Open AccessIn silico modeling of the interaction between TEX19 and LIRE1, and analysis of TEX19 gene missense SNPs
Author(s) -
Alzahrani Faisal A.,
Hawsawi Yousef MohammedRabaa,
Altayeb Hisham N.,
Alsiwiehri Naif O.,
Alzahrani Othman R.,
Alatwi Hanan E.,
AlAmer Osama M.,
Alomar Suliman,
Mansour Lamjed
Publication year - 2021
Publication title -
molecular genetics and genomic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.765
H-Index - 29
ISSN - 2324-9269
DOI - 10.1002/mgg3.1707
Subject(s) - missense mutation , in silico , computational biology , gene , biology , docking (animal) , genetics , single nucleotide polymorphism , genome , mutation , medicine , genotype , nursing
Background Testis expressed 19 ( TEX19 ) is a specific human stem cell gene identified as cancer‐testis antigen (CTA), which emerged as a potential therapeutic drug target. TEX19.1, a mouse paralog of human TEX19, can interact with LINE‐1 retrotransposable element ORF1 protein (LIRE1) and subsequently restrict mobilization of LINE‐1 elements in the genome. Aim This study aimed to predict the interaction of TEX19 with LIRE1 and analyze TEX19 missense polymorphisms. TEX19 model was generated using I‐TASSER and the interaction between TEX19 and LIRE1 was studied using the HADDOCK software. Methods The stability of the docking formed complex was studied through the molecular dynamic simulation using GROMACS. Missense SNPs (n=102) of TEX19 were screened for their potential effects on protein structure and function using different software. Results Outcomes of this study revealed amino acids that potentially stabilize the predicted interaction interface between TEX19 and LIRE1. Of these SNPs, 37 were predicted to play a probably damaging role for the protein, three of them (F35S, P61R, and E55L) located at the binding site of LIRE1 and could disturb this binding affinity. Conclusion This information can be verified by further in vitro and in vivo experimentations and could be exploited for potential therapeutic targets.