©1996-2016. All Rights Reserved. Online Journal of Bioinformatics . You may not store these pages in any form except for your own personal use. All other usage or distribution is illegal under international copyright treaties. Permission to use any of these pages in any other way besides the before mentioned must be gained in writing from the publisher. This article is exclusively copyrighted in its entirety to OJB publications. This article may be copied once but may not be, reproduced or re-transmitted without the express permission of the editors. This journal satisfies the refereeing requirements (DEST) for the Higher Education Research Data Collection (Australia). Linking: To link to this page or any pages linking to this page you must link directly to this page only here rather than put up your own page.
Online Journal of Bioinformatics ©
Volume 16 (2): 144-155, 2015.
In silico model simulation docking of tyrosine kinase inhibiting leukemia quinazolines.
Raju Bathula, Shobha Rani Satla
Centre for Pharmaceutical Sciences, Institute of Science and Technology, JNTUH, Kukatpally, HYD-85. India
Bathula R, Rani Satla S., In silico model simulation docking of tyrosine kinase inhibiting leukemia quinazolines, Onl J Bioinform., 16 (2): 144-155, 2015. Acute myeloid Leukemia cancer of blood and bone marrow is characterized by abnormal proliferation of white blood cells. Genes regulating hematopoiesis affect susceptibility to leukemia. Tyrosine kinase plays an important role in cell proliferation and differentiation. We generated a 3D model of the enzyme using 1Z3S as a template and Modeller7v7, verified by Procheck and Verify 3D. After energy minimization, the 3D structure of tyrosine was compared with a template. Molecular docking of 6-thiogunaosine (6-TG) analogs was performed on the ATR1 model and inhibitors were selected based on docking performance. Results showed that residues GSN235, AsN257, and ILE289 in the enzyme were essential for hydrogen bonding with analogues. The data suggested that interactions of these residues may be necessary for stronger binding of tyrosine kinase with synthetized molecules.
KEY WORDS: Acute mylenoid Leukemia, Tyrosine Kinase, Modelling, Molecular Dynamics, Docking studies.