在NF-kappa B转录因子的明显细胞质前体中激活DNA结合活性
1Whitehead Institute for Biomedical Research Cambridge, Massachusetts 02142.
Cell
|April 22, 1988
概括
卡帕增强剂结合蛋白NF-kappa B存在但不活跃在未刺激细胞的细胞质中. 博 Ester 激活NF-卡帕B结合并导致其核转位.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 核因子kappa B (NF-kappa B) 是一个关键的转录因子,参与免疫反应和细胞信号传递.
- 通常在未受刺激的细胞中以不活跃的细胞质形式发现NF-kappa B.
- 卡帕增强元件对于免疫球蛋白卡帕轻链基因表达至关重要.
研究的目的:
- 在缺乏卡帕免疫球蛋白轻链表达的细胞中研究NF-kappa B的细胞局部化和激活状态.
- 确定NF-kappa B在pre-B细胞中受调节的机制.
- 了解醇在NF-kappa B激活和核转移中的作用.
主要方法:
- 使用细胞系,如70Z/3前B细胞和HeLa细胞.
- 采用生物化学技术,包括去化,大小分化和重新化,以评估蛋白质活性.
- 使用脱离剂,如脱氧化和形式胺,从细胞分数中提取和分析NF-kappa B.
- 通过比较非刺激细胞和醇刺激细胞的细胞和核分数中的NF-kappa B水平.
主要成果:
- 在未受刺激的70Z/3细胞的细胞质部分中检测到NF-kappa B,这表明它存在但缺乏DNA结合活性.
- 在未刺激的70Z/3细胞中发现了大量不活跃的细胞系NF-kappa B,与刺激细胞中的激活的核NF-kappa B相当.
- 博治疗导致NF-kappa B结合抑制的释放,并诱导其转移到细胞核.
- 70Z/3和HeLa细胞都含有NF-kappa B的细胞解质形式,不积极结合DNA.
结论:
- 细胞质NF-kappa B存在于70Z/3和HeLa细胞中的抑制状态.
- 博 Ester 在NF-kappa B调节中起着双重作用:释放结合抑制和促进核转位.
- 这些发现阐明了NF-kappa B激活与免疫细胞发育和功能相关的关键调节机制.
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