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Jean-François Tanti

Jean-François Tanti

Current position and studies

I’m the team leader of the team Cellular and Molecular Pathophysiology of Obesity at the Mediterranean Research Center of Molecular Medicine, an INSERM Research center in Nice, France. I’m also the deputy director of the Center. The studies of my team deal with the cellular and molecular mechanisms involved in the development of insulin resistance in obese and type diabetic patients.”

Career

“I did my PhD in the laboratory of Pr Emmanuel Van Obberghen in Nice under the supervision of Dr Yannick Le Marchand-Brustel where I studied the role of PKC and cAMP dependent kinase in the modulation of the insulin signaling and metabolic effects. In 1990, I obtained a tenured position in CNRS (Centre National de la Recherche Scientifique) to work in the team of Dr Yannick Le Marchand-Brustel on the insulin signaling pathways involved in glucose transport. In 2003, I moved to the new laboratory of Dr Y Le Marchand-Brustel focusing mainly on the posttranslational modifications of insulin receptor substrate and the role of different serine kinases in the development of insulin resistance. In 2007, I became a group leader in the Mediterranean Research Center for Molecular Medicine where my team focuses on three related and highly integrated areas which are central to insulin resistance and T2D development : 1) mechanisms of insulin signaling and glucose transport in adipocytes and how they are altered in insulin resistant state 2) identification of stress-signaling pathways involved in adipose tissue inflammation and dysfunction 3) identification of new genetic and epigenetic players controlling hepatic gluconeogenesis. I was author of 95 original articles or reviews in peer-reviewed journals.”

Main Discoveries

  • Implication of the PI3 kinase/PKB axis in insulin induced glucose transport
  • Demonstration that IRS-1 serine phosphorylation is mechanism involved in the desensitization of insulin response
  • Implication of the Tpl2/ERK pathway in adipose tissue inflammation and inflammatory cytokines induced insulin resistance
  • Role of DNA damage and p53 pathway in adipose tissue dysfunction
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