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Parvez Alam

Researcher at Aligarh Muslim University

Publications -  54
Citations -  2830

Parvez Alam is an academic researcher from Aligarh Muslim University. The author has contributed to research in topics: Human serum albumin & Amyloid. The author has an hindex of 31, co-authored 49 publications receiving 2358 citations.

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Elucidating the interaction of limonene with bovine serum albumin: a multi-technique approach

TL;DR: The present study will be helpful in understanding the binding mechanism of limonene and associated stability and conformational changes.
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Vitamin k3 inhibits protein aggregation: Implication in the treatment of amyloid diseases

TL;DR: It is demonstrated that vitamin k3 significantly inhibits fibril formation as well as the inhibitory effect is dose dependent manner, paving the way for discovery of other small molecules that may exert similar effect against amyloid formation and its associated neurodegenerative diseases.
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Biophysical and molecular docking insight into the interaction of cytosine β-D Arabinofuranoside with Human serum albumin

TL;DR: This study will be helpful to understand the binding mechanism of cytosine β-D arabinofuranoside with HSA and associated alterations and help understand the topology of protein in absence and presence of drug.
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Protein aggregation: From background to inhibition strategies.

TL;DR: Better therapeutics could be developed by using cocktail of small molecule inhibitors for the treatment of amyloid diseases by summarizes the background information on the protein folding, misfolding, cellular strategies against protein aggregation, factors affecting protein aggregation and mechanism of protein aggregation.
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Ascorbic acid inhibits human insulin aggregation and protects against amyloid induced cytotoxicity.

TL;DR: It is demonstrated that ascorbic acid significantly inhibits the fibrillation of HI in a dose-dependent manner and Interestingly ascorBic acid destabilise the preformed amyloid fibrils and protects human neuroblastoma cell line (SH- SY5Y) against amyloids induced cytotoxicity.