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ASK1 and its role in cardiovascular and other disorders: available treatments and future prospects.
Expert Review of Proteomics ( IF 3.8 ) Pub Date : 2019-10-17 , DOI: 10.1080/14789450.2019.1676735
Mohammad Hassan Baig 1 , Abu Baker 2 , Ghulam M Ashraf 3 , Jae-June Dong 1
Affiliation  

Introduction: Apoptosis signal-regulating kinase 1 (ASK1), also known as MAP3K5, is a member of mitogen-activated protein kinase kinase kinase (MAP3K) family and is well reported as crucial in the regulation of the JNK and P38 pathways. ASK1 is activated in response to a diverse array of stresses such as endoplasmic reticulum stress, lipopolysaccharides, tumor necrosis factor alpha, and reactive oxygen species. The activation of ASK1 induces various stress responses.

Areas covered: Considering ASK1 as an important therapeutic drug target, here we have discussed the role of ASK1 in the progression of various diseases. We have also provided an overview of the available inhibitors for ASK1. The success of computational-based approaches toward ASK1 inhibitor design has also been discussed.

Expert opinion: A number of reports have outlined the prominent role of ASK1 in the pathogenesis of several diseases. The discovery of novel ASK1 inhibitors would have a wide range of applications in medical science. In-silico techniques have been successfully used in the design of some novel ASK1 inhibitors. The use of machine learning-based approaches in combination with structure-based virtual screening (SBVS) and ligand-based virtual screening (LBVS) will be helpful toward the development of potent ASK1 inhibitors.



中文翻译:

ASK1及其在心血管疾病和其他疾病中的作用:可用的治疗方法和未来前景。

简介:细胞凋亡信号调节激酶1(ASK1),也称为MAP3K5,是有丝分裂原激活的蛋白激酶激酶激酶(MAP3K)家族的成员,并且据报道在调节JNK和P38途径中至关重要。ASK1被激活以响应各种各样的压力,例如内质网压力,脂多糖,肿瘤坏死因子α和活性氧。ASK1的激活诱导各种应激反应。

涵盖的领域:考虑到ASK1是重要的治疗药物靶标,在这里我们讨论了ASK1在各种疾病进展中的作用。我们还提供了ASK1抑制剂的概述。还讨论了基于计算的ASK1抑制剂设计方法的成功。

专家意见:许多报告概述了ASK1在几种疾病的发病机理中的重要作用。新型ASK1抑制剂的发现将在医学中具有广泛的应用。电子技术已成功用于某些新型ASK1抑制剂的设计中。将基于机器学习的方法与基于结构的虚拟筛选(SBVS)和基于配体的虚拟筛选(LBVS)结合使用,将有助于开发有效的ASK1抑制剂。

更新日期:2019-10-17
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