Marine Groslambert

ORCID: 0000-0003-3258-0268
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About
Contact & Profiles
Research Areas
  • Inflammasome and immune disorders
  • IL-33, ST2, and ILC Pathways
  • Gout, Hyperuricemia, Uric Acid
  • Ubiquitin and proteasome pathways
  • Toxoplasma gondii Research Studies
  • Eicosanoids and Hypertension Pharmacology
  • French Urban and Social Studies
  • Sphingolipid Metabolism and Signaling
  • Climate Change and Geoengineering
  • Sustainable Industrial Ecology
  • Sustainability and Climate Change Governance
  • Immunotherapy and Immune Responses
  • Heme Oxygenase-1 and Carbon Monoxide

Centre National de la Recherche Scientifique
2016-2024

Centre International de Recherche en Infectiologie
2016-2024

École Normale Supérieure de Lyon
2016-2024

Université Claude Bernard Lyon 1
2016-2024

Inserm
2016-2024

Institut de Génomique Fonctionnelle de Lyon
2018

MRC University of Glasgow Centre for Virus Research
2015

Laboratoire Reproduction et Développement des Plantes
2014

Abstract NLRP3 controls the secretion of inflammatory cytokines IL-1β/18 and pyroptosis by assembling inflammasome. Upon coordinated priming activation stimuli, recruits NEK7 within hetero-oligomers that nucleate ASC caspase-1 filaments, but apical molecular mechanisms underlying inflammasome assembly remain elusive. Here we show recruitment to is controlled phosphorylation status S803 located interaction surface, in which phosphorylated upon later dephosphorylated activation. Phosphomimetic...

10.1038/s41467-021-26142-w article EN cc-by Nature Communications 2021-10-06

NLRP3-associated autoinflammatory disease is a heterogenous group of monogenic conditions caused by NLRP3 gain-of-function mutations. The poor functional characterization most variants hinders diagnosis despite efficient anti-IL-1 treatments. Additionally, while controlled priming and activation signals, gain-of-functions have only been investigated in response to priming. Here, we characterize 34 vitro, evaluating their activity upon induction, priming, and/or sensitivity four inhibitors....

10.1084/jem.20231200 article EN cc-by The Journal of Experimental Medicine 2024-03-26

Abstract NLRP3 inflammasome plays a key role in the intracellular activation of caspase‐1, processing pro‐inflammatory interleukin‐1β (IL‐1β), and pyroptotic cell death cascade. The overactivation is implicated pathogenesis autoinflammatory diseases, known as cryopyrin‐associated periodic syndromes (CAPS), progression several such atherosclerosis, type‐2 diabetes, gout, Alzheimer's disease. In this study, synthesis acrylamide derivatives their pharmaco‐toxicological evaluation potential...

10.1002/cmdc.201600055 article EN ChemMedChem 2016-03-17

Covalent linkage to members of the small ubiquitin-like (SUMO) family proteins is an important mechanism by which functions many cellular are regulated. Sumoylation has roles in control protein stability, activity and localization, involved regulation transcription, gene expression, chromatin structure, nuclear transport RNA metabolism. also linked, both positively negatively, with replication different viruses terms modification viral modulation sumoylated that influence efficiency...

10.1371/journal.ppat.1005059 article EN cc-by PLoS Pathogens 2015-07-22

Abstract NLRP3-associated autoinflammatory disease (NLRP3-AID or CAPS) is an heterogenous group of monogenic autoinflammations associated with NLRP3 gain-of-function mutations. The poor functional characterization most variants a barrier to diagnosis although patients can be efficiently treated anti-IL-1 approaches. In addition, while inflammasome controlled by coordinated priming and activation signals, gain-of-functions have been only investigated in response priming. Here, we functionally...

10.1101/2023.09.22.558949 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-09-22
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