Stress priming and thermotolerance model - Pfeuty et al. 2021

ABSTRACT: The model describes cellular adaptation to proteotoxic stress through four dynamical variables: protein damage, cell survival, molecular chaperone mRNA and molecular chaperone protein. Heat increases the production of misfolded proteins, which are either degraded or repaired by chaperones. Accumulated damage decreases cell survival and also activates chaperone transcription through a negative-feedback mechanism representing HSF1-mediated regulation. The induced increase in chaperone abundance during a first sublethal heat shock can protect cells against a subsequent stress, thereby reproducing thermotolerance and allowing the effects of priming temperature, duration and recovery time to be explored.

SUBMITTER: Quentin Thommen  

PROVIDER: MODEL2608180005 | BioModels | 2026-09-02

REPOSITORIES: BioModels