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Gael Nicolas

  • Academic Researcher / PhD
  • Research Fellow
  • National Institute of Health and Medical Research
  • 26h-indexImpact measure calculated using publication and citation counts. Updated daily.
  • 5075CitationsNumber of citations received by Gael's publications. Updated daily.

Research interests

http://cvscience.aviesan.fr/cv/76/gael-nicolas

About

In 2001, we described for the first time the critical and irreplaceable role of hepcidin in the regulation of iron homeostasis. At that time, we made the pioneer demonstration that hepcidin is an hyposideremic hormone acting to repress the iron availability into the body (read this comment). We also made the demonstration that hepcidin expression is regulated by anemia, hypoxia and more importantly by inflammation. By developing a turpentine abcess-induced inflammation in hepcidin-deficient mice we are the first to unambiguously demonstrate the crucial role of hepcidin in the dysregulation of iron homeostasis during inflammation. We were the first to describe that erythropoietin injection completely turns off hepcidin expression, a mechanism required to allow strong iron avaibility for production of new red blood cells. This protocol based on erythropoietin injection could be used to discover new proteins involved in the downregulation of hepcidin expression. Finally, we demonstrated that hemochromatosis is an hepatic metabolic disease due an insufficient production of hepcidin. We made the proof-of-principle that restoring a normal or higher production of hepcidin completely protects the organism against iron overload.

Co-authors (408)

Publications (5)

  • MED13L-related intellectual disability: involvement of missense variants and delineation of the phenotype

    • Smol T
    • Petit F
    • Piton A
    • et al.
    N/AReaders
    N/ACitations
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  • Mutation in the 3'untranslated region of APP as a genetic determinant of cerebral amyloid angiopathy

    • Nicolas G
    • Wallon D
    • Goupil C
    • et al.
    N/AReaders
    N/ACitations
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  • XPR1 mutations are a rare cause of primary familial brain calcification

    • Anheim M
    • López-Sánchez U
    • Giovannini D
    • et al.
    N/AReaders
    N/ACitations
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  • Improving Significance in Association Studies: a New Perspective for Association Studies Submitted to the Journal of Molecular Neuroscience

    • Nicolas G
    • Charbonnier C
    • Oliveira J
    N/AReaders
    1Citations
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  • A diagnosis of idiopathic basal ganglia calcification in an 82-year-old man

    • Nicolas G
    • Wallon D
    • Salle B
    • et al.
    N/AReaders
    0Citations
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Professional experience

Research Fellow

INSERM

October 2002 - Present