Cytokine pleiotropy and redundancy: a view from the receptor.
Cytokine pleiotropy and redundancy: a view from the receptor.
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作者：
N. Nicola
所有的细胞因子或多或少都表现出多效性(多个生物作用)和冗余(共享的生物作用)。对细胞因子受体的研究表明，冗余可能是由相关细胞因子利用共同的受体亚基(通常称为β-亚基)和独特的配体特异性α-亚基来解释的。另一方面，生物多效性要求细胞因子受体在不同的细胞上发挥不同的活性。潜在地，这可以通过使用不同的β亚基、阿尔法亚基的独特信号能力、受体复合体不同区域的不同信号能力或以不同方式对相同信号做出反应的不同细胞机制来解释。对参与受体激活的蛋白质-蛋白质相互作用的分子细节的了解可能有助于理解这些现象和设计新的干预策略。
All cytokines, to a greater or lesser extent, exhibit pleiotropy (multiple biological actions) and redundancy (shared biological actions). The study of cytokine receptors, most of which belong to a structurally related hemopoietin domain family, has revealed that redundancy might be explained by the usage by related cytokines of a common receptor subunit usually termed the beta-subunit and a unique ligand-specific alpha-subunit. Biological pleiotropy, on the other hand, requires that cytokine receptors exert differential activities on different cells. Potentially, this could be explained by the use of different beta-subunits, unique signaling capacities of the alpha-subunit, differential signaling capacities of different regions of the receptor complex, or differential cellular machinery that responds to the same signal in different ways. An understanding in molecular detail of the protein-protein interactions involved in receptor activation may help in understanding these phenomena and in designing novel intervention strategies.