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首页> 外文期刊>Journal of Cellular Physiology >A-type lamins and signaling: the PI 3-kinase/Akt pathway moves forward.
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A-type lamins and signaling: the PI 3-kinase/Akt pathway moves forward.

机译：a类型核纤层蛋白和信号:π3-kinase / Akt通路往前移动。

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Lamin A/C is a nuclear lamina constituent mutated in a number of human inherited disorders collectively referred to as laminopathies. The occurrence and significance of lamin A/C interplay with signaling molecules is an old question, suggested by pioneer studies performed in vitro. However, this relevant question has remained substantially unanswered, until data obtained in cellular and organismal models of laminopathies have indicated two main aspects of lamin A function. The first aspect is that lamins establish functional interactions with different protein platforms, the second aspect is that lamin A/C activity and altered function may elicit different effects in different cells and tissue types and even in different districts of the same tissue. Both these observations strongly suggest that signaling mechanisms targeting lamin A/C or its binding partners may regulate such a plastic behavior. A number of very recent data show involvement of kinases, as Akt and Erk, or phosphatases, as PP1 and PP2, in lamin A-linked cellular mechanisms. Moreover, altered activation of signaling in laminopathies and rescue of the pathological phenotype in animal models by inhibitors of signaling pathways, strongly suggest that signaling effectors related to lamin A/C may be implicated in the pathogenesis of laminopathies and may represent targets of therapeutic intervention. In face of such an open perspective of basic and applied research, we review current evidence of lamin A/C interplay with signaling molecules, with particular emphasis on the lamin A-Akt interaction and on the biological significance of their relationship.
机译：核纤层蛋白A / C核板组成变异在许多人类遗传疾病集体称为laminopathies。核纤层蛋白A / C的存在和意义与信号分子相互作用是一个古老的问题,建议的先驱研究体外。仍大幅回答,直到数据获得的细胞和有机体的模型laminopathies表示的两个主要方面核纤层蛋白一个函数。建立功能相互作用不同第二个方面是,蛋白质平台核纤层蛋白A / C活动和功能改变在不同的细胞,引起不同的效果组织类型,甚至在不同的地区相同的组织。建议针对核纤层蛋白的信号机制A / C或其约束力的合作伙伴可能调节等塑料的行为。显示激酶,参与的一种蛋白激酶Erk,或在核纤层蛋白磷酸酶,PP1 PP2链细胞机制。laminopathies和救援的信号病理表型在动物模型信号通路的抑制剂,强劲表明信号效应器与核纤层蛋白有关A / C可能涉及的发病机制laminopathies,可能代表的目标治疗性干预。基础和应用研究的角度来看,我们审查当前核纤层蛋白A / C相互作用的证据与特定的信号分子强调核纤层蛋白A-Akt交互他们的生物学意义的关系。

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