Protein kinase C, delta binding protein, or Cavin-3, forms a complex with cavin-1 (polymerase I and transcript release factor) and caveolin to anchor caveolae to the plasma membrane at the actin cytoskeleton via myosin 1c protein.  Cavin-3 is involved in ERK and AKT signaling and circadian clock regulation.  These mice carry a targeted mutation in which exon 1 and most of exon 2 is replaced by a floxed NEO cassette.  Homozygous mice are viable and fertile, although with a shortened lifespan.  At 12 months of age homozygotes have an approximately 80% survival rate, dropping to an approximately 40% survival rate at 24 months of age.  No gene product (protein) is detected by Western blot analysis of tissue (lung) or of MEFs isolated from homozygous animals. Homozygotes exhibit cachexia (40% reduction in body weight and severe lipodystrophy), hepatic steatosis, and increased glycolytic metabolism. MEFs from homozygous animals proliferate faster than MEFs from wildtype controls, exhibit Warburg metabolism, are more resistant to TNF-alpha and the MAPK/ERK Kinase (MEK) inhibitor, PD98059, and are more sensitive to the PI3K inhibitor, LY294002. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background.

Cavin-3 knock-out mice exhibit cachexia and increased glycolytic metabolism. They are suitable for use in applications related to the study of ERK and Akt signaling.

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.