©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.
OJBTM
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
ABSTRACT
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.
FULL-TEXT(SUBSCRIPTION) OR PURCHASE ARTICLE