@article {1011,
	title = {Molecular mechanism of interactions between Chrysin and I-kappa-B kinase epsilon (IKKe)/Tank Binding Kinase-1(TBK1): Cell based assay and insilico molecular docking studies [High Throughput Screening Facility].},
	journal = {J Biomol Struct Dyn},
	year = {2019},
	month = {2019 Feb 15},
	pages = {1-9},
	abstract = {<p>Chrysin, a bioactive flavonoid, was investigated for its potential to inhibit the activity of I-kappa-B kinase epsilon (IKKe) / Tank Binding Kinase-1(TBK1) an enzyme responsible for production of pro inflammatory cytokine and suppression of energy expenditure genes, finally causing insulin resistance and obesity. Expressions of majority of polyinosinic-polycytidylic acid (poly IC) mediated genes are mediated through Toll/interleukin-1 receptor domainߝcontaining adapter-inducing interferon (TRIF) dependent signalling pathway. To check the therapeutic potential of chrysin its effect was examined on Toll/interleukin-1 receptor domainߝcontaining adapter-inducing interferon (TRIF) dependent pathway. Chrysin showed significant inhibition of I-kappa-B kinase epsilon (IKKe) / Tank Binding Kinase-1(TBK1) enzyme activity by kinase assay. Chrysin suppressed the I-kappa-B kinase epsilon expression induced by polyinosinic-polycytidylic acid resulting into decrease expression of target genes interferon gamma-induced protein 10 (IP10), monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) in macrophage-like cell line. Chrysin also showed increase in oxygen consumption in osteosarcoma cell line hence alleviating energy expenditure and thermogenesis. Moreover, insilico analysis shows that chrysin interact weakly with I-kappa-B kinase epsilon (IKKe) but displayed good interaction with Tank Binding Kinase-1 (TBK1). Overall these results suggested that I-kappa-B kinase epsilon (IKKe) / Tank Binding Kinase-1(TBK1) may be a novel target for chrysin that possesses anti-inflammatory and insulin sensitivity effects at I-kappa-B kinase epsilon (IKKe) / Tank Binding Kinase-1(TBK1) binding sites.</p>
},
	issn = {1538-0254},
	doi = {10.1080/07391102.2019.1581086},
	author = {Siddiqui, Amir M and Akhtar, Juber and M S, Shahab Uddin and Khan, Mohammad Irfan and Khalid, Mohammad}
}
