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Systematic evaluation of the role of IRE1 in the modulation of chronological aging via ER -mitochondrial crosstalk during chronic ER stress

Implementing Organization

Birla Institute of Technology
Principal Investigator
Dr. shuvadeep Maity
Birla Institute of Technology

About

Chronic endoplasmic reticulum (ER) stress is a key regulator of diseases like diabetes, neurodegeneration, and cancer. However, our understanding of ER stress pathways is limited, especially in the context of chronic ER stress, which is physiologically more relevant to late-onset diseases like neurodegenerative diseases. A recent study found that ER stress sensor Inositol-requiring enzyme 1 (IRE1) mediated modulation of metabolic flux results in altered lifespan during calorie restriction. The known molecular modulator of aging is also highly conserved. The current project aims to systematically dissect the effect of chronic ER stress in aging and the role of IRE1 in the modulation of aging via ER-mitochondrial communication. The project will use a previously established budding yeast-based in vivo chronic ER stress system to determine the IRE1-dependent effect over aging, elucidate the ER-mitochondrial crosstalk during chronic ER stress via IRE1, and identify the IRE1 dependent signaling network during chronic ER stress. The goal is to identify the conserved molecular route of regulation related to aging and age-related diseases, and identify potential therapeutic targets for chronic ER stress-related diseases. The proteomics data will help identify IRE1-mediated signaling routes, allowing for the identification of conserved molecular routes of regulation related to aging and age-related diseases.
Funding Organization
Funding Organization
Science and Engineering Research Board (SERB), New Delhi
Anusandhan National Research Foundation (ANRF)
Quick Information
Area of Research
Life Sciences & Biotechnology
Start Year
2022
End Year
2024
Sanction Amount
₹ 28.16 L
Status
Completed
Output
No. of Research Paper
00
Technologies (If Any)
00
No. of PhD Produced
N/A
Startup (If Any)
00
No. of Patents
Filed :00
Grant :00
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