These Rab3a knock-out mice exhibit synaptic depression after repetitive stimulation. They are suitable for use in applications related to the study of neuron synapsis.
Dr. Thomas C. Sudhof, Stanford University School of Medicine
Mice homozygous for the Rab3atm1Sud targeted mutation are viable, fertile, and comparable in weight and health to normal wild type siblings. Most of their synaptic parameters are normal, although synaptic depression after repetitive stimulation is significantly increased, suggesting a role for Rab3a in synaptic vesicle docking. Mutant mice do not express Rab3a and levels of rabphilin (a protein that associates with the GTP-bound form of Rab3) are decreased by 70%. Expression of over 20 other synaptic proteins is unchanged.
|Allele Name||targeted mutation 1, Thomas C Sudhof|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Rab3a, RAB3A, member RAS oncogene family|
|Strain of Origin||129|
|Molecular Note||A neomycin cassette replaced the promoter and the first two exons of the gene. Western blots of brain extracts did not detect any encoded protein in homozygous mice.|
|Mutations Made By|| |
Dr. Thomas Sudhof, Stanford University School of Medicine
The strain can be maintained by mating homozygous siblings.
When using the Rab3a- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002443 in your Materials and Methods section.