Abstract
DC-SIGN receptor articulated by macrophages and dendritic cells is encoded by CD209 gene and plays a role to activate and proliferate the T-lymphocytes in response of virus attack. The dysfunctional activity of DC-SIGN receptor because of missense SNPs can lead to cause dengue haemorrhage fever, HIV-1 infection etc. Out of 11 transcripts of CD209, all missense SNPs of canonical transcript were retrieved from Ensembl database and evaluated by their deleteriousness by using Polyphen-2, PMut, SIFT, MutPred, PROVEAN and PhD-SNP together with stimulation of its complete 3D structure. 10 nsSNPs were chosen depending on both the significance value of nsSNP and their prediction among SNPs evaluating servers which are based on different algorithms. Moreover, the position and native role of 10 nsSNPs in wild 3D model has been described which assist to acknowledge their importance. This study urges the researcher’s community to experimentally validate these SNPs and their association in causing the diseases like dengue fever, Tuberculosis etc.
Highlights
CD209 gene encodes dendritic cell-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) receptor which is articulated by macrophages and dendritic cells [1,2,3] that participant in innate immune response
The C-lectin domain of CD209 is the core site for recognition and binding of carbohydrate moieties of pathogens and our results suggested that mostly deleterious nsSNPs were annotated in C-lectin domain only, where wild type residues can develop interactions with ligands as well as may involve maintaining the conformation. we assessed the interactions developed by substituted residues with neighbouring amino acids
The role of missense single nucleotide polymorphism (SNPs) leading to development of several diseases has always been under discussion demanding their rapid identification to understand the origin of pathologies
Summary
CD209 gene encodes dendritic cell-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) receptor which is articulated by macrophages and dendritic cells [1,2,3] that participant in innate immune response. Several studies have described an association of single nucleotide polymorphism (SNPs) and human diseases. Coding SNPs are either synonymous, having a nucleotide transition that does not bring about the amino acid shift, or non-synonymous (nsSNPs), a nucleotide transition concordant with the amino acid shift. NsSNPs. Coding SNPs are either synonymous, having a nucleotide transition that does not bring about the amino acid shift, or non-synonymous (nsSNPs), a nucleotide transition concordant with the amino acid shift. A small fraction of nsSNPs is deleterious which are always been a great interest for scientific community as being associated to cause various complex diseases in humans [9,10,11]
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