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11 results on '"Amaya P."'

5. Physical drivers of the summer 2019 North Pacific marine heatwave.

Author

Amaya, Dillon J, Miller, Arthur J, Xie, Shang-Ping, and Kosaka, Yu

Abstract

Summer 2019 observations show a rapid resurgence of the Blob-like warm sea surface temperature (SST) anomalies that produced devastating marine impacts in the Northeast Pacific during winter 2013/2014. Unlike the original Blob, Blob 2.0 peaked in the summer, a season when little is known about the physical drivers of such events. We show that Blob 2.0 primarily results from a prolonged weakening of the North Pacific High-Pressure System. This reduces surface winds and decreases evaporative cooling and wind-driven upper ocean mixing. Warmer ocean conditions then reduce low-cloud fraction, reinforcing the marine heatwave through a positive low-cloud feedback. Using an atmospheric model forced with observed SSTs, we also find that remote SST forcing from the central equatorial and, surprisingly, the subtropical North Pacific Ocean contribute to the weakened North Pacific High. Our multi-faceted analysis sheds light on the physical drivers governing the intensity and longevity of summertime North Pacific marine heatwaves.

Published
2020

7. A caveolin-dependent and PI3K/AKT-independent role of PTEN in β-catenin transcriptional activity.

Author

Conde-Perez, Alejandro, Gros, Gwendoline, Longvert, Christine, Pedersen, Malin, Petit, Valérie, Aktary, Zackie, Viros, Amaya, Gesbert, Franck, Delmas, Véronique, Rambow, Florian, Bastian, Boris C, Campbell, Andrew D, Colombo, Sophie, Puig, Isabel, Bellacosa, Alfonso, Sansom, Owen, Marais, Richard, Van Kempen, Leon CLT, and Larue, Lionel

Subjects
Cell Line, Tumor, Melanocytes, Animals, Mice, Transgenic, Humans, Mice, Melanoma, Skin Neoplasms, GTP Phosphohydrolases, Glycogen Synthase Kinase 3, Cadherins, Membrane Proteins, MicroRNAs, Microscopy, Fluorescence, Blotting, Western, Prognosis, Immunohistochemistry, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, beta Catenin, Caveolin 1, Transcriptional Activation, Feedback, Physiological, Phosphatidylinositol 3-Kinases, Glycogen Synthase Kinase 3 beta, Cell Line, Tumor, Transgenic, Microscopy, Fluorescence, Blotting, Western, Feedback, Physiological
Abstract

Loss of the tumour suppressor PTEN is frequent in human melanoma, results in MAPK activation, suppresses senescence and mediates metastatic behaviour. How PTEN loss mediates these effects is unknown. Here we show that loss of PTEN in epithelial and melanocytic cell lines induces the nuclear localization and transcriptional activation of β-catenin independent of the PI3K-AKT-GSK3β axis. The absence of PTEN leads to caveolin-1 (CAV1)-dependent β-catenin transcriptional modulation in vitro, cooperates with NRAS(Q61K) to initiate melanomagenesis in vivo and induces efficient metastasis formation associated with E-cadherin internalization. The CAV1-β-catenin axis is mediated by a feedback loop in which β-catenin represses transcription of miR-199a-5p and miR-203, which suppress the levels of CAV1 mRNA in melanoma cells. These data reveal a mechanism by which loss of PTEN increases CAV1-mediated dissociation of β-catenin from membranous E-cadherin, which may promote senescence bypass and metastasis.

Published
2015

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