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

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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 Torktaz^{2, 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.