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首页> 外文期刊>Molecular and Cellular Biology >Rapid induction in regenerating liver of RL/IF-1 (an I kappa B that inhibits NF-kappa B, RelB-p50, and c-Rel-p50) and PHF, a novel kappa B site-binding complex.
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Rapid induction in regenerating liver of RL/IF-1 (an I kappa B that inhibits NF-kappa B, RelB-p50, and c-Rel-p50) and PHF, a novel kappa B site-binding complex.

机译：快速再生的RL / IF-1（一种抑制NF-κB，RelB-p50和c-Rel-p50的IκB）和PHF（一种新颖的κB位点结合复合体）在肝脏中快速诱导。

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The liver is one of the few adult tissues that has the capacity to regenerate following hepatectomy or toxic damage. In examining the early growth response during hepatic regeneration, we found that a highly induced immediate-early gene in regenerating liver encodes RL/IF-1 (regenerating liver inhibitory factor) and is the rat homolog of human MAD-3 and probably of chicken pp40. RL/IF-1 has I kappa B activity of broad specificity in that it inhibits the binding of p50-p65 NF-kappa B, c-Rel-p50, and RelB-p50, but not p50 homodimeric NF-kappa B, to kappa B sites. Like RL/IF-1, several members of the NF-kappa B and rel family of transcription factors are immediate-early genes in regenerating liver and mitogen-treated cells. We examined changes in kappa B site binding activity during liver regeneration and discovered a rapidly induced novel kappa B site-binding complex designated PHF [posthepatectomy factor(s)]. PHF is induced over 1,000-fold within minutes posthepatectomy in a protein synthesis-independent manner, with peak activity at 30 min, and is not induced by sham operation. PHF is distinct from p50-p65 NF-kappa B, which is present only in the inactive form in liver posthepatectomy. Although early PHF complexes do not interact strongly with anti-p50 antibodies, PHF complexes present later (3 to 5 h) posthepatectomy react strongly, suggesting that they contain a p50 NF-kappa B subunit. Unlike p50-p65 NF-kappa B, c-Rel-p50, and RelB-p50 complexes, PHF binding to kappa B sites is not inhibited by RL/IF-1. One role of RL/IF-1 in liver regeneration may be to inhibit p50-p65 NF-kappa B activity present in hepatic cells, allowing for the preferential binding of PHF to kappa B sites. Because PHF is induced immediately posthepatectomy in the absence of de novo protein synthesis, PHF could have a role in the regulation of liver-specific immediate-early genes in regenerating liver.
机译：肝脏是少数在肝切除或毒性损伤后具有再生能力的成年组织之一。在检查肝再生过程中的早期生长反应时，我们发现再生肝中高度诱导的立即早期基因编码RL / IF-1（再生肝抑制因子），并且是人MAD-3和大鼠pp40的大鼠同源物。 。 RL / IF-1具有广泛的I kappa B活性，因为它抑制p50-p65 NF-kappa B，c-Rel-p50和RelB-p50，而不是p50同型二聚体NF-kappa B的结合B网站。像RL / IF-1一样，NF-κB和rel转录因子家族的几个成员是再生肝脏和有丝分裂原处理的细胞中的早期基因。我们检查了肝再生过程中κB位点结合活性的变化，发现了一种快速诱导的新型κB位点结合复合物，称为PHF [后皮切除因子]。在肝切除术后数分钟内，PHF以一种不依赖蛋白质合成的方式被诱导超过1,000倍，在30分钟时达到峰值活性，并且不是由假手术诱导的。 PHF与p50-p65NF-κB不同，后者在肝切除术后仅以非活性形式存在。尽管早期的PHF复合物不能与抗p50抗体强烈相互作用，但是肝切除术后晚些（3-5小时）出现的PHF复合物反应强烈，表明它们含有p50NF-κB亚基。与p50-p65NF-κB，c-Rel-p50和RelB-p50复合物不同，RLF / IF-1不会抑制PHF与Kappa B位点的结合。 RL / IF-1在肝再生中的一种作用可能是抑制肝细胞中存在的p50-p65NF-κB活性，从而允许PHF与κB位点优先结合。因为在没有从头合成蛋白的情况下，肝切除术后会立即诱导PHF，所以PHF可能在再生肝脏中调节肝脏特有的早期基因。

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