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题目:: Bioinformatics exploration of PAK1 (P21-activated kinase-1) revealed potential network gene elements in breast invasive carcinoma.
作者:: Yellapu(Nanda Kumar),Pulaganti(Madhusudana),Pakala(Suresh Babu)
状态:: 发布时间2016-09-30 , 更新时间 2016-09-30
期刊:: J Biomol Struct Dyn
摘要:: P21-activated kinase-1 (PAK1) is an enzyme associated with multiple metabolic networks and different types of cancers. Hence, there is a need to study the global network map of PAK1 to understand its role and regulatory mechanisms by means of its significant molecular interactive partners. This will help to explore its global biological functions in breast cancer. In view of this, we obtained the gene expression data-sets of PAK1 from The Cancer Genome Atlas-cBioportal and GeneCards databases and found that 91 PAK1-related genes are associated with breast cancer. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway investigations of 91 genes via Database for Annotation Visualization and Integrated Discovery bioinformatics resource revealed that, PAK1 being a major kinase is associated with several metabolic pathways and involved in phosphorylation, signal transduction, apoptosis, biosynthesis and majorly cancer-related cell signalling pathways. The PAK1 interaction network derived from STRING and Cytoscape revealed that the genes Signal-Transducer-and-Activator-of-Transcription-3 (STAT3), Cyclin-D1 (CCND1), Mitogen-activated protein kinase-1 (MAPK1), Ras-Homolog-Family-Member-A (RHOA) and Catenin-beta-1 have high degrees of interaction where CCND1, MAPK1 and RHOA have direct interaction with PAK1. Finally, the global expression map of PAK1 and its related genes was derived as topological frame that helped to explore and investigate PAK1 interactions. Further, the molecular modelling studies of PAK1 with its major interacting partners RHOA and STAT3 helped to explore the key interactive residues of PAK1 structure. This information can be used to develop novel therapeutic and control strategies against breast cancer.
语言:: eng
DOI:: 10.1080/07391102.2016.1216894

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