Mice homozygous for the Lyntm1Sor targeted mutation are viable and fertile. However, age-related autoimmunity has been observed in homozygotes which may make it preferable to maintain the strain heterozygously, at least on a 129 background. Lyn-deficient mice are useful in analyzing the role of Lyn in B cell antigen receptor (BCR) signaling. Mutant mice have a reduced number of peripheral B cells with a greater proportion of immature cells and a higher than normal turnover rate. Aged homozygotes develop splenomegaly, produce autoantibodies, and have an expanded population of B lymphoblasts of the B1 lineage. Splenic B cells from young homozygotes initiate early BCR signaling events, although in a delayed fashion. B cells exhibit an enhanced MAP kinase activation and an increased proliferative response to BCR engagement.

These Lyn knock-out mice exhibit a reduced number of peripheral B cells; splenic B cells have enhanced mitogen-activated protein (MAP) kinase activation and an increased proliferative response to B cell antigen receptor (BCR) engagement.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

<a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> for more information.