In response to mitogenic stimulation, B cells activate different pro-anabolic signaling pathways such as c-Myc- and mTORC1-dependent networks to satisfy the energetic demands of biomass synthesis and proliferation. In order to preserve viability and function, cell growth cannot progress unchecked and must be adjusted according to the availability of nutrients. Nutrient-sensing proteins such as AMPK antagonize mTORC1 activity in response to starvation. If pro-anabolic signaling pathways are aberrantly activated, B cells may lack the metabolic capacity to accommodate their energetic needs, which can lead to cell death. On the other hand, metabolic hyperactivation is a salient feature of cancer cells, suggesting that mechanisms exist, which allow B cells to cope with metabolic stress. The aim of this review is to discuss how B cells respond to a mismatch between energy supply and demand and what the consequences are of metabolic dysregulation in normal and malignant B cells.

中文翻译：

---

代谢检查点调节剂在B细胞存活和转化中的作用。

响应有丝分裂刺激，B细胞激活不同的促代谢信号通路，例如c-Myc-和mTORC1依赖性网络，以满足生物质合成和增殖的能量需求。为了保持活力和功能，细胞生长不能不受限制地进行，必须根据营养素的可用性进行调整。营养敏感的蛋白质（例如AMPK）可拮抗饥饿引起的mTORC1活性。如果异常代谢前信号通路被激活，B细胞可能缺乏代谢能力来适应其能量需求，这可能导致细胞死亡。另一方面，代谢过度活化是癌细胞的显着特征，表明存在机制，该机制可使B细胞应对代谢应激。