The Akap12 gene, also known as SSeCKS, encodes for a scaffold protein that is involved in signal transduction, cell growth and blood–brain barrier regulation. In human prostate cancer, AKAP12 is downregulated. In these knock-out mice, exon 2 of the Akap12 gene has been replaced by a lacZ-NEO cassette. No gene product (protein) is detected by Western blot analysis of testes, bladder, lung, brain, heart, ovary, or prostate tissue from homozygous animals. 3-4% of mice homozygous for the knock-out allele on the B6;129 background die spontaneously as early as 4 months of age, and 10-25% of surviving homozygotes on the B6;129 background are infertile or exhibit delayed fertility (requiring breeding pairs to be housed for up to 3 weeks). Homozygous males on the B6;129 background at 2 months of age exhibit increased prostate gland weight. Homozygotes develop hyperplasia in the anterior and ventral prostate lobes. At one year of age, less than 30% of homozygous males develop prostatic focal dysplasia. Apoptosis in prostate tissue is increased. Histological analysis reveals
liver granulomas, larger cell size and vascularization of the lung, and increased germinal center red pulp layer.
Alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
