铁金库的制衡机制。
Checks and balances for the iron bank.
作者信息
Outten Caryn E
机构信息
From the Department of Chemistry and Biochemistry, University of South Carolina, Columbia, South Carolina 29208
出版信息
J Biol Chem. 2017 Sep 22;292(38):15990-15991. doi: 10.1074/jbc.H117.785741.
Abstract
The RNA-binding iron regulatory proteins IRP1 and IRP2 are inactivated by either Fe-S cluster insertion or protein degradation mediated by the E3 ligase component FBXL5. However, the mechanisms for coordination between Fe-S cluster assembly, FBXL5, and IRP1/IRP2 activity are poorly defined. A new study reveals that FBXL5 plays a critical role in limiting IRP1 and IRP2 overaccumulation when cytosolic Fe-S cluster assembly is impaired in order to maintain optimal iron levels for cell viability.
摘要
RNA结合铁调节蛋白IRP1和IRP2可通过铁硫簇插入或由E3连接酶组分FBXL5介导的蛋白质降解而失活。然而，铁硫簇组装、FBXL5和IRP1/IRP2活性之间的协调机制尚不清楚。一项新研究表明，当胞质铁硫簇组装受损时，FBXL5在限制IRP1和IRP2过度积累方面发挥关键作用，以维持细胞存活的最佳铁水平。
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