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Ayeman Amanullah

Researcher at Indian Institute of Technology, Jodhpur

Publications -  22
Citations -  451

Ayeman Amanullah is an academic researcher from Indian Institute of Technology, Jodhpur. The author has contributed to research in topics: Ubiquitin ligase & Ubiquitin. The author has an hindex of 12, co-authored 20 publications receiving 339 citations.

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E3 Ubiquitin Ligases Neurobiological Mechanisms: Development to Degeneration

TL;DR: To understand how few E3 ubiquitin ligases sense major molecular events, which are crucial for human brain development from its early embryonic stages to throughout adolescence period, is explained.
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Evidences for Piperine inhibiting cancer by targeting human G-quadruplex DNA sequences

TL;DR: In-vitro studies show that Piperine causes apoptosis-mediated cell death that further emphasizes the potential of this natural product, Piperine, as a promising candidate for targeting G-quadruplex structure and thus, acts as a potent anti-cancer agent.
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A Decade of Boon or Burden: What Has the CHIP Ever Done for Cellular Protein Quality Control Mechanism Implicated in Neurodegeneration and Aging?

TL;DR: A wide range of functionality of CHIP inside cells is explored by a detailed presentation of its co-chaperone, E3 and E4 enzyme like functions, with central focus on its protein quality control roles in neurodegenerative diseases.
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Polyphenolic flavonoid (Myricetin) upregulated proteasomal degradation mechanisms: Eliminates neurodegenerative proteins aggregation.

TL;DR: It is shown that Myricetin, a flavonoid, can eliminate various abnormal proteins from the cellular environment via modulating endogenous levels of Hsp70 chaperone and quality control (QC)‐E3 ubiquitin ligase E6‐AP and reduce the misfolded proteins inclusions, which further alleviates cytotoxicity.
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Lanosterol Suppresses the Aggregation and Cytotoxicity of Misfolded Proteins Linked with Neurodegenerative Diseases

TL;DR: It is demonstrated that treatment of lanosterol diminishes aberrant proteotoxic aggregation and mitigates their cytotoxicity via induced expression of co-chaperone CHIP and elevated autophagy and suggested that upregulation of cellular molecular chaperones, primarily using small molecules, can probably offer an efficient therapeutic approach in the future against misfolding of different disease-causing proteins and neurodegenerative disorders.