Mesh : Humans Cystic Fibrosis Transmembrane Conductance Regulator / metabolism genetics chemistry Endoplasmic Reticulum / metabolism Membrane Proteins / metabolism chemistry Protein Folding Ubiquitin-Protein Ligases / metabolism Ubiquitination

来  源:   DOI:10.1083/jcb.202405160   PDF(Pubmed)

Abstract:
During ER-associated decay, unfolded membrane-resident proteins are targeted for removal and degradation by ubiquitin ligases whose identities and precise operations remain unclear. In this issue, Guerriero and Brodsky discuss new results from Kamada et al. (https://doi.org/10.1083/jcb.202308003) showing the clearance of misfolded CFTR by the E3 ligase HERC3.
摘要:
在ER相关衰变期间,未折叠的膜驻留蛋白被泛素连接酶靶向去除和降解,泛素连接酶的身份和精确操作尚不清楚。在这个问题上,Guerriero和Brodsky讨论了Kamada等人的新结果。(https://doi.org/10.1083/jcb.202308003)显示E3连接酶HERC3清除错误折叠的CFTR。
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