摘要
感染是病原体侵入的过程,也是宿主对外来药物的反应。脯氨酸定向磷酸化是调节感染和感染引起的癌症基本蛋白功能的主要调节机制.。最近,该磷酸化依赖的脯氨酸异构酶Pin1的鉴定揭示了一个独特的信号转导机制控制蛋白质的构象和功能后磷酸化。Pin1是唯一的脯氨酸异构酶特异性地识别某些亲执导的丝氨酸/苏氨酸磷酸化的酶。Pin1作为肿瘤病毒和细菌感染主要是通过激活Toll样受体信号和NF-κB途径的主要调节方式。本文将具体研究Pin1在癌症相关的病毒和细菌感染,并讨论新发现Pin1抑制剂作为有前途的药物对病毒和细菌感染有关的肿瘤的预防和治疗作用。
关键词: 脯氨酸异构酶Pin1,癌症相关的病毒和细菌感染、ATRA、炎症反应、NF-κBκ,Toll样受体
Current Molecular Medicine
Title:The Roles of the Unique Prolyl Isomerase Pin1 in Cancer-Related Viral and Bacterial Infections
Volume: 16 Issue: 9
Author(s): J. Wang, X.-H. Liao, M. Zheng, D. Yang, X. Z. Zhou, H. Liu, K. P. Lu
Affiliation:
关键词: 脯氨酸异构酶Pin1,癌症相关的病毒和细菌感染、ATRA、炎症反应、NF-κBκ,Toll样受体
摘要: Infection is the process of pathogen invasion, as well as the host reaction to the foreign agents. Proline-directed phosphorylation is a major regulatory mechanism that regulates the function of fundamental proteins involved in infection and infection-induced cancer. Recently, the identification of the phosphorylation-dependent prolyl isomerase Pin1 has uncovered a unique regulatory signaling mechanism controlling protein conformation and function after phosphorylation. Pin1 is the only proline isomerase that specifically recognizes certain Pro-directed Ser/Thr phosphorylation motifs. Pin1 has emerged as a major regulator of cancerrelated viral and bacterial infections notably via activating Toll-like receptor signaling and NF-κB pathways. This paper will specifically review recent findings on the role of Pin1 in cancer-related viral and bacterial infections and also discuss newly discovered Pin1 inhibitors as promising drugs for the prevention and treatment of viral and bacterial infections and associated tumorigenesis.
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Cite this article as:
J. Wang, X.-H. Liao, M. Zheng, D. Yang, X. Z. Zhou, H. Liu, K. P. Lu , The Roles of the Unique Prolyl Isomerase Pin1 in Cancer-Related Viral and Bacterial Infections, Current Molecular Medicine 2016; 16 (9) . https://dx.doi.org/10.2174/1566524016666161124103654
DOI https://dx.doi.org/10.2174/1566524016666161124103654 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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