Cfp- knock-out mice have exons 3-5 of the X-linked complement factor properdin (Cfp) gene removed. Properdin encodes a plasma glycoprotein that is involved in the regulation of the alternative pathway of the complement system of innate immunity. The complement pathway plays an essential role in the migration of cells during development and in innate and adaptive immune responses that help the body clear foreign material by recognizing pathogens and neutralizing them. In cells and in circulation, properdin stabilizes the activation of C3 and leads to formation of the membrane attack complex and lysis of the target cell, both of which contribute to tissue injury and pathogen recognition and elimination. The complement system plays an important role in the pathogenesis of ischemia-reperfusion injury (IRI). IRI occurs when reperfusion into ischemic tissue is crucial to prevent further tissue damage, yet the restoration of blood flow can intensify the initial injury. LPS-induced alternative pathway (AP) complement activation is impaired in these Cfp- mice. Homozygous females and hemizygous males are viable and fertile.

Use of MICE only available to non-profit entities.

Cfp- knock-out mice have exons 3-5 of the X-linked Cfp gene deleted. These mice are useful for studying diseases mediated by the alternative pathway of the complement system, such as asthma, autoimmune arthritis, extravascular hemolysis, abdominal aortic aneurysm formation, and kidney diseases like renal ischemia-reperfusion injury, glomerulonephritis and atypical hemolytic uremic syndrome.

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.