UNH - Unité de Nutrition Humaine
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Daniel Taillandier
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Taillandier Daniel
daniel.taillandier@inrae.fr
04 73 62 48 44
INRAE
PROTEOSTASIS
Researcher

Research activity

The long-term goal of my work is to preserve muscle mass in situations of protein wasting. Within the Proteolysis team, I initially conducted fundamental work on the characterization of protein degradation mechanisms involved in the skeletal muscle contractile system (alpha-actin, the most abundant contractile protein, and telethonin, which plays a major role in stabilizing the sarcomeric structure). Furthermore, the E3 ligase enzyme MuRF1 has been shown to be the key player in targeting contractile proteins. These results are fundamental to developing innovative strategies to block or limit muscle protein wasting during multiple catabolic states.

The main strategy we are implementing to combat muscle atrophy involves targeting enzymes of the Ubiquitin Proteasome proteolytic system. More specifically, our research has identified E2-MuRF1 enzyme pairs responsible for the degradation of contractile proteins. We are currently working to identify pharmacological drugs capable of preserving muscle mass during catabolic situations.

The second component of my research is a translational project made sustainable thanks to a long-term collaboration with the Nephrology Department of the Clermont-Ferrand University Hospital. We were thus able to identify blood markers of muscle atrophy in patients with kidney failure or cancer that can be used in a hospital setting. These major results have been patented. A clinical test to assess/predict the catabolic state of patients is currently being developed with the support of Clermont-Auvergne Innovation.

Most notable publications

  • Muscle actin is polyubiquitinylated in vitro and in vivo and targeted for breakdown by the E3 ligase MuRF1. Polge C, Heng AE, Jarzaguet M, Ventadour S, Claustre A, Combaret L, Béchet D, Matondo M, Uttenweiler-Joseph S, Monsarrat B, Attaix D, Taillandier D. FASEB J. 2011 Nov;25(11):3790-802. doi: 10.1096/fj.11-180968
  • A muscle-specific MuRF1-E2 network requires stabilization of MuRF1-E2 complexes by telethonin, a newly identified substrate. Polge C, Cabantous S, Deval C, Claustre A, Hauvette A, Bouchenot C, Aniort J, Béchet D, Combaret L, Attaix D, Taillandier D. J Cachexia Sarcopenia Muscle. 2018 Feb;9(1):129-145. doi: 10.1002/jcsm.12249.
  • UBE2E1 Is Preferentially Expressed in the Cytoplasm of Slow-Twitch Fibers and Protects Skeletal Muscles from Exacerbated Atrophy upon Dexamethasone Treatment. Cells 2018, 7, 214. Polge C, Aniort J, Armani A, Claustre A, Coudy-Gandilhon C, Tournebize C, Deval C, Combaret L, Béchet D, Sandri M, Attaix D, Taillandier D. Cells. 2018 Dec 4;7(12):242. doi: 10.3390/cells7120242.
  • Muscle wasting in patients with end-stage renal disease or early-stage lung cancer: common mechanisms at work. Aniort J, Stella A, Philipponnet C, Poyet A, Polge C, Claustre A, Combaret L, Béchet D, Attaix D, Boisgard S, Filaire M, Rosset E, Burlet-Schiltz O, Heng AE, Taillandier D. J Cachexia Sarcopenia Muscle. 2019 Apr;10(2):323-337. doi: 10.1002/jcsm.12376.
  • UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin. Peris-Moreno D, Malige M, Claustre A, Armani A, Coudy-Gandilhon C, Deval C, Béchet D, Fafournoux P, Sandri M, Combaret L, Taillandier D, Polge C. Cells. 2021 Aug 3;10(8):1974. doi: 10.3390/cells10081974.

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PROTEOSTASIS