Arthur Aubry

ORCID: 0000-0002-4344-1194
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About
Contact & Profiles
Research Areas
  • Ocular Oncology and Treatments
  • Cancer-related Molecular Pathways
  • Ubiquitin and proteasome pathways
  • Lung Cancer Research Studies
  • Cytokine Signaling Pathways and Interactions
  • Protein Degradation and Inhibitors
  • Lung Cancer Treatments and Mutations
  • Neuroblastoma Research and Treatments
  • RNA Interference and Gene Delivery
  • CAR-T cell therapy research
  • Bacteriophages and microbial interactions
  • Cancer-related gene regulation
  • Hippo pathway signaling and YAP/TAZ
  • Prostate Cancer Treatment and Research
  • Immune Cell Function and Interaction
  • interferon and immune responses
  • Glioma Diagnosis and Treatment

Lunenfeld-Tanenbaum Research Institute
2017-2023

Sinai Health System
2020-2023

Mount Sinai Hospital
2019-2023

Université de Toulouse
2015-2023

Université Toulouse III - Paul Sabatier
2015-2023

University of Toronto
2019-2023

Centre Hospitalier Universitaire de Toulouse
2023

RB1 loss (RB1null) or MYCN amplification (MYCNamp ) in fetal human retina causes retinoblastoma. SKP2 kills RB1null cells, but small molecule inhibitors remain unexplored therapeutically. Whether is synthetic lethal MYCNamp retinoblastoma unclear. the substrate recognition component of two Cullin-RING Ligase complexes (CRL1SKP2/SCFSKP2, and CRL4SKP2), a family multiprotein E3 ubiquitin ligases. NEDD8 activating enzyme (NAE) required for Cullin neddylation thus CRL activation. Here, we show...

10.1038/s41420-020-0237-8 article EN cc-by Cell Death Discovery 2020-01-20

STAT1 and IRF1 collaborate to induce interferon-γ (IFNγ) stimulated genes (ISGs), but the extent which they act alone or together is unclear. The effect of single nucleotide polymorphisms (SNPs) on in vivo binding also largely unknown. We show that binds at proximal distant ISG sites twice as often STAT1, increasing sixfold MHC class I locus. almost always bound with IRF1, while most events were isolated. Dual remote enhancers distinguished ISGs responsive IFNγ versus cell-specific resistant...

10.1186/s12867-017-0084-1 article EN cc-by BMC Molecular Biology 2017-03-09

Abstract Local intravitreal or intra-arterial chemotherapy has improved therapeutic success for the pediatric cancer retinoblastoma (RB), but toxicity remains a major caveat. RB initiates primarily with RB1 loss or, rarely, MYCN amplification, critical downstream networks are incompletely understood. We set out to uncover perturbed molecular hubs, identify synergistic drug combinations target these vulnerabilities, and expose overcome resistance. applied dynamic transcriptomic analysis...

10.1038/s41388-020-1372-7 article EN cc-by Oncogene 2020-06-22

The neddylation inhibitor MLN4924/Pevonedistat is in clinical trials for multiple cancers. Efficacy generally attributed to cullin RING ligase (CRL) inhibition, but the contribution of non-CRL targets unknown. Here, CRISPR screens map MLN4924-monotherapy sensitivity retinoblastoma a classic DNA damage-induced p53/E2F3/BAX-dependent death effector network, which synergizes with Nutlin3a or Navitoclax. In monotherapy-resistant cells, MLN4924 plus standard-of-care topotecan overcomes...

10.1016/j.celrep.2023.112925 article EN cc-by Cell Reports 2023-08-01

Abstract ALK is a receptor tyrosine kinase with an oncogenic role in various types of human malignancies. Despite constitutive activation the through gene alterations, such as chromosomal translocation, amplification or mutation, treatments inhibitors invariably lead to development resistance. Aiming develop new tools for targeting, we took advantage our previous demonstration identifying dependence receptor, implying that absence ligand kinase-inactive triggers enhances apoptosis. Here,...

10.1038/cddis.2015.102 article EN cc-by Cell Death and Disease 2015-05-07
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