Upregulation of p53 caused by Rpl22 was linked to immune-deficiency.

Scientists at Lexicon Pharmaceuticals and Fox Chase Cancer Center (FCCC) discovered that deletion of the ubiquitously expressed ribosomal protein L22 (Rpl22) gene resulted in the upregulation of p53, a key tumor suppressor gene that triggers apoptosis. Further, it was determined that this upregulation of p53 was responsible for blocking alpha-beta+ T-cell development, thereby creating an immune-deficient state.

“The connection between Rpl22 and the p53-mediated apoptosis pathway is exciting,” said David Wiest Ph.D., member of the basic science division at FCCC. “If research confirms our theories, Rpl22 may prove to be an important biomarker for certain T-cell immune deficiency diseases and some types of lymphoid cancers.”

“These findings could help us to further define the pathways involved in T lymphocyte development and regulation,” said Tamas Oravecz, Ph.D., Lexicon’s vp of immunology and oncology. “While Rpl22 will likely prove difficult for development as a classic drug target, understanding its role could contribute significantly to its potential as a biomarker for disease.”

These findings have been published in the June issue of Immunity.

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