Ripk3m1Btlr ENU-induced mutant mice have a mutation within the donor splice site of intron 2 of the Ripk3 gene. This strain may be useful when studying inflammation, oxidative stress and apoptosis.
Bruce Beutler, University of Texas Southwestern Medical
This strain was generated by Dr. Bruce Beutler at The University of Texas Southwestern Medical Center. Ripk3m1Btlr ENU-induced knock-out mice have a mutation within the donor splice site of intron 2 (1 bp from exon 2) of the receptor-interacting serine-threonine kinase 3 (Ripk3) gene. RIPK3 is a cytoplasmic member of the receptor-interacting protein (RIP) family of serine/threonine protein kinases and is a trigger for pro-inflammatory apoptotic cell death. In these mice, RIP3 deletion protects against brain
injury through inhibiting inflammation, oxidative stress and apoptosis, potentially making RIP3 a therapeutic target against traumatic brain injury. Homozygotes are viable and fertile.
For additional information on this mutation, please see the Mutagenetix website.
Following multidose N-ethyl-N-nitrosourea (ENU) treatments to induce mutations in founder male C57BL/6J mice, whole exome sequencing of the G1 grandsire identified a C to T transition at base pair 55788237 (v38) on chromosome 14, within the donor splice site of intron 2 of Ripk3. The Ripk3m1Btlr mice were maintained on a C57BL/6J background. Upon arrival at The Jackson Laboratory, mice were bred to C57BL/6J (Stock No. 000664) for at least one generation.
|Allele Name||mutation 1, Bruce Beutler|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Ripk3, receptor-interacting serine-threonine kinase 3|
|Strain of Origin||C57BL/6J|
|Molecular Note||ENU-mutagenesis induced a C to T transition at base pair 55788237 (v38) on chromosome 14, within the donor splice site of intron 2|
When maintaining a live colony, homozygous mice may be bred together.
When using the C57BL/6J-Ripk3m1Btlr/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #025738 in your Materials and Methods section.