BACK TO CONTENTS   |    PDF   |    PREVIOUS   |    NEXT

Title

Docking studies and network analyses reveal capacity of compounds from Kandelia rheedii to strengthen cellular immunity by interacting with host proteins during tuberculosis infection

 

Authors

Aubhishek Zaman

 

Affiliation

Molecular Biology Laboratory, Department of Biochemistry and Molecular Biology and Department of Genetic Engineering and Biotechnology, University of Dhaka, Dhaka-1000, Bangladesh.

 

Email

aubhishek@gmail.com; *Corresponding author

 

Article Type

Hypothesis

 

Date

Received October 07, 2012; Accepted October 15, 2012; Published October 31, 2012

Abstract

Kandelia rheedii (locally known as Guria or Rasunia), widely found and used in Indian subcontinent, is a well-known herbal cure to tuberculosis. However, neither the mechanism nor the active components of the plant extract responsible for mediating this action has yet been confirmed. Here in this study, molecular interactions of three compounds (emodin, fusaric acid and skyrin) from the plant extract with the host protein targets (casein kinase (CSNK), estrogen receptor (ERBB), dopamine -hydroxylase (DBH) and glucagon receptor (Gcgr)) has been found. These protein targets are known to be responsible for strengthening cellular immunity against Mycobacteria tuberculosis. The specific interactions of these three compounds with the respective protein targets have been discussed here. The insights from study should further help us designing molecular medicines against tuberculosis.

 

Keywords

Kandelia rheedii, Emodin, Fusaric acid, Skyrin, Casein kinase, Estrogen receptor, Dopamine beta hydroxylase, Glucagon receptor

 

Citation

Zaman, Bioinformation 8(21): 1012-1020 (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.