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Effect of mutation on aggregation propensity in homology model structures of syntaxin-3 from <i style="mso-bidi-font-style:normal">Homo sapiens</i>

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Title Effect of mutation on aggregation propensity in homology model structures of syntaxin-3 from Homo sapiens
 
Creator Maheshwari, Amutha Selvaraj
Rajesh, Durairaj
Padmanabhan, Parasuraman
Archunan, Govindaraju
 
Subject Aggregation propensity
Cancer therapy
Directed evolution
Homology modeling
Membrane protein
Syntaxin-3
 
Description 335-342
Perception of molecular mechanism would provide
potent additional knowledge on mammalian membrane proteins involved in causing
diseases. In human, syntaxin-3 (STX3) is a significant apical targeting protein
in the epithelial membrane and in exocytosis process; it also acts as a vesicle
transporter by cellular receptor in neutrophils, which is crucial for protein
trafficking event. Structurally, syntaxin-3 has hydrophobic domain at carboxyl
terminus that directs itself to intra-cellular compartments. In addition, the
experimental structure of STX3 is not available and no mutational study has
been carried out with natural variants of proteins. Moreover, there is no evidence so
far for the natural variant Val286 of STX3 causing any diseases. Hence, in the present study, analyses of residue-based properties
of the homology model STX3 were carried out along with mutations at carboxyl
terminus of STX3 by implementing protein engineering and
in silico approaches. The model
structure of STX3 was constructed adopting Modeller v9.11 and the aggregation
propensity was analyzed with BioLuminate tool. The results showed that there
was reduction in aggregation propensity with point mutation at Val286, instead
of Ile, resulting into increasing the structural stability of STX3. In
conclusion, the Ccap exposed residue would be a suitable position for further
mutational studies, particularly with Val286 of STX3 in human. This approach
could gainfully be applied to STX3 for efficient drug designing which would be
a valuable target in the cancer treatment.
 
Date 2014-11-12T11:04:28Z
2014-11-12T11:04:28Z
2014-10
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/29889
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.51(5) [October 2014]