Development of spontaneous uterine tumors in low molecular mass polypeptide-2 knockout mice.

Abstract

The presentation of antigenic peptides by MHC class I molecules is important for tumor rejection by CTLs. Such antigenic peptides are generated as a result of the degradation of intracellular proteins by the proteasome pathway, a process that is influenced by the IFN-gamma-inducible low molecular mass polypeptide-2 (LMP2) subunit of the proteasome complex. LMP2 knockout mice thus exhibit a defect in proteasome function. Female LMP2(-/-) mice are now shown to develop uterine neoplasms, with a disease prevalence of approximately 36% by 12 months of age. This observation indicates that proteasome function is essential for MHC class I-mediated tumor rejection by CTLs.

• Authors: Takuma Hayashi, Denise L Faustman
• Journal: Cancer research (Cancer Res) Vol. 62 Issue 1 Pg. 24-7 (Jan 01 2002) ISSN: 0008-5472 [Print] United States
• PMID: 11782352 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Histocompatibility Antigens Class I
• Proteins
• LMP-2 protein
• Interferon-gamma
• Cysteine Endopeptidases

Topics

• Animals
• Cysteine Endopeptidases
• Female
• Histocompatibility Antigens Class I (immunology)
• Immunologic Surveillance (genetics, immunology)
• Interferon-gamma (pharmacology)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Mice, Nude
• Protein Biosynthesis
• Proteins (genetics, immunology)
• Uterine Neoplasms (genetics, immunology)