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Related Experiment Video

Updated: Jul 17, 2026

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Published on: April 13, 2018

Reduced eIF2alpha phosphorylation and increased proapoptotic proteins in aging.

Syed G Hussain¹, Kolluru V A Ramaiah

¹Department of Biochemistry, University of Hyderabad, Hyderabad 500 046, AP, India.

Biochemical and Biophysical Research Communications

|February 16, 2007

Summary

Aging reduces eukaryotic initiation factors (eIFs) and S6 phosphorylation in rat tissues. Young tissues show better endoplasmic reticulum (ER) stress adaptation, which declines with age.

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Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

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Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

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Published on: September 7, 2021

Area of Science:

Molecular Biology
Cellular Aging
Biochemistry

Background:

Chronological aging is associated with decreased protein synthesis and cellular stress.
Eukaryotic initiation factors (eIFs) regulate protein translation, a process crucial for cellular function.
Endoplasmic reticulum (ER) stress is implicated in aging and age-related diseases.

Purpose of the Study:

To investigate the changes in protein synthesis machinery and ER stress response during aging in rat tissues.
To determine the role of eIF2alpha phosphorylation and its regulatory kinases/phosphatases in the aging process.
To elucidate the adaptive mechanisms of ER stress in young versus aged tissues.

Main Methods:

Quantitative analysis of eIFs, ribosomal protein S6, eIF2alpha kinases (PKR, PERK), eIF2B, ATF4, BiP, GADD34, CHOP, and phospho JNK levels in young and aged rat tissues.
Assessment of eIF2alpha phosphorylation status.
Evaluation of kinase activity and ER stress markers.

Main Results:

Aged rat tissues showed reduced levels and phosphorylation of eIFs and S6.
Elevated levels of eIF2alpha kinases (PKR, PERK) were observed in aged tissues, but their activity was not increased.
Young tissues exhibited higher eIF2B, ATF4, and BiP levels, indicating a more robust ER stress adaptive response, which declined in aged tissues.
Aged tissues had increased GADD34, CHOP, and phospho JNK, suggesting impaired ER stress handling and a pro-apoptotic shift.

Conclusions:

Aging leads to a decline in protein synthesis initiation and adaptive ER stress mechanisms in rat tissues.
Young tissues possess a more efficient ER stress response system that diminishes with chronological aging.
The observed changes suggest that impaired ER stress handling contributes to cellular dysfunction during aging.