Authors

Yuan Chen

Type

Text

Type

Thesis

Advisor

Raleigh, Daniel P | Laughlin, Scott | Green, David.

Date

2015-08-01

Keywords

Chemistry

Department

Department of Chemistry.

Language

en_US

Source

This work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.

Identifier

http://hdl.handle.net/11401/77102

Publisher

The Graduate School, Stony Brook University: Stony Brook, NY.

Format

application/pdf

Abstract

Amyloid formation in vivo plays a role in the pathology of more than 25 diseases. Amyloid formation by Islet Amyloid Polypeptide (IAPP) in the pancreas is a pathophysiological feature of type-2 diabetes. Much work has been performed in order to unravel the mechanisms of IAPP amyloid formation in vitro and recent studies suggest that toxic oligomers are generated during the formation of amyloids. Thus, it may be useful to look for compounds that accelerate fibril formation and reduce the lifetime of toxic intermediates. (S)-(+)-Flurbiprofen has been previously proven to accelerate IAPP amyloid formation. Computational simulation suggested the N-terminus of IAPP plays an important role in the interaction. In order to further understand the mechanism, the effect of (S)-(+)-Flurbiprofen were tested with different mutants of IAPP. The results suggest that the overall charge of IAPP is important in the interaction between negatively charged (S)-(+)-Flurbiprofen and positively charged IAPP. Moreover, a new compound, 4-[(4-chlorophenyl) thio] thiophene-3-carboxylic acid was identified and shown to accelerate amyloid formation by IAPP. | 90 pages

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