Inka marti biography template
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A hyperspectral and multi-angular synthetic dataset for algorithm development in waters of varying trophic levels and optical complexity
Lewis, Edouard Leymarie, Aude Leynaert, Thomas Linkowski, Martine Lizotte, Adriana Lopes dos Santos, Claudie Marec, Dominique Marie, Guillaume Massé, Philippe Massicotte, Atsushi Matsuoka, Lisa A. Miller, Sharif Mirshak, Nathalie Morata, Brivaela Moriceau, Philippe-Israël Morin, Simon Morisset, Anders Mosbech, Alfonso Mucci, Gabrielle Nadaï, Christian Nozais, Ingrid Obernosterer, Thimoté Paire, Christos Panagiotopoulos, Marie Parenteau, Noémie Pelletier, Marc Picheral, Bernard Quéguiner, Patrick Raimbault, Joséphine Ras, Eric Rehm, Llúcia Ribot Lacosta, Jean-François Rontani, Blanche Saint-Béat, Julie Sansoulet, Noé Sardet, Catherine Schmechtig, Antoine Sciandra, Richard Sempéré, Caroline Sévigny, Jordan Toullec, Margot Tragin, Jean-Éric Tremblay, Annie-Pier Trottier, Daniel Vaulot, Anda Vladoiu, Lei Xue, Gustavo Yunda-Guarin, and Marcel Babin
Earth Syst. Sci. Data, 14, 4607–4642, https://doi.org/10.5194/essd-14-4607-2022,https://doi.org/10.5194/essd-14-4607-2022, 2022
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Abstract
In Birt–Hogg–Dubé (BHD) syndrome, germline loss-of-function mutations in the Folliculin (FLCN) gene lead to an increased risk of renal cancer. To address how FLCN inactivation affects cellular kinase signaling pathways, we analyzed comprehensive phosphoproteomic profiles of FLCNPOS and FLCNNEG human renal tubular epithelial cells (RPTEC/TERT1). In total, 15,744 phosphorylated peptides were identified from 4329 phosphorylated proteins. INKA analysis revealed that FLCN loss alters the activity of numerous kinases, including tyrosine kinases EGFR, MET, and the Ephrin receptor subfamily (EPHA2 and EPHB1), as well their downstream targets MAPK1/3. Validation experiments in the BHD renal tumor cell line UOK257 confirmed that FLCN loss contributes to enhanced MAPK1/3 and downstream RPS6K1/3 signaling. The clinically available MAPK inhibitor Ulixertinib showed enhanced toxicity in FLCNNEG cells. Interestingly, FLCN inactivation induced the phosphorylation of PIK3CD (Tyr524) without altering the phosphorylation of canonical Akt1/Akt2/mTOR/EIF4EBP1 phosphosites. Also, we identified that FLCN inactivation resulted in dephosphorylation of TFEB Ser109, Ser114, and Ser122, which may be linked to increased oxidative stress levels in FLCNNEG cells. Together, our study high
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Open Access
Peer-reviewed
- Yibing Wang,
- Parliamentarian Suchland,
- Amy Hua,
- Steven Carrell,
- Book Rockey,
- Kevin Hybiske
- Yibing Wang,
- Robert Suchland,
- Amy Hua,
- Steven Carrell,
- Daniel Rockey,
- Kevin Hybiske
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Figures
Abstract
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