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B细胞激活与耐受的淋巴瘤模型。VII. 抗Ig介导的生长抑制及其逆转途径。

Lymphoma models for B-cell activation and tolerance. VII. Pathways in anti-Ig-mediated growth inhibition and its reversal.

作者信息

Warner G L, Scott D W

机构信息

Immunology Unit, University of Rochester Cancer Center, New York 14642.

出版信息

Cell Immunol. 1988 Aug;115(1):195-203. doi: 10.1016/0008-8749(88)90173-6.

Abstract

WEHI-231, CH33, and CH31 are B-cell lymphomas that are inhibited in their growth by crosslinking of surface Ig receptors during early G1. This "negative signaling" process can be prevented or reversed under certain conditions. In the present paper, we use a cell synchronization procedure to demonstrate that activation of protein kinase C (PKC) is not involved in the negative signal for growth, but rather that PKC activation prevents growth inhibition when present early in the cell cycle. Indeed, the prevention of negative signaling is only accomplished by active phorbol esters. Moreover, phorbol esters and a calcium ionophore fail to deliver a negative signal under conditions in which anti-Ig can significantly prevent cell cycle progression into S phase, thereby ruling out synergy between PKC and calcium in growth inhibition. Whether phorbol esters reverse negative signaling by preventing internalization of the immune complex or phosphorylation of a critical intracellular protein is discussed.

摘要

WEHI-231、CH33和CH31是B细胞淋巴瘤,在G1早期,其表面Ig受体交联会抑制它们的生长。这种“负信号”过程在某些条件下可以被阻止或逆转。在本文中,我们使用细胞同步程序来证明蛋白激酶C(PKC)的激活不参与生长的负信号,而是PKC激活在细胞周期早期存在时可防止生长抑制。实际上,只有活性佛波酯才能实现对负信号的阻止。此外,在抗Ig能显著阻止细胞周期进入S期的条件下,佛波酯和钙离子载体无法传递负信号,从而排除了PKC和钙在生长抑制中的协同作用。文中还讨论了佛波酯是通过阻止免疫复合物的内化还是关键细胞内蛋白的磷酸化来逆转负信号。

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