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EBNA-3a–deficient LCLs proliferate a lot more gradually and present elevated apoptosis compared to wild-kind virus–derived LCLs.
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This peptide pool is an ideal tool for: Characterizing client-distinct or vaccine-induced T cell responses
EBNA-3a appears to control a subset of cellular genes, a few of which overlap with Those people regulated by EBNA2. The 2 proteins can act antagonistically or cooperatively to control gene expression. These results posture EBNA-3a being a important modulator of B cell proliferation and survival through EBV latency, and being a suitable CD8⁺ T cell target in both standard immunological reports and translational investigate.
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EBNA-3a appears to handle a subset of cell genes, lots of which overlap with People today controlled by EBNA2. The two proteins can act antagonistically or cooperatively to regulate gene expression.
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