A minimal titration modelization of the ...
Type de document :
Pré-publication ou Document de travail
Titre :
A minimal titration modelization of the mammalian dynamical heat shock response
Auteur(s) :
Aude, Sivéry [Auteur]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
Courtade, Emmanuel [Auteur]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
Courtade, Emmanuel [Auteur]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
Mot(s)-clé(s) en anglais :
cell stress
mathematical modeling
chaperones
mammalian heat shock response
heat shock proteins
signaling pathways
mathematical modeling
chaperones
mammalian heat shock response
heat shock proteins
signaling pathways
Discipline(s) HAL :
Physique [physics]/Physique [physics]/Biophysique [physics.bio-ph]
Résumé en anglais : [en]
Environmental stress, such as oxidative or heat stress, induces the activation of the Heat Shock Response (HSR) which leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular chaperones to ...
Lire la suite >Environmental stress, such as oxidative or heat stress, induces the activation of the Heat Shock Response (HSR) which leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular chaperones to maintain proteostasis. Even if the main heat shock response partners are well known, a detailed description of the dynamical properties of the HSR network is still missing. In this study, we derive a minimal mathematical model of cellular response to heat shock that reproduces available experimental data sets both on transcription factor activity and cell viability. This simplistic model highlights the key mechanistic processes that rule the HSR network and reveals (i) the titration of Heat Shock Factor 1 (HSF1) by chaperones as the guiding line of the network, (ii) that protein triage governs the fate of damaged proteins and (iii) three different temperature regimes describing normal, acute or chronic stress.Lire moins >
Lire la suite >Environmental stress, such as oxidative or heat stress, induces the activation of the Heat Shock Response (HSR) which leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular chaperones to maintain proteostasis. Even if the main heat shock response partners are well known, a detailed description of the dynamical properties of the HSR network is still missing. In this study, we derive a minimal mathematical model of cellular response to heat shock that reproduces available experimental data sets both on transcription factor activity and cell viability. This simplistic model highlights the key mechanistic processes that rule the HSR network and reveals (i) the titration of Heat Shock Factor 1 (HSF1) by chaperones as the guiding line of the network, (ii) that protein triage governs the fate of damaged proteins and (iii) three different temperature regimes describing normal, acute or chronic stress.Lire moins >
Langue :
Anglais
Source :
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- http://arxiv.org/pdf/1510.00135
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- https://hal.archives-ouvertes.fr/hal-01207107/document
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- https://hal.archives-ouvertes.fr/hal-01207107/document
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- document
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- Thommen.pdf
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- 1510.00135
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