{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Whillock AL"],"funding":["U.S. Department of Health & Human Services | National Institutes of Health","BLRD VA","NIEHS NIH HHS","NIAID NIH HHS","NCI NIH HHS","NIGMS NIH HHS","Center for Integrated Healthcare, U.S. Department of Veterans Affairs"],"pagination":["12884"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6733949"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["TRAF3 is a versatile intracellular adapter protein with multiple context-specific roles. Uniquely in B cells, TRAF3 deficiency enhances survival and increases the risk of transformation, as loss of TRAF3 is observed in several types of B cell cancers. Here, we report a new mechanism for TRAF3 in the restraint of B cell survival. We found that TRAF3 deficiency was associated with induction of the pro-survival kinase Pim2 in mouse primary B cells and human malignant B cell lines. The increase in Pim2 was independent of NF-κB2 activation but was ameliorated with inhibition of STAT3 expression or function. TRAF3 deficiency also led to a Pim2-dependent increase in c-Myc protein levels and was associated with reduced c-Myc ubiquitination. TRAF3-deficient primary B cells were less sensitive to ce"],"journal":["Scientific reports"],"pubmed_title":["TRAF3 regulates the oncogenic proteins Pim2 and c-Myc to restrain survival in normal and malignant B cells."],"pmcid":["PMC6733949"],"funding_grant_id":["T32 AI07485","P30 ES005605","P30 CA086862","T32 AI007485","I01 BX001702","T32 GM007337","T32 AI007533","MR I01 BS001702","P50 CA097274","P50 CA97274"],"pubmed_authors":["Stunz LL","Whillock AL","Lin WW","Mambetsariev N","Bishop GA"],"additional_accession":[]},"is_claimable":false,"name":"TRAF3 regulates the oncogenic proteins Pim2 and c-Myc to restrain survival in normal and malignant B cells.","description":"TRAF3 is a versatile intracellular adapter protein with multiple context-specific roles. Uniquely in B cells, TRAF3 deficiency enhances survival and increases the risk of transformation, as loss of TRAF3 is observed in several types of B cell cancers. Here, we report a new mechanism for TRAF3 in the restraint of B cell survival. We found that TRAF3 deficiency was associated with induction of the pro-survival kinase Pim2 in mouse primary B cells and human malignant B cell lines. The increase in Pim2 was independent of NF-κB2 activation but was ameliorated with inhibition of STAT3 expression or function. TRAF3 deficiency also led to a Pim2-dependent increase in c-Myc protein levels and was associated with reduced c-Myc ubiquitination. TRAF3-deficient primary B cells were less sensitive to ce","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Sep","modification":"2025-04-21T23:22:11.701Z","creation":"2020-05-21T18:59:38Z"},"accession":"S-EPMC6733949","cross_references":{"pubmed":["31501481"],"doi":["10.1038/s41598-019-49390-9"]}}