Luciano F., et al. – Investigation of the 6 antiapoptotic human Bcl-2 family members showed that Nur77/TR3 binds most strongly to Bcl-B, which is prominently expressed in plasma cells and multiple myeloma. Nur77 converts the Bcl-B phenotype from antiapoptotic to proapoptotic. A Nur77-mimicking peptide killed RPMI 8226 myeloma cells through a Bcl-B–dependent mechanism. Because Bcl-B is abundantly expressed in plasma cells and some myelomas, these findings suggest exploiting the Nur77/Bcl-B mechanism for apoptosis to eradicate autoimmune plasma cells or myeloma.
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