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Title

Comparative modeling of CCRL1, a key protein in masked immune diseases and virtual screening for finding inhibitor of this protein

 

Authors

Mohaddeseh Behjati1, Ibrahim Torktaz2, 4, Mehrdad Mohammadpour3, Gholamreza Ahmadian4*, Andrew J Easton5

 

Affiliation

1Isfahan University of Medical Sciences, Isfahan, Iran; 2Department of Biotechnology, Faculty of Advanced science and technologies, University of Isfahan, Hezarjarib St., 81746-73441, Isfahan, Iran; 3Department of Medicinal Chemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, 81746-73461, Isfahan, Iran; 4Department of Molecular Genetics, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran; 5School of Life Sciences, University of Warwick, Coventry, UK.

 

Email

gholamrezaahmadian@yahoo.ca; *Corresponding author

 

Article Type

Hypothesis

Date

Received February 22, 2012; Accepted March 08, 2012; Published April 13, 2012

 

Abstract

Human CCRL1 belongs to the family of silent chemokine receptors. This transmembrane protein plays a role in blunting function of chemokines through binding to them. This will attenuate immune responses. Interaction between CCRL1 and CCL21 determines this immune extinction. Thus inhibiting the action of this atypical chemokine seems to stimulate immune responses especially in the case of suppressed and immune deficient conditions. In this study we predicted 3D structure of CCRL1 using comparative modeling and Hiddebn Markov Model algorithm. Final predicted model optimized by Modeller v9.8 and minimized regarding energy level using UCSF chimera candidate version1.5.3. ClasPro webserver was used to find interacting residues between CCRL1 and CCL21. Interacting residues were used as target for chemical inhibitors by simulated docking study. For finding potential inhibitors, library of KEGG compounds screened and 97 obtained chemicals docked against interacting residues between CCRL1-CCL21 and MolDock was used as docking scoring function. Results indicated that Hexadecanal is a potential inhibitor of CCRL1- CCL21 interaction. Inhibition of this interaction will increase intercellular level of CCl21 and interaction between CCL21 and CCR7 causes immune potentiaiton.

 

Keywords

CCRL1, CCL21, CCR7, Docking, MolDock, Hexadecanal.

 

Citation

Behjati et al. Bioinformation 8(7): 336-340 (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.