKII alpha promoter was injected into the pronuclei of B6CBF1 fertilized egges. The transgenic mice were backcross to C57BL/6J mice for 26 generations.
|Strain description||B6.Cg-Tg(Camk2a-Fyn-531)1Nko/Rbrc. Transgenic mice overexpressing activated form of Fyn under the control of the calcium/calmodulin-dependent protein kinase II alpha promoter. The transgenic mutant Fyn is expressed at high levels in neurons of the forebrain. The transgenic mice exhibit seizure activity by stimulus of drug and light, accelerated kindling, and spontaneous death after weaning. The survival rate of these mice correlates inversely with the expression level of mutant Fyn. This strain is useful for elucidation of the role of Fyn tyrosine kinase in synaptic plasticity.|
|Colony maintenance||Backcross to C57BL/6 (Hemizygote x C57BL/6JJcl)
Reproductive performance is good.
BRC facility Health Report in the last year and a half
|Promoter||mouse Camk2a promoter|
|Symbol name||Fyn proto-oncogene|
|Common name||No Data|
|Symbol description||No Data|
|References||Learn Mem. 1998 Nov-Dec;5(6):429-45.
Higher seizure susceptibility and enhanced tyrosine phosphorylation of N-methyl-D-aspartate receptor subunit 2B in fyn transgenic mice.
|Research applications||Neurobiology Research|
|Specific Term and Conditions||The following terms and conditions will be requested by the DEPOSITOR.
In publishing the research results obtained by use of the BIOLOGICAL RESOURCE, a citation of the following literature(s) designated by the DEPOSITOR is requested.
Learning and Memory, 5, 429-445 (1998).
|2||Genotyping protocol <PCR>|
|Depositor||Kojima, Nobuhiko (RIKEN Center for Brain Science)|
|Strain Status /