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Title

The Potential effect of G915C polymorphism in regulating TGF-β1 transport into Endoplasmic Reticulum for cytokine production

 

Authors

Hani Susianti1*, Atma Gunawan2, Jayarani Fatimah Putri3, Basuki B Purnomo4 Kusworini Handono1 & Handono Kalim2

 

Affiliation

1Departement of Clinical Pathology, Faculty of Medicine, Brawijaya University, Malang, Indonesia; 2Departement of Internal Medicine, Faculty of Medicine, Brawijaya University, Malang, Indonesia; 3Departement of Biology, Faculty of Sciences, Brawijaya University, Malang, Indonesia; 4Department of Urology, Faculty of Medicine, Brawijaya University, Malang, Indonesia

 

Email

hanisusianti.fk@ub.ac.id; *Corresponding author

 

Article Type

Hypothesis

 

Date

Received July 17, 2014; Accepted July 26, 2014; Published August 30, 2014

 

Abstract

The TGF-β1 cytokine concentration is known to be higher in nephritis with implied Lupus Nephritis severity. The production of TGF-β1 cytokine is associated with G915C polymorphism. Therefore, it is of interest to study G915C polymorphism. The G915C polymorphism changes codon 25 which encodes arginine into proline in the signal peptide of TGF-β1. The amino acid substitution affects signal peptide properties that may inhibit the transport of TGF-β1 into the endoplasmic reticulum and eventually decline the cytokine production. Hence, the effect of G915C polymorphism on the properties of the signal peptide, the ability of TGF-β1 transport into the endoplasmic reticulum and the concentrations of urinary TGF-β1 in Lupus Nephritis patients was studied. The arginine substitution into proline decreased the polarity of the signal peptide for TGF-β1. The increased hydrophobicity with increased binding energy of the signal peptide for TGF-β1 to Signal Recognition Particle (SRP) and translocon is shown. This implies decreased protein complex stability in potentially blocking the transport of TGF-β1 into the endoplasmic reticulum. This transport retention possibly hampers the synthesis and maturation of TGF-β1 leading to decreased cytokine production.

 

Citation

Susianti et al. Bioinformation 10(8): 487-490 (2014)
 

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.