The ATM protein is a DNA double-strand break sensor protein, delaying cell cycle by activating CHK2 checkpoint homolog or arresting cell cycle/initiate apoptosis by phosphorylating p53.  These mice carry a targeted mutation of the <i>Atm</i> gene in which the exon encoding the ATM kinase domain and the adjacent 3' exon is disrupted by a PGK-NEO cassette.  Mice that are homozygous for the allele are viable, but exhibit retarded growth, and are infertile due to meiotic failure.  Homozygotes develop thymic lymphomas that eventually block the thoracic cavity and die before 4 months of age.  Mutant mice have fewer pre-B cells and thymocytes, and lower IgG levels.  Although ataxia is not observed, homozygotes develop neurodegeneration in the neocortex (large vacuoles in the cerebellar Purkinje cell layer).  Heterozygotes are viable and fertile.

In this strain a PGK-NEO cassette replaces the exon encoding the ATM kinase domain and the adjacent 3' exon of the <i>Atm</i> gene. Mice homozygous for this targeted mutation succumb to thymic lymphomas by 4 months of age, exhibit neurodegeneration and have applications in studies related to Ataxia-Telangiectasia.

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

Typically mice are recovered in 12-16 weeks. <a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> to place an order or for more information.