Development of spontaneous uterine tumors in low molecular mass polypeptide-2 knockout mice
T Hayashi, DL Faustman - Cancer Research, 2002 - AACR
T Hayashi, DL Faustman
Cancer Research, 2002•AACRThe 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-γ-
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∼ 36% by 12 …
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-γ-
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∼ 36% by 12 …
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-γ-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 ∼36% by 12 months of age. This observation indicates that proteasome function is essential for MHC class I-mediated tumor rejection by CTLs.
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