Reference | <p style=/line-height:25px/>
<br>[1]. Picard C, Casanova JL, Puel A. Infectious diseases in patients with IRAK-4, MyD88, NEMO, or IκBα deficiency. Clin Microbiol Rev. 2011 Jul;24(3):490-7. doi: 10.1128/CMR.00001-11.
<br>[2]. Pourbasheer E, Riahi S, Ganjali MR, Norouzi P. Quantitative structure-activity relationship (QSAR) study of interleukin-1 receptor associated kinase 4 (IRAK-4) inhibitor activity by the genetic algorithm and multiple linear regression (GA-MLR) method. J Enzyme Inhib Med Chem. 2010 Dec;25(6):844-53.
<br>[3]. Dunne A, Carpenter S, Brikos C, Gray P, Strelow A, Wesche H, Morrice N, O/’Neill LA. IRAK1 and IRAK4 promote phosphorylation, ubiquitination, and degradation of MyD88 adaptor-like (Mal). J Biol Chem. 2010 Jun 11;285(24):18276-82.
<br>[4]. Wang Z, Wesche H, Stevens T, Walker N, Yeh WC. IRAK-4 inhibitors for inflammation. Curr Top Med Chem. 2009;9(8):724-37.
<br>[5]. Buckley GM, Fosbeary R, Fraser JL, Gowers L, Higueruelo AP, James LA, Jenkins K, Mack SR, Morgan T, Parry DM, Pitt WR, Rausch O, Richard MD, Sabin V. IRAK-4 inhibitors. Part III: a series of imidazo[1,2-a]pyridines. Bioorg Med Chem Lett. 2008 Jun 15;18(12):3656-60.
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