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Last update: May 2021

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Human Nutrition Unit

Zone de texte éditable et éditée et rééditée

To tackle

   

Improving Patient Health by correcting AA/protein homeostasis in chronic diseases



    Inhibition of muscle atrophy during catabolic states
Contractile proteins represent a major AA reservoir of the organism and their degradation by the ubiquitin proteasome system (UPS) requires 2 classes of enzymes...
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Lutter_ImageProjetDTCP


Contractile proteins represent a major AA reservoir of the organism and their degradation by the ubiquitin proteasome system (UPS) requires 2 classes of enzymes that, through their interaction, confer targeting selectivity: the E2s (≈40 members) generally bring the catalytic activity and the E3s (> 700 members) recognize the substrate, an E2 being able to interact with several E3s and vice versa.

There is currently no treatment to limit muscle wasting that occurs during catabolic states. Our goal is to better understand the degradation of contractile proteins by the UPS to open new avenues for fighting against muscle atrophy: 

  • We aim to identify among the 14 poorly characterized muscular E2s, those involved in muscle atrophy. We already identified the E2 enzymes functionally interacting with MuRF1, the only E3 known to target contractile proteins.
  • Since MuRF1 is the major actor of contractile protein degradation, we are currently looking for MuRF1 pharmacological inhibitors.


ReferencesInvestigators
Agnès Claustre, Cécile Coudy-Gandilhon, Mélodie Malige, Dulce Peris-Moreno, Cécile Polge, Daniel Taillandier

Tackle_Pi-coll-fundings-ProjetDTCP




    Nutrient-medication interaction
We investigate the metabolic side effects of paracetamol treatment on amino acids/proteins homeostasis.
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Hypothesis
The eIF2α-ATF4 signaling pathway could contribute to paracetamol-induced sarcopenia



Context
Paracetamol is the first intention treatment of chronic pain. Its detoxification  occurs in the liver and utilises sulfates and glutathione, both of which are issued from cysteine (Cys) . The detoxification-induced siphoning of cysteine can reduce the bioavailbility of cysteine and aggravate sarcopenia.

Project
We aim to determine the role of the eIF2a-ATF4 signaling pathway could contribute to paracetamol-induced sarcopenia.

Perspectives
To optimize nutritional sulfur amino acid supplementation and methionine/cysteine ratio in order to promote the healthiest metabolic response to a large range of paracetamol treatments.



References

Investigators
Alain Bruhat, Valérie Cararro, Isabelle Papet