Post-translational myristoylation at the cross roads of cell death, autophagy and neurodegeneration

被引:17
作者
Martin, Dale D. O. [1 ]
Hayden, Michael R. [1 ]
机构
[1] Univ British Columbia, Dept Med Genet, Child & Family Res Inst, Ctr Mol Med & Therapeut, Vancouver, BC, Canada
关键词
apoptosis; autophagy; caspases; huntingtin; Huntington disease; post-translational myristoylation; MUTANT HUNTINGTIN; CASPASE CLEAVAGE; CYTOPLASMIC DYNEIN; N-MYRISTOYLATION; APOPTOSIS; PROTEINS; DISEASE; DIFFERENTIATION; IDENTIFICATION; PROLIFERATION;
D O I
10.1042/BST20140281
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In a little more than a decade, post-translational myristoylation (PTMyr) has become an established post-translational modification during cell death. It involves the addition of the fatty acid myristate to newly exposed N-terminal glycines following caspase cleavage. It promotes membrane binding and relocalization of functional protein domains released by caspase cleavage during apoptosis, or programmed cell death. However, as the requirement of caspase cleavage has expanded beyond just cell death, it has become apparent that PTMyr may play a role in cell survival, differentiation and now autophagy. Herein, we describe how myristoylation may play a role in autophagy with an emphasis on PTMyr.
引用
收藏
页码:229 / 234
页数:6
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