Title

Authors

Affiliation

Department of Bioinformatics and Biotechnology, International Islamic University, Women Campus, Sector H-10, Islamabad, Pakistan

Email

shagufta.kanwal@iiu.edu.pk; *Corresponding authors

Article Type

Hypothesis

Date

Received January 06, 2012; Accepted 17, 2012; Published February 03, 2012

Motivation: Rhodopsin is a visual pigment present in rod cells of retina. It belongs to GPCR family and involves photoisomerization of 11-cis-retinal to all-trans-retinal isomers, conformational changes in rhodopsin and signal transduction cascade to generate a nerve impulse. This signaling pathway has been targeted to eliminate the effect of a mutation (Gly90àAsp) responsible for abnormal activation of G-protein without retinal conformations in the absence of light leading to congenital night blindness. A theoretical model of rhodopsin with induced mutation has been deliberated in order to find potential ligands which can offset this mutational effect. The binding interactions between the target mutated rhodopsin model and potential ligands have been predicted with the help of molecular docking. The results indicated strong functional benefits of ligands as an inhibitor and an agonist for mutated rhodopsin model. Therefore, we propose a new visual cascade model which can initiate the normal signaling of rhodopsin mutant with the help of proposed ligands and can provide a hope for vision in future.

Keywords

Molecular Docking, Arrestin, Rutinoside, Agonist, Cyanidin, Congenital Night Blindness, Rhodopsin

Citation

Kanwal et al. Bioinformation 8(3): 128-133 (2012)
 

Edited by

P Kangueane

ISSN

0973-2063

Publisher

Biomedical Informatics

License

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.