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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Homeostatic cell-cycle control by BLyS: Induction of cell-cycle entry but not G1/S transition in opposition to p18INK4c and p27Kip1.
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Homeostatic cell-cycle control by BLyS: Induction of cell-cycle entry but not G1/S transition in opposition to p18INK4c and p27Kip1.

机译：BLyS的稳态细胞周期控制：诱导细胞周期进入，但与p18INK4c和p27Kip1相反，不会发生G1 / S过渡。

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摘要

Cell-cycle entry is critical for homeostatic control in physiologic response of higher organisms but is not well understood. The antibody response begins with induction of naive mature B cells, which are naturally arrested in G(0)/G(1) phase of the cell cycle, to enter the cell cycle in response to antigen and cytokine. BLyS (BAFF), a cytokine essential for mature B cell development and survival, is thought to act mainly by attenuation of apoptosis. Here, we show that BLyS alone induces cell-cycle entry and early G(1) cell-cycle progression, but not S-phase entry, in opposition to the cyclin-dependent kinase inhibitors p18(INK4c). Independent of its survival function, BLyS enhances the synthesis of cyclin D2, in part through activation of NF-kappaB, as well as CDK4 and retinoblastoma protein phosphorylation. By convergent activation of the same cell-cycle regulators in opposition to p18(INK4c), B cell receptor signaling induces cell-cycle entry and G(1) progression in synergy with BLyS, but also DNA replication. The failure of BLyS to induce S-phase cell-cycle entry lies in its inability to increase cyclin E and reduce p27(Kip1) expression. Antagonistic cell-cycle regulation by BLyS and p18(INK4c) is functionally linked to apoptotic control and conserved from B cell activation in vitro to antibody response in vivo, further indicating a physiologic role in homeostasis.
机译：细胞周期的进入对于高等生物的生理反应中的稳态控制至关重要，但尚未广为人知。抗体反应始于天真成熟的B细胞的诱导，该细胞自然停滞在细胞周期的G（0）/ G（1）阶段，以响应抗原和细胞因子进入细胞周期。 BLyS（BAFF）是成熟B细胞发育和存活所必需的细胞因子，被认为主要通过减少细胞凋亡来发挥作用。在这里，我们表明，BLyS单独诱导细胞周期进入和早期G（1）细胞周期进展，但不诱导S期进入，这与细胞周期蛋白依赖性激酶抑制剂p18（INK4c）相反。不依赖于其生存功能，BLyS部分地通过激活NF-κB以及CDK4和成视网膜细胞瘤蛋白磷酸化来增强细胞周期蛋白D2的合成。通过对p18（INK4c）的相同细胞周期调节剂的收敛激活，B细胞受体信号传导诱导细胞周期进入和G（1）进程与BLyS协同作用，但也可以复制DNA。 BLyS诱导S期细胞周期进入的失败在于其无法增加细胞周期蛋白E和减少p27（Kip1）表达。 BLyS和p18（INK4c）的拮抗细胞周期调控在功能上与细胞凋亡控制相关，并且在体外B细胞对体内抗体反应的激活中是保守的，进一步表明了体内稳态的生理作用。

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