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L'Institut de biologie Valrose (iBV)
Postdoctoral Positions in Neurobiology
L'Institut de biologie Valrose (iBV)
L'Institut de biologie Valrose (iBV) à Nice est un institut de recherche international financé par le CNRS, l’INSERM, l'Université Nice Sophia Antipolis, le centre régional de lutte contre le cancer Antoine Lacassagne et l'Union Européenne.
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Publié: il y a 6 mois
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Localisation: Nice , France
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Postdoctoral Positions in Neurobiology

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Several positions in Neurobiology/Pharmacology/Electrophysiology are available at the “Institut de Biologie Valrose” (iBV) located in Nice, France. The Institute of Biology Valrose (http://ibv.unice.fr/EN/index.php) is a multi-disciplinary, international scientific environment with over 200 researchers working in 27 different groups. We are looking for highly motivated and enthusiastic scientists to join our research team “Biology of ion channels” to investigate the role of K2P potassium channels using new optical and optogenetic approaches.

Maintenance of a negative resting membrane potential underlies the basis of neuronal excitability. This negative potential is generated by a potassium leak current mediated by K2P channels. K2P channels are notably involved in pain perception, mood regulation and migraine. Our projects aim to address TREK channel’s physiological (neuroexcitability, plasticity, pain perception) and pathological (such as depression and migraine) functions and to determine the channel subtypes which are involved in these aforementioned processes.

To address the role of the K2P channels, we are using optical and optogenetic tools. Notably, a TREK1 channel that is controlled by light both in-vitro (TREKlight, TREK1-PCS) and in-vivo (StarTREK mouse model) in combination with single molecule fluorecsence assays (SiMPull)—

The candidate will work on two aspects:

  1. At the fundamental level the applicant will study:
    1. The TREK channel function using optogenetic tools. Notably a TREK1 channel that is controlled by light both in-vitro (TREKlight, TREK1-PCS) and in-vivo (StarTREK mouse model).
    2. The functional coupling between TRAAK and AT2R. We recently demonstrate how mycolactone (toxin secreted by the bacterium) generates its analgesic effect. This involves the pain-killing action associated with the toxin binding onto the angiotensin 2 receptors (AT2R) (belonging to the GPCR family), and thus inducing the activation of TRAAK channels and reduction of neuronal excitability.
  1. At the technical level:  the applicant will develop, in collaboration, new optical tools to endow optical control of K2P channels. 

The ideal candidates will have a solid background in electrophysiology (slice-patching experience would be appreciated) and molecular biology and/or cell imaging and/or optogenetic.

Position: Contract with the French CNRS Institution. The salary is commensurate with experience.

Interested candidates should e-mail a letter of application, including a CV and the names and addresses of at least two references to: Guillaume Sandoz, sandoz@unice.fr.

References:

Levitz J, Royal P, Comoglio Y, Wdziekonski B, Schaub S, Clemens D, Isacoff EY and Sandoz G, Heterodimerization within the TREK channel subfamily produces a diverse family of highly regulated potassium channels. Proc Natl Acad Sci U S A. 12;113(15):4194-9.

Comoglio Y, Levitz J, Kienzler M, Lesage F, Isacoff EY and Sandoz G. Specific regulation of TREK channels by phosphatidic acid due to direct association with Phospholipase D2. Proc Natl Acad Sci U S A. 111: 13547-52

Marion E, Song OR, Christophe T, Babonneau J, Fenistein D, Eyer J, Letournel F, Henrion D, Clere N, Paille V, Guérineau NC, Saint André JP, Gersbach P, Altmann KH, Stinear TP, Comoglio Y, Sandoz G, Preisser L, Delneste Y, Yeramian E, Marsollier L, Brodin P. Mycobacterial toxin induces analgesia in buruli ulcer by targeting the Angiotensin pathways. Cell. 157: 1565-76.

Sandoz G, Levitz J, Kramer R & Isacoff E. Optical control of endogenous proteins with a photo-switchable conditional subunit reveals a role for TREK1 in GABAB signaling.  Neuron. 74; 1005-14.

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