BK通道的失活的氨基末端beta2辅助单元:一个重要的角色一个终端三个疏水残基的肽段。
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夏XM,丁JP, Lingle CJ
BK通道的失活的氨基末端beta2辅助单元:一个重要的角色一个终端三个疏水残基的肽段。
J创杂志。2003年2月,121 (2):125 - 48。
- PubMed ID
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12566540 (在PubMed]
- 文摘
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一个辅助beta2亚基,当coexpressed Sloα亚基,生产产生的large-conductance失活,Ca(2 +)和压敏K (+) (BK-type)通道。失活是介导的胞质NH(2)终点站beta2亚基。了解失活的结构要求,我们做了一个突变分析的角色NH(2)终点站的失活过程。beta2 NH(2)终点站包含46个残留物被认为是第一个跨膜胞质部分(TM1)。在这里,我们解决两个问题。首先,我们定义的关键部分残留产生的失活。第二,我们检查的角色之间的链接器失活段和TM1。结果表明,失活的关键决定因素的初始段三个氨基酸(残留2 - 4:FIW)后启动蛋氨酸。删除扫描的位置从5到残留的36改变失活,但不能废除它。相比之下,删除FIW或组合内的点突变FIW三合废除失活。 Mutational analysis of the three initial residues argues that inactivation does not result from a well-defined structure formed by this epitope. Inactivation may be better explained by linear entry of the NH(2)-terminal peptide segment into the permeation pathway with residue hydrophobicity and size influencing the onset and recovery from inactivation. Examination of the ability of artificial, polymeric linkers to support inactivation suggests that a variety of amino acid sequences can serve as adequate linkers as long as they contain a minimum of 12 residues between the first transmembrane segment and the FIW triplet. Thus, neither a specific distribution of charge on the linker nor a specific structure in the linker is required to support the inactivation process.