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
Tuesday, September 22, 2009
Monday, September 21, 2009
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.
Joanne Fieldinga, b, c,, Louise Corbend, e, Phillip Cremerf, Lynette Millistc, Owen Whiteb, c and Martin Delatyckid, g
Keywords: Friedreich ataxia (FRDA); cognition; saccades; cerebellum
Received 1 April 2009; revised 21 July 2009; accepted 11 September 2009.
Available online 17 September 2009.
Joanne Fieldinga, b, c,, Louise Corbend, e, Phillip Cremerf, Lynette Millistc, Owen Whiteb, c and Martin Delatyckid, 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
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
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
Saturday, September 19, 2009
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
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.
Wednesday, September 16, 2009
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.
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.
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.
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.
Tuesday, September 15, 2009
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
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
Monday, September 14, 2009
Friedreich's ataxia: Oxidative stress and cytoskeletal abnormalities
Journal of the Neurological Sciences
Article in Press, Corrected Proof
Marco Sparacoa, 1, Laura Maria Gaetab, 1, Filippo Maria Santorellib, Chiara Passarellib, Giulia Tozzib, Enrico Bertinib, Alessandro Simonatic, Francesco Scaravillid, Franco Taronie, Charles Duyckaertsf, Michele Feleppaa and Fiorella Piemonteb,
, 
Received 2 April 2009;
Keywords: Glutathione; Oxidative stress; Friedreich's ataxia; Cytoskeletal proteins, frataxin, Complexes I, II, III, aconitase, fibroblasts, tubulin, neurofilaments, motor neurons.
Article in Press, Corrected Proof
Marco Sparacoa, 1, Laura Maria Gaetab, 1, Filippo Maria Santorellib, Chiara Passarellib, Giulia Tozzib, Enrico Bertinib, Alessandro Simonatic, Francesco Scaravillid, Franco Taronie, Charles Duyckaertsf, Michele Feleppaa and Fiorella Piemonteb,
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
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.
Sunday, September 13, 2009
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 Garc
a-Serres§
, Meng Li‡, William E. Broderick
, Boi Hanh Huynh*§ and Joan B. Broderick*
‡ 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+ , FeIII, FeII, redox state, 5′-deoxyadenosine, AMP, ADP, and methylthioadenosine, oxidative damage.
Subscribe to:
Posts (Atom)
