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调节钙离子稳态的转录机制。

Transcriptional mechanisms regulating Ca(2+) homeostasis.

机构信息

Department of Biochemistry, Temple University School of Medicine, Philadelphia, PA 19140, United States.

出版信息

Cell Calcium. 2011 May;49(5):314-21. doi: 10.1016/j.ceca.2010.10.001. Epub 2010 Nov 13.

Abstract

Ca(2+) is a dynamic cellular secondary messenger which mediates a vast array of cellular responses. Control over these processes is achieved via an extensive combination of pumps and channels which regulate the concentration of Ca(2+) within not only the cytosol but also all intracellular compartments. Precisely how these pumps and channels are regulated is only partially understood, however, recent investigations have identified members of the Early Growth Response (EGR) family of zinc finger transcription factors as critical players in this process. The roles of several other transcription factors in control of Ca(2+) homeostasis have also been demonstrated, including Wilms Tumor Suppressor 1 (WT1), Nuclear Factor of Activated T cells (NFAT) and c-myc. In this review, we will discuss not only how these transcription factors regulate the expression of the major proteins involved in control of Ca(2+) homeostasis, but also how this transcriptional remodeling of Ca(2+) homeostasis affects Ca(2+) dynamics and cellular responses.

摘要

钙离子是一种动态的细胞二级信使,介导着广泛的细胞反应。通过广泛的泵和通道组合来控制这些过程,这些泵和通道不仅可以调节细胞质内的钙离子浓度,还可以调节所有细胞内隔室中的钙离子浓度。然而,这些泵和通道是如何被调节的,我们只是部分了解,最近的研究已经确定了早期生长反应(EGR)家族的锌指转录因子成员是这个过程中的关键参与者。其他几种转录因子在控制钙离子稳态中的作用也已经得到证实,包括 Wilms 肿瘤抑制因子 1(WT1)、激活 T 细胞的核因子(NFAT)和 c-myc。在这篇综述中,我们不仅将讨论这些转录因子如何调节参与钙离子稳态控制的主要蛋白质的表达,还将讨论钙离子稳态的这种转录重塑如何影响钙离子动力学和细胞反应。

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