Epstein-Barr Virus Latent Membrane Protein 1 Increases Calcium Influx through Store-operated Channels in B

2011 
Ca 2 signaling plays an important role in B cell survival and activation and is dependent on Ca 2 trapped in the endoplasmic reticulum (ER) and on extracellular Ca 2 . Epstein-Barr virus (EBV) can immortalize B cells and contributes to lymphomagenesis. Previously, we showed that the ER Ca 2 content of Burkitt lymphoma cell lines was increased following infection with immortalization-competent virus expressing the full set of EBV latency genes (B95– 8). In contrast, infection with an immortalization-deficient virus (P3HR-1) not expressing LMP-1 is without effect. LMP-1 protein expression was sufficient to increase the ER Ca 2 content and to increase the cytosolic Ca 2 concentration ([Ca 2 ]cyt). In this follow-up study, we showed that the resting [Ca 2 ]cyt of P3HR-1-infected cells was
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