Abstract

ABSTRACTFirst Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms, helping early-career researchers promote themselves alongside their papers. Kriti Chaplot is first author on ‘SOD1 activity threshold and TOR signalling modulate VAP(P58S) aggregation via reactive oxygen species-induced proteasomal degradation in a Drosophila model of amyotrophic lateral sclerosis’, published in DMM. Kriti is a PhD student in the lab of Dr Girish Ratnaparkhi at the Indian Institute of Science Education and Research, Pune, India. Her main research interest is delineating cellular mechanisms that perturb aggregation in neurodegenerative diseases.

Highlights

  • “[...] I have identified one such process that acts as a garbage disposal machine in the neuron, helping to reduce a particular kind of mutant protein aggregate.”

  • Kriti Chaplot approved amyotrophic lateral sclerosis (ALS) drug that works by altering the levels of reactive oxygen species (ROS)

  • What are the potential implications of these results for your field of research? The study highlights a functional interaction between two diseasecausing loci in ALS, namely Sod1 and VAP

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Summary

Introduction

“[...] I have identified one such process that acts as a garbage disposal machine in the neuron, helping to reduce a particular kind of mutant protein aggregate.”. Kriti Chaplot approved ALS drug that works by altering the levels of ROS. The study highlights a functional interaction between two diseasecausing loci in ALS, namely Sod1 and VAP. Our study serves as an example of how aggregates of one protein (mutant VAP) are regulated by the other (SOD1 activity).

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Conclusion

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