Yann Chéli

ORCID: 0000-0001-9839-4332
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About
Contact & Profiles
Research Areas
  • melanin and skin pigmentation
  • Melanoma and MAPK Pathways
  • Advanced biosensing and bioanalysis techniques
  • Photochromic and Fluorescence Chemistry
  • RNA regulation and disease
  • Platelet Disorders and Treatments
  • Click Chemistry and Applications
  • Cell Adhesion Molecules Research
  • Immunotherapy and Immune Responses
  • Cutaneous Melanoma Detection and Management
  • Protein Degradation and Inhibitors
  • Telomeres, Telomerase, and Senescence
  • Immune Cell Function and Interaction
  • Cancer Cells and Metastasis
  • Ocular Oncology and Treatments
  • CRISPR and Genetic Engineering
  • Cytokine Signaling Pathways and Interactions
  • Lower Extremity Biomechanics and Pathologies
  • Viral Infectious Diseases and Gene Expression in Insects
  • Venomous Animal Envenomation and Studies
  • Blood disorders and treatments
  • Chronic Lymphocytic Leukemia Research
  • bioluminescence and chemiluminescence research
  • Cancer-related gene regulation
  • Virus-based gene therapy research

Inserm
2012-2024

Centre Méditerranéen de Médecine Moléculaire
2009-2024

Observatoire de la Côte d’Azur
2020-2024

Université Côte d'Azur
2009-2021

Discovery Institute
2015-2017

Sanford Burnham Prebys Medical Discovery Institute
2015-2017

KU Leuven
2016

Center for Human Genetics
2016

Scripps Research Institute
2004-2013

Centre Hospitalier Universitaire de Nice
2010

Abstract T-cells play a crucial role in progression of autoimmunity, including vitiligo, yet the initial steps triggering their activation and tissue damage remain unknown. Here we demonstrate increased presence type-1 innate lymphoid cells (NK ILC1)-producing interferon gamma (IFNγ) blood non-lesional skin vitiligo patients. Melanocytes patients have strong basal expression chemokine-receptor-3 (CXCR3) isoform B which is directly regulated by IFNγ. CXCR3B CXCL10 at surface cultured human...

10.1038/s41467-019-09963-8 article EN cc-by Nature Communications 2019-05-16

Apoptosis and senescence are cellular failsafe programs that counteract excessive mitogenic signaling observed in cancer cells. Melanoma is known for its notorious resistance to apoptotic processes; therefore, senescence, which remains poorly understood melanomas, can be viewed as a therapeutic alternative. Microphthalmia-associated transcription factor (MITF), M transcript specifically expressed melanocyte cells, plays critical role melanoma proliferation, specific inhibition associated...

10.1158/0008-5472.can-09-2913 article EN Cancer Research 2010-04-14

Melanins are synthesized in melanocytes within specialized organelles called melanosomes. Numerous studies have shown that the pH of melanosome plays a key role regulation melanin synthesis. However, until now, acute by physiological stimulus has never been demonstrated. In present study, we show activation cAMP pathway alphaMSH or forskolin leads to an alkalinization melanosomes and concomitant vacuolar ATPases ion transporters solute carrier family. The family members include SLC45A2,...

10.1074/jbc.m109.005819 article EN cc-by Journal of Biological Chemistry 2009-04-24

// Mickaël Ohanna 1,2,* , Yann Cheli Caroline Bonet 1,2 Vanessa F Bonazzi 4 Marylin Allegra 1,3 Sandy Giuliano Karine Bille Philippe Bahadoran 1,2,3 Damien Giacchero 3 Jean Lacour 2,3 Glen M Boyle Nicholas Hayward Corine Bertolotto and Robert Ballotti 1,2,3,* . 1 Inserm U1065, Centre Méditerranéen de Médecine Moléculaire, Equipe 1, Biologie et pathologies des mélanocytes: la pigmentation cutanée au mélanome. labellisée Ligue 2013, Nice, F-06204, France 2 Université Nice Sophia-Antipolis, UFR...

10.18632/oncotarget.1143 article EN cc-by Oncotarget 2013-08-19

Specific BRAFV600E inhibitors (BRAFi) are highly effective in the treatment of melanoma. However, acquired drug resistances invariably develop after initial response. Therefore, identification new mechanisms resistance gives important clues towards development therapies that could elicit long lasting responses. Here we report CD271 confers to BRAFi melanoma cells. The expression is increased by through a stimulation tumor necrosis factor-alpha (TNFα) secretion leads NF-κB signaling pathway...

10.1038/celldisc.2015.30 article EN cc-by Cell Discovery 2015-10-27

// Yann Cheli 1,2 , Vanessa F. Bonnazi Arnaud Jacquel 4,2 Maryline Allegra 1,2,3 Gian Marco De Donatis Philippe Bahadoran 1,2,3,5 Corine Bertolotto and Robert Ballotti 1 INSERM U1065, Equipe 1, Biologie et pathologies des mélanocytes: de la pigmentation cutanée au mélanome, labellisée Ligue 2013, Centre Méditerranéen Médecine Moléculaire, Nice, France 2 Université Nice Sophia-Antipolis, UFR Médecine, 3 CHU Service Dermatologie, 4 2, Cell death, differentiation cancer, 5 Clinical Research...

10.18632/oncotarget.1967 article EN Oncotarget 2014-05-13

Disrupting the eukaryotic translation initiation factor 4F (eIF4F) complex offers an appealing strategy to potentiate effectiveness of existing cancer therapies and overcome resistance drugs such as BRAF inhibitors (BRAFi). Here, we identified characterized small molecule SBI-0640756 (SBI-756), a first-in-class inhibitor that targets eIF4G1 disrupts eIF4F complex. SBI-756 impaired assembly independently mTOR attenuated growth BRAF-resistant BRAF-independent melanomas. also suppressed AKT...

10.1158/0008-5472.can-15-0885 article EN Cancer Research 2015-11-25

MITF encodes an oncogenic lineage-specific transcription factor in which a germline mutation ( MITFE318K ) was identified human patients predisposed to both nevus formation and, among other tumor types, melanoma. The molecular mechanisms underlying the activity of E318K remained uncharacterized.Here, we compared SUMOylation status endogenous by proximity ligation assay melanocytes isolated from wild-type (n = 3) or 4) donors. We also used newly generated Mitf knock-in (KI) mouse model assess...

10.1093/jnci/djw340 article EN JNCI Journal of the National Cancer Institute 2016-12-24

Chronic myelogenous leukemia (CML) is a cytogenetic disorder resulting from the expression of p210BCR-ABL. Imatinib, an inhibitor BCR-ABL, has emerged as leading compound to treat CML patients. Despite encouraging clinical results, resistance imatinib represents major drawback for therapy, substantial proportion patients are refractory this treatment. Recent publications have described existence small cancer cell population with potential exhibit phenotypic switch responsible...

10.1093/jmcb/mjs010 article EN Journal of Molecular Cell Biology 2012-03-31

Metastatic uveal melanomas are highly resistant to all existing treatments. To address this critical issue, we performed a kinome-wide CRISPR-Cas9 knockout screen, which revealed the LKB1-SIK2 module in restraining melanoma tumorigenesis. Functionally, LKB1 loss enhances proliferation and survival through SIK2 inhibition upregulation of sodium/calcium (Na

10.15252/emmm.202317719 article EN cc-by EMBO Molecular Medicine 2023-11-15
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