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- W4313386493 abstract "Abstract TNF-receptor associated factor 3 (TRAF3), a negative regulator of CD40 and BAFF-receptor- mediated signaling pathways, also serves as a potentially important tumor suppressor in B cell malignancies. Deletion or loss of function mutations of the traf3 gene are highly associated with multiple myeloma (MM) and different subtypes of B cell lymphoma. Current dogma has attributed TRAF3’s role of restraining cell survival to its negative regulatory role in activating the non-canonical NF-κB2 pathway. However, studying cell-type-specific TRAF3-deficient mouse strains we produced, we found that TRAF3 deletion in B cells, T cells or dendritic cells all results in constitutive NF-κB2 activation, while enhanced cell survival is unique to TRAF3 deficient B cells. This indicates that TRAF3 must negatively regulate additional survival or anti-apoptotic pathways in a B-cell-specific manner. Our recent results show that TRAF3 deficient B cells, but not other TRAF3-deficient cell types, highly express the pro-survival kinase Pim2. Pim2 expression levels also correlate with copy number and loss of function mutations in the traf3 gene in human MM cell lines. TRAF3 deficient B cells also display higher basal levels of the activated form of the B cell-specific kinase Btk, a kinase implicated in MM pathogenesis. These findings reveal B cell-specific mechanisms by which TRAF3 can exert its cell-specific impact on regulation of survival, and are being further explored in ongoing work." @default.
- W4313386493 created "2023-01-06" @default.
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- W4313386493 date "2013-05-01" @default.
- W4313386493 modified "2023-09-27" @default.
- W4313386493 title "The role of TRAF3 in B cell specific regulation of survival and malignancy (P1112)" @default.
- W4313386493 doi "https://doi.org/10.4049/jimmunol.190.supp.64.3" @default.
- W4313386493 hasPublicationYear "2013" @default.
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