Biophysical Characterization of the Iron in Mitochondria from Atm1p-Depleted Saccharomyces cerevisiae

Biochemistry, Article ASAP DOI: 10.1021/bi901110n
Publication Date (Web): September 17, 2009
 
Ren Miao, Hansoo Kim, Uma Mahendra Kumar Koppolu, E. Ann Ellis, Robert A. Scott and Paul A. Lindahl*

‡ Department of Chemistry § Microscopy and Imaging Center,
Department of Biochemistry and Biophysics
Texas A&M University, College Station, Texas 77843-3255
Department of Chemistry, University of Georgia, Athens, Georgia 30602-2556

Keywords: Atm1p, ABC transporter, mitochondrial inner membrane, cytosol, cellular iron metabolism, cytosolic Fe/S cluster assembly, mitochondrial Fe/S cluster assembly,  Mssbauer spectroscopy, EPR, electronic absorption spectroscopy, X-ray absorption spectroscopy, and electron microscopy, aerobically grown cells, iron(III) phosphate nanoparticles,  yeast frataxin Yfh1p-deleted, yeast ferredoxin Yah1p-depleted,  Atm1p-depleted, nonheme Fe(II) ions, oxidative damage,  cytosolic Fe/S cluster assembly,  oxygen.

Chemical Probes Identify a Role for Histone Deacetylase 3 in Friedreich's Ataxia Gene Silencing

Chemistry & Biology, Volume 16, Issue 9, 980-989, 25 September 2009
Chunping Xu1, Elisabetta Soragni1, C. James Chou1, David Herman1, Heather L. Plasterer2, James R. Rusche2 and Joel M. Gottesfeld1,

1 Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
2 Repligen Corporation, Waltham, MA 02453, USA

Keywords: pimelic diphenylamide histone deacetylase (HDAC) inhibitors, Friedreich's ataxia (FRDA), Huntington's disease, HDAC3.

Neurophysiological evaluation in children with Friedreich's ataxia.

Early Hum Dev. 2009 Sep 21.

Sival DA, du Marchie Sarvaas GJ, Brouwer OF, Uges DR, Verschuuren-Bemelmans CC, Maurits NM, Brunt ER, van der Hoeven JH.


Department of Pediatrics, Beatrix Children's Hospital, University Medical Center Groningen, University of Groningen, The Netherlands.

Keywords:  Friedreich's ataxia (FRDA children), ICARS, idebenone treatment, longitudinal neurophysiological parameters,   two-year study,  period, cardiomyopathy (6-18years), sensory evoked potentials (SEPs), F response, peripheral nerve conduction , dynamometry, SEPs , peroneal nerve conduction velocity,  not substantiate neurologic improvement.

SCA-LSVD: a repeat-oriented locus-specific variation database for genotype to phenotype correlations in spinocerebellar ataxias.

Hum Mutat. 2009 Jul;30(7):1037-42
Faruq M, Scaria V, Singh I, Tyagi S, Srivastava AK, Mukerji M.


Genomics and Molecular Medicine, Institute of Genomics and Integrative Biology-Council of Scientific and Industrial Research (IGIB-CSIR), Delhi, India.

Keyword: Repeat expansion, autosomal dominant cerebellar ataxias (ADCAs), spinocerebellar ataxias (SCAs),   clinical classification,  prevalence, phenotypic expression,  ethnic groups, SCA-locus-specific variation database (LSVD),  SCA1, SCA 2, SCA 3, SCA 6, SCA 7, SCA 8, SCA 12, SCA 17, Friedreich's ataxia [FRDA], dentatorubral-pallidoluysian atrophy [DRPLA]),  Leiden Open (source) Variation Database (LOVD) software,  clinical features, HGVS Nomenclature guidelines.

High frequency of Friedreich's ataxia carriers in the Paphos district of Cyprus.

Acta Myol. 2009 Jul;28(1):24-6.

Zamba-Papanicolaou E, Koutsou P, Daiou C, Gaglia E, Georghiou A, Christodoulou K.
The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.

Keyword: Friedreich's ataxia, Paphos, Cyprus,  GAA triplet repeat, frataxin gene,  carrier frequency,  organized prevention programme.

Mitochondrial Superoxide Radicals Differentially Affect Muscle Activity and Neural Function

Genetics, Vol. 183, 175-184, September 2009

Tanja Godenschwege*,1, Renée Forde,1, Claudette P. Davis, Anirban Paul,2, Kristopher Beckwith and Atanu Duttaroy,3


* Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida 33431 and Biology Department, Howard University, Washington, DC 20059

Disruption to higher order processes in Friedreich ataxia

doi:10.1016/j.neuropsychologia.2009.09.009
Received 1 April 2009; revised 21 July 2009; accepted 11 September 2009. 

Available online 17 September 2009.

Joanne Fielding^{a, b, c,}, Louise Corben^{d, e}, Phillip Cremer^f, Lynette Millist^c, Owen White^{b, c} and Martin Delatycki^{d, g}

^aCentre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia
^bCentre for Developmental Psychiatry and Psychology, School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Clayton, Victoria, Australia
^cDepartment of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia
^dBruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Victoria, Australia
^eExperimental Neuropsychology Research Unit, School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Clayton, Victoria, Australia
^fRoyal North Shore Hospital, N.S.W., Australia
^gDepartment of Paediatrics, University of Melbourne, Victoria, Australia

 Keywords: Friedreich ataxia (FRDA); cognition; saccades; cerebellum  

Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival

Journal of Neural Transmission,

Makoto Naoi1 , Wakako Maruyama2, Hong Yi1, Keiko Inaba1, Yukihiro Akao1, 3 and Masayo Shamoto-Nagai2


(1) Department of Neurosciences, Gifu International Institute of Biotechnology, 1-1 Nakafudogaoka, Kakamigahara Gifu, 504-0838, Japan

(2) Department of Geriatric Medicine, National Institute for Geriatrics and Gerontology, Obu, Aichi, Japan

(3) United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu, Japan

Received: 4 March 2009 Accepted: 30 August 2009 Published online: 18 September 2009

Keywords:  Apoptosis - Mitochondria - Oxidative stress - Redox state - Neuroprotection - MAO inhibitor

Functional MRI study of Friedreich's ataxia using Simon task

NeuroImage, Volume 47, Supplement 1, July 2009, Pages S39-S41

H Akhlaghi, L Corben, E Storey, J Bradshaw, A Churchyard, N Georgiou-Karistianis, M Delatycki and G Egan

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WNP-4X3PHYG-13&_user=10&_coverDate=07%2F31%2F2009&_alid=1016977109&_rdoc=1&_fmt=high&_orig=search&_cdi=6968&_sort=r&_docanchor=&view=c&_ct=23&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=b42469b7f822812d2217b37f2f5f0bc5

 

(From Wikipedia, the free encyclopedia) In psychology, the Simon effect reaction times are usually faster and more accurate when the stimulus occurs in the same relative location as the response, even if the stimulus location is irrelevant to the task.

Negative feedback maintenance of heme homeostasis by its receptor, Rev-erbα

Genes & Development, Received May 29, 2009, Accepted August 7, 2009.

Nan Wu, Lei Yin, Elyisha A. Hanniman, Shree Joshi and Mitchell A. Lazar

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, and The Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA

Keywords: Intracellular heme levels, mitochondrial respiration, iron  toxicity, negative feedback mechanism,  nuclear heme receptor, Rev-erbα,  NCoR/histone deacetylase 3 (HDAC3),  coactivator PGC-1α, heme synthesis, cellular energy metabolism.

Histone Deacetylase Inhibitors and Neurodegenerative Disorders: Holding the Promise.

Curr Pharm Des. 2009 Sep 15:Antonello-Mai

Rotili D, Valente S, Kazantsev AG.
Harvard Medical School, Massachusetts General Hospital, CNY114 16th, Street, Charlestown, MA 02129, USA. akazantsev@partners.org.

Keywords: Neurodegenerative disorders (NDs), Huntington's disease, Alzheimer's disease, Parkinson disease, amyotrophic lateral sclerosis, spinal muscular atrophy, Friedreich's ataxia,  pathologic phenotype,   acetylation homeostasis,  histone acetyltransferase (HAT),  histone deacetylase (HDAC) , recent applications, HDAC inhibitors, HDAC/SIRT, CNS pathologies.

Human Ind1, an iron-sulfur cluster assembly factor for respiratory complex I.

Mol Cell Biol. 2009 Sep 14.

Sheftel AD, Stehling O, Pierik AJ, Netz DJ, Kerscher S, Elsässer HP, Wittig I, Balk J, Brandt U, Lill R.

Institut für Zytobiologie, Philipps-Universität Marburg, Robert-Koch-Strasse 6, 35033 Marburg, Germany; Goethe-Universität, Zentrum der Biologischen Chemie, Molekulare Bioenergetik, Cluster of Excellence "Macromolecular Complexes", 60590 Frankfurt am Main, Germany; Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge CB2 3EA, UK.

Keywords: Respiratory complex I, NADH:ubiquinone oxidoreductase, iron-sulfur (Fe/S) clusters, mitochondrial diseases,  Fe/S cofactors, huInd1, HeLa cells,  RNAi technology, NDUFS1, NDUFV1, NDUFS3, NDUFA13, radiolabelling technique, iron.

El factor neurotrófico BDNF disminuye la neurodegeneración inducida por la deficiencia de frataxina en cultivos neuronales.

(The neurotrophic factor BDNF reduces neurodegeneration induced by frataxin deficiency in neuronal cultures. )



Comunicacion: (sección Bases Moleculares de la Patología )

Y.M. Katsu, F. Lim, J. Díaz-Nido
UAM-CSIC, Madrid.

 
XXXII Congreso de la Sociedad Española de Bioquímica y Biología Molecular (SEBBM)
Oviedo, 23-26 de septiembre, 2009

Friedreich's ataxia: Oxidative stress and cytoskeletal abnormalities

Journal of the Neurological Sciences
Article in Press, Corrected Proof

  Marco Sparaco^{a, 1}, Laura Maria Gaeta^{b, 1}, Filippo Maria Santorelli^b, Chiara Passarelli^b, Giulia Tozzi^b, Enrico Bertini^b, Alessandro Simonati^c, Francesco Scaravilli^d, Franco Taroni^e, Charles Duyckaerts^f, Michele Feleppa^a and Fiorella Piemonte^{b, ,}

^aDivision of Neurology, Department of Neurosciences, Azienda Ospedaliera “G. Rummo”, 82100 Benevento, Italy
^bMolecular Medicine Unit, Children's Hospital and Research Institute “Bambino Gesù”, Roma, Italy
^cDepartment of Neurological and Visual Sciences, Section of Neurology, University of Verona, Policlinico G.B. Rossi, 37134 Verona, Italy
^dDivision of Neuropathology, Institute of Neurology, University College London, WC1N 3BG London, UK
^eUO Biochimica e Genetica, Fondazione IRCCS Istituto Neurologico “Carlo Besta”, Milano, Italy
^fLaboratoire de Neuropathologie Raymond Escourolle, Hôpital de La Salpêtrière, 75651 Paris, France

Received 2 April 2009; 

revised 24 July 2009; 

accepted 13 August 2009. 

Available online 12 September 2009.

Keywords: Glutathione; Oxidative stress; Friedreich's ataxia; Cytoskeletal proteins,  frataxin, Complexes I, II, III,  aconitase, fibroblasts, tubulin,  neurofilaments, motor neurons.

The Iron−Sulfur Cluster of Pyruvate Formate-Lyase Activating Enzyme in Whole Cells: Cluster Interconversion and a Valence-Localized [4Fe-4S]2+ State

Biochemistry, Article ASAP

DOI: 10.1021/bi9010286

Publication Date (Web): August 27, 2009

Jian Yang‡, Sunil G. Naik§, Danilo O. Ortillo§, Ricardo Garca-Serres§, Meng Li‡, William E. Broderick, Boi Hanh Huynh*§ and Joan B. Broderick*

Department of Chemistry and Biochemistry, Montana State University, Bozeman, Montana 59718

^‡ Department of Chemistry, Michigan State University, East Lansing, Michigan 48824

^§ Department of Physics, Emory University, Atlanta, Georgia 30322

KEYWORDS: Pyruvate formate-lyase activating enzyme (PFL-AE),  glycyl radical, pyruvate formate-lyase (PFL),  [4Fe-4S] cluster, cluster interconversions,  [4Fe-4S]²⁺  , [2Fe-2S]²⁺ , Fe^III,  Fe^II,  redox state, 5′-deoxyadenosine, AMP, ADP, and methylthioadenosine, oxidative damage.

Recurrent Ventricular Tachycardia in Patient with Friedreich's Ataxia in the Absence of Clinical Myocardial Disease.

Pacing Clin Electrophysiol. 2009 Sep 10

Asaad N, El-Menyar A, Al Suwaidi J.

From the Department of Cardiology and Cardiovascular Surgery, Hamad General Hospital and Weill Cornell Medical College, Doha, Qatar.

Uptake of ferrous iron by cultured rat astrocytes

Journal of Neuroscience Research, Published Online: 10;Sep;2009


Ketki Tulpule ^{1 2}, Stephen R. Robinson ³, Glenda M. Bishop ³, Ralf Dringen ^{1 2 3 *1}Center for Biomolecular Interactions Bremen, University of Bremen, Bremen, Germany
²Center for Environmental Research and Sustainable Technology, Bremen, Germany
³School of Psychology, Psychiatry and Psychological Medicine, Monash University, Clayton, Victoria, Australia

TARGETING NUCLEIC ACIDS IN BACTERIA WITH SYNTHETIC LIGANDS

Abbas Nikravesh (Thesis for doctoral degree (Ph.D.))         
Stockholm 2008
From the Programme for Genomics and Bioinformatics
Department of Cell and Molecular Biology
Karolinska Institutet, Stockholm, Sweden



 .../...

3.4 PAPER IV
Friedreich’s ataxia (GAA)n triplex DNA structures are stabilized by Benzoquinoquinoxaline derivatives

.../...


5 FUTURE PERSPECTIVES
.../...

The experiments on (GAA)n repeat sequences described in this thesis were restricted to in vitro studies and probing of E. coli plasmid DNA. Nevertheless, the evidence that we provide for the existence of triplex structures within FA (GAA)n repeats suggests that destabilization of these structures could provide a possible therapeutic strategy for patients. Whereas BQQ stabilizes triplex structures, other DNA ligands may destabilize triplex structures. Such strategies may offer hope for developing small molecule DNA ligands to treat FA or other conditions that involve triplex DNA structures that arise from tri nucleotide repeat expansions.

.../...

Structure-Specific Recognition of Friedreich's Ataxia (GAA)n Repeats by Benzoquinoquinoxaline Derivatives

ChemBioChem, Published Online: 10 Sep 2009

Helen Bergquist 1, Abbas Nikravesh, Dr. 2, Raquel Domingo Fernández 1, Veronica Larsson 1, Chi-Hung Nguyen, Dr. 3, Liam Good, Dr. 2 4, Rula Zain, Dr. 1 *


1Department of Molecular Biology and Functional Genomics, Stockholm University, Svante Arrhenius väg 20C, 10691 Stockholm (Sweden), Fax: (+46) 8-166488

2Department of Cell and Molecular Biology, Karolinska Institutet, Berzelius väg 35, 17177 Stockholm (Sweden)

3UMR176 CNRS-Institut Curie, Laboratoire de Pharmacochimie, Centre Universitaire, Bâtiment 110, 91405 Orsay (France)

4Department of Pathology and Infectious Diseases, Royal Veterinary College, University of London, Hawkshead Lane, N. Mymms AL9 7TA (UK)

Friedreich’s Ataxia Symposium 2009 - Children’s Hospital of Philadelphia

The symposium will take place on November 13 and 14.
Further information can be obtained from the Continuing Medical Education Department at the Children’s Hospital of Philadelphia at (215) 590 5263.

Elucidation of the mechanism of mitochondrial iron loading in Friedreich's ataxia by analysis of a mouse mutant

Proceedings of the National Academy of Science USA

Edited by Solomon H. Snyder, Johns Hopkins University School of Medicine, Baltimore, MD, and approved July 30, 2009 (received for review June 17, 2009)

Michael Li-Hsuan Huanga, Erika M. Beckera, Megan Whitnalla, Yohan Suryo Rahmantoa, Prem Ponkab,1 and Des R. Richardson.

Keywords: muscle creatine kinase (MCK), frataxin knockout mouse, frataxin deficiency, iron metabolism, neurologic and cardiologic degeneration, iron-sulfur cluster (ISC) synthesis, cysteine desulferase Nfs1, mitochondrial ferritin, 5-aminolevulinate dehydratase, coproporphyrinogen oxidase, hydroxymethylbilane synthase, uroporphyrinogen III synthase, ferrochelatase, Sec15l1, mitoferrin-2 (Mfrn2).

The roles of SbcCD and RNaseE in the transcription of GAA·TTC repeats in Escherichia coli

DNA Repair, article in press.

Xuefeng Pan^{a, b, ,} , Yunfeng Ding^{a, 1} and Lingfeng Shi^{a, 1}

^aSchool of Life Science, Beijing Institute of Technology, Beijing 100081, China

^bInstitute of Cell and Molecular Biology, Edinburgh University, Edinburgh EH9 3JR, Scotland, UK

Received 17 February 2009;

revised 24 July 2009;

accepted 9 August 2009.

Available online 4 September 2009.

Keyword: Frataxin, GAA·TTC repeats , FXN gene, Frederich's ataxia, α-Complementation SbcCD; RNaseE .

The dorsal root ganglion in Friedreich's ataxia.

Acta Neuropathol. 2009 Aug 30. [Epub ahead of print]

Koeppen AH, Morral JA, Davis AN, Qian J, Petrocine SV, Knutson MD, Gibson WM, Cusack MJ, Li D.
Research Service (151), Veterans Affairs Medical Center, 113 Holland Ave, Albany, NY, 12208, USA, arnulf.koeppen@med.va.gov.

Keywords: Atrophy of dorsal root ganglia (DRG), thinning of dorsal roots (DR), Friedreich's ataxia (FRDA), selective vulnerability of larger neurons in DRG, selective vulnerability of thicker myelinated DR axons, ventral roots (VR), Schwann cells, laminin, ferritin, mitochondrial ferritin, ferroportin.

AAV9-mediated erythropoietin gene delivery into the brain protects nigral dopaminergic neurons in a rat model of Parkinson's disease

Gene Therapy, advance online publication 3 September 2009; doi: 10.1038/gt.2009.113

Y-Q Xue1,7, B-F Ma1,7, L-R Zhao1,2,3, J B Tatom4, B Li2, L-X Jiang5, R L Klein3,4 and W-M Duan1,3,6
1Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA, USA
2Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
3Gene Therapy Program, Louisiana State University Health Sciences Center, Shreveport, LA, USA
4Department of Pharmacology, Toxicology and Neuroscience, Louisiana State University Health Sciences Center, Shreveport, LA, USA
5Vector Gene Technology Company LTD, Beijing, PR China
6Department of Anatomy and Neurobiology, Capital Medical University, Beijing, PR China
Correspondence: Dr W-M Duan, Department of Cellular Biology & Anatomy, LSU Health Sciences Center in Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA. E-mail: wduan@lsuhsc.edu
7These authors contributed equally to this work.
Received 17 March 2009; Revised 3 August 2009; Accepted 5 August 2009; Published online 3 September 2009.

Promise Of Nanodiamonds For Safer Gene Therapy

Article Date: 03 Sep 2009 - 0:00 PDT
Medical News Today
Gene therapy holds promise in the treatment of a myriad of diseases, including cancer, heart disease and diabetes, among many others. However, developing a scalable system for delivering genes to cells both efficiently and safely has been challenging.
Read more.....

China cracks down on stem cell tourism

NewScientist

00:01 03 September 2009 by Andy Coghlan


Chinese and European researchers have today published ethical guidelines aimed at discouraging Chinese doctors from offering patients unproven or sham treatments based on stem cells.
The authors hope the move will reinforce legal curbs on stem cell treatments introduced on 1 May by China's ministry of health.



Read more ....

Neuroprotective effects of compounds with antioxidant and anti-inflammatory properties in a Drosophila model of Parkinson's disease

OPEN ACCESS

Katharina Faust , Stephan Gehrke , Yufeng Yang , Lichuan Yang , Flint Beal and Bingwei Lu
BMC Neuroscience 2009, 10:109doi:10.1186/1471-2202-10-109
Published: 1 September 2009

Abstract (provisional)

Background
Parkinson's disease (PD) is the most common movement disorder. Extrapyramidal motor symptoms stem from the degeneration of the dopaminergic pathways in patient brain. Current treatments for PD are symptomatic, alleviating disease symptoms without reversing or retarding disease progression. Although the cause of PD remains unknown, several pathogenic factors have been identified, which cause dopaminergic neuron (DN) death in the substantia nigra (SN). These include oxidative stress, mitochondrial dysfunction, inflammation and excitotoxicity. Manipulation of these factors may allow the development of disease-modifying treatment strategies to slow neuronal death. Inhibition of DJ-1A, the Drosophila homologue of the familial PD gene DJ-1, leads to oxidative stress, mitochondrial dysfunction, and DN loss, making fly DJ-1A model an excellent in vivo system to test for compounds with therapeutic potential.
Results
In the present study, a Drosophila DJ-1A model of PD was used to test potential neuroprotective drugs. The drugs applied are the Chinese herb celastrol, the antibiotic minocycline, the bioenergetic amine coenzyme Q10 (coQ10), and the glutamate antagonist 2,3-dihydroxy-6-nitro-7-sulphamoylbenzo[f]-quinoxaline (NBQX). All of these drugs target pathogenic processes implicated in PD, thus constitute mechanism-based treatment strategies. We show that celastrol and minocycline, both having antioxidant and anti-inflammatory properties, confer potent dopaminergic neuroprotection in Drosophila DJ-1A model, while coQ10 shows no protective effect. NBQX exerts differential effects on cell survival and brain dopamine content: it protects against DN loss but fails to restore brain dopamine level.
Conclusions
The present study further validates Drosophila as a valuable model for preclinical testing of drugs with therapeutic potential for neurodegenerative diseases. The lower cost and amenability to high throughput testing make Drosophila PD models effective in vivo tools for screening novel therapeutic compounds. If our findings can be further validated in mammalian PD models, they would implicate drugs combining antioxidant and anti-inflammatory properties as strong therapeutic candidates for mechanism-based PD treatment.


Full text: http://www.biomedcentral.com/content/pdf/1471-2202-10-109.pdf

Finding The ZIP-code For Gene Therapy: Scientists Imitate Viruses To Deliver Therapeutic Genes

ScienceDaily (Aug. 31, 2009) — A research report featured on the cover of the September 2009 print issue of The FASEB Journal describes how Australian scientists developed a new gene therapy vector that uses the same machinery that viruses use to transport their cargo into our cells. As a result of this achievement, therapeutic DNA can be transferred to a cell's nucleus far more efficiently than in the past, raising hopes for more effective treatment of genetic disorders and some types of cancers. Read more ....

Original scientific source: Multifunctional protein nanocarriers for targeted nuclear gene delivery in nondividing cells. Dominic J. Glover, Su May Ng, Adam Mechler, Lisandra L. Martin, and David A. Jans

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system

Nature Reviews Drug Discovery 8, 733-750 (September 2009) doi:10.1038/nrd2927
Antoine Taly1, Pierre-Jean Corringer2, Denis Guedin3, Pierre Lestage3 & Jean-Pierre Changeux


Laboratoire de Chimie Biophysique, Institut de Science et d'Ingénierie Supramoléculaires, UMR 7006 (CNRS-Université de Strasbourg), 8 Allée Gaspard Monge, 67000 Strasbourg, France. Email: a.taly@isis.u-strasbg.fr
Channel Receptors, CNRS URA 2182, Institut Pasteur, 25 rue du Dr Roux, 75015 Paris, France. Email: pjcorrin@pasteur.fr
Institut de Recherches Servier, 125 Chemin de Ronde, 78290 Croissy-sur-Seine. Email: denis.guedin@fr.netgrs.com; Email: pierre.lestage@fr.netgrs.com
CNRS URA 2182, Institut Pasteur, 25 rue du Dr Roux, 75015 Paris, France. Email: changeux@pasteur.fr

Highlight: "Varenicline (Chantix or Champix) is a nicotinic receptor partial agonist"