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SMYD2-PARP1复合物的结构揭示了肽结合的有效模式和变构模式。

Structure of the SMYD2-PARP1 Complex Reveals Both Productive and Allosteric Modes of Peptide Binding.

作者信息

Zhang Yingxue, Alshammari Eid, Sobota Jacob, Spellmon Nicolas, Perry Emerson, Cao Tianxin, Mugunamalwaththa Thamarahansi, Smith Sheila, Brunzelle Joseph, Wu Gensheng, Stemmler Timothy, Jin Jianping, Li Chunying, Yang Zhe

机构信息

Department of Biochemistry, Microbiology, and Immunology, Wayne State University School of Medicine, Detroit, MI, USA.

Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.

出版信息

bioRxiv. 2024 Dec 4:2024.12.03.626679. doi: 10.1101/2024.12.03.626679.

Abstract

Allosteric regulation allows proteins to dynamically respond to environmental cues by modulating activity at sites away from the catalytic center. Despite its importance, the SET-domain protein lysine methyltransferase superfamily has been understudied. Here, we present four crystal structures of SMYD2, a unique family member with a MYND domain. Our findings reveal a novel allosteric binding site with high conformational plasticity and promiscuity, capable of binding peptides, proteins, PEG, and small molecules. This site exhibits positive cooperativity with substrate binding, influencing catalytic activity. Mutations here significantly alter substrate affinity, changing the enzyme's kinetic profile. Specificity studies show interaction with PARP1 but not histones, suggesting targeted regulation. Interestingly, this site's function remains unaffected by active site changes, indicating unidirectional mechanisms. Our discovery provides novel insights into SMYD2's biochemical regulation and lays the foundation for broader research on allosteric control in lysine methyltransferases. Given SMYD2's role in various cancers, this work opens exciting avenues for designing specific allosteric inhibitors with reduced off-target effects.

摘要

变构调节使蛋白质能够通过调节催化中心以外位点的活性来动态响应环境信号。尽管其很重要,但SET结构域蛋白赖氨酸甲基转移酶超家族一直未得到充分研究。在此,我们展示了SMYD2(一种具有MYND结构域的独特家族成员)的四个晶体结构。我们的研究结果揭示了一个具有高构象可塑性和多配体结合性的新型变构结合位点,该位点能够结合肽、蛋白质、聚乙二醇和小分子。此位点与底物结合表现出正协同性,影响催化活性。此处的突变会显著改变底物亲和力,改变酶的动力学特征。特异性研究表明其与PARP1相互作用,但不与组蛋白相互作用,提示存在靶向调节。有趣的是,该位点的功能不受活性位点变化的影响,表明存在单向机制。我们的发现为SMYD2的生化调节提供了新见解,并为赖氨酸甲基转移酶变构调控的更广泛研究奠定了基础。鉴于SMYD2在多种癌症中的作用,这项工作为设计具有降低脱靶效应的特异性变构抑制剂开辟了令人兴奋的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ee/11642878/84fb1ee21ce4/nihpp-2024.12.03.626679v1-f0001.jpg

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