NDLI: Restoration of p53–DNA interaction loss upon R273H mutation by CP-31398: an ultra accelerated quantum chemical molecular dynamics approach

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Restoration of p53–DNA interaction loss upon R273H mutation by CP-31398: an ultra accelerated quantum chemical molecular dynamics approach

Content Provider	Springer Nature Link
Author	Rauf, Shah Md. Abdur Sahu, Kamlesh Kumar Tsuboi, Hideyuki Hatakeyama, zomu Endou, Akira Takaba, Hiromitsu Del Carpio, Carlos A. Miyamoto, Akira
Copyright Year	2010
Abstract	The mutation of Arginine273 to Histidine in the DNA binding domain of p53 is one of the most common mutations found in human cancer. Though R273H mutation retains wild-type conformation, the sequence-specific DNA binding is impaired and subsequently lack of trans-activation function and the ability to suppress cell growth. CP-31398 can restore DNA binding activity to mutant p53 has shown by a chromatin immunoprecipitation assay but the underlying mechanism at atomistic level is not well understood. Our aim is to investigate theoretically the effect of R273H mutation on DNA binding and the mechanism of restoration of DNA binding by CP-31398, using docking and newly developed ultra accelerated quantum chemical molecular dynamics. Our results show that due to R273H mutation, p53 lost two hydrogen bonds with DNA at the binding site during interaction. CP-31398 helps to reestablish the lost hydrogen bond interactions at p53–DNA binding site, thus restore DNA binding activity and transcriptional activity. This will provide a deeper insight to structure-based drug designing.
Starting Page	239
Ending Page	244
Page Count	6
File Format	PDF
ISSN	10542523
Journal	Medicinal Chemistry Research
Volume Number	21
Issue Number	2
e-ISSN	15548120
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-12-25
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Quantum chemical molecular dynamics Docking p53-DNA interaction Mutation Cell Biology Pharmacology/Toxicology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Pharmacology, Toxicology and Pharmaceutics

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