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The Plymouth Student Scientist

Authors

Riya Roychan

Document Type

Biomedical and Healthcare Sciences Articles

Abstract

Autophagy is a fundamental cellular process that maintains homeostasis by the degradation of damaged organelles and proteins. It plays crucial roles in cellular remodelling, development, and disease progression. These roles apply to the study of neurodegenerative diseases which is heavily linked to the toxicity produced by unwarranted accumulation of cellular material. A key player in autophagy is LC3, which translocate to autophagosomal membranes during the process. Detecting fluorescently labelled LC3-II through immunofluorescence provides a valuable method for assessing autophagy levels in samples. In a similar premise p62, also known as sequestosome-1 (SQSTM-1), is an adaptor between LC3 and ubiquitinated substrates, facilitating their incorporation into autophagosomes for degradation. Consequently, p62 levels can reflect autophagic activity and this study explores the viability of the protein as an autophagy biomarker. Using a variety of autophagy inhibitors, autophagic flux could be assessed and a comparison could be made between the response to the inhibition between LC3 and p62. The absence of statistically significant results in any of the test markers, whether it is the inhibitors in immunofluorescence, or the western blotting results does not support the original hypothesis. Consequently, this study concludes that p62 is unsuitable as an autophagy biomarker. Even though p62 has been extensively studied as a biomarker, it remains controversial. Further investigations are required to clarify its role and address any technical challenges whilst for now, LC3 remains the gold standard biomarker. However, understanding p62’s nuances and alternative functions could potentially enhance our understanding of autophagy dynamics.

Publication Date

2025-07-29

Publication Title

The Plymouth Student Scientist

Volume

18

Issue

1

ISSN

1754-2383

Deposit Date

2025-07-29

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

Available for download on Wednesday, July 30, 2025

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