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In-Silico characterization of SCN9A: A protein that mediates voltage-dependent sodium ion permeability of excitable membranes

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Research Paper 01/11/2017
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In-Silico characterization of SCN9A: A protein that mediates voltage-dependent sodium ion permeability of excitable membranes

Humaira Aziz Sawal, Rubina Dad, Sarmad Mehmood, Umme Kalsoom, Peter John, Muhammad Jawad Hassan
Int. J. Biosci.11( 5), 378-385, November 2017.
Certificate: IJB 2017 [Generate Certificate]
Key: CharacterizationCIPCongenital insensitivity to painIn-silicoSCN9A

Abstract

Sodium channel NaV 1.7, SCN9A gene encodes the SCN9A protein which is associated with either pain insensitivity typically with loss-of-function mutations, and chronic pain disorders typical with gain-of-function mutations. In the present study, we tried to characterize the SCN9A structure and predict its interactions with different proteins using different on-line tools. Protscale server predicted an unstable protein structure for SCN9A based on several parameters including accessibility, hydrophilicity, mutability, refractivity bulkiness, flexibility and polarity. Signal Server predicted no signal peptide in SCN9A. No acetylation site was present in SCN9A: as predicted by Net Acet. Different threonine, serine and tyrosine specific phosphorylation sites were predicted in SCN9A at different positions. Kinases like PKA and PKC were shown to be involved in phosphorylation of SCN9A. We also predicted different physiochemical parameters for SCN9A. The study also predicted that SCN9A might interact with other members of sodium channel family including SCN2A, SCN3A, SCN5A, SCN8A, SCN10A, SCN11A, SCN1B, SCN2B, SCN4B ABCB1 and CALM2 proteins. These results might be helpful to understand disease pathogenesis and molecular mechanisms of different inherited disorders of nervous system including congenital sensitivity to pain caused by SCN9A mutations.

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