The programmed cell death 4 protein is a proinflammatory agent and tumor suppressor that also inhibits translation initiation and cap-dependent translation. MicroRNA-21 (miR-21) downregulates Pdcd4 expression post-translationally.
Mice homozygous for this knockout mutation of Pdcd4 are viable and fertile, however 86% of homozygotes die due to lymphoma by 106 weeks of age (mean life expectancy of homozygotes is reduced to 101 weeks). At approximately 20 months of age, many homozygotes develop spontaneous lymphoma (primarily diffuse B cell), often with metastasis to liver and kidney. Approximately half of homozygotes at 20 weeks of age exhibit kidney, ovary, or prostate cysts. No Pdcd4 mRNA or protein is detected by Northern or Western blot analysis of thymus. Homozygotes are resistant to STZ (streptozotocin) induced diabetes (5% compared to 59% in controls), and exhibit reduced severity and mortality of EAE (experimental autoimmune encephalomyelitis). IL-4, IL-10, and
IFNG cytokine secretion is elevated in homozygous animals. Homozygotes display reduced susceptibility to and lower circulating IL-6 levels after lipopolysaccharide (LPS) challenge, and lower resulting mortality compared to wildtype controls. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background.

This knockout mutant of the Pdcd4 (programmed cell death 4) gene exhibits reduced cytokine secretion, lower susceptibility to LPS challenge and EAE, resistance to STZ- induced diabetes, and develops spontaneous lymphoma.

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