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Détail de l'auteur
Auteur Emanuel DICICCO-BLOOM |
Documents disponibles écrits par cet auteur (3)
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ENGRAILED2 and Cerebellar Development in the Pathogenesis of Autism Spectrum Disorders / Ian T. ROSSMAN
Titre : ENGRAILED2 and Cerebellar Development in the Pathogenesis of Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Ian T. ROSSMAN, Auteur ; Emanuel DICICCO-BLOOM, Auteur Année de publication : 2008 Importance : p.3-40 Langues : Anglais (eng) Mots-clés : Engrailed 2 Neurodéveloppement Modelage; Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=703 ENGRAILED2 and Cerebellar Development in the Pathogenesis of Autism Spectrum Disorders [Texte imprimé et/ou numérique] / Ian T. ROSSMAN, Auteur ; Emanuel DICICCO-BLOOM, Auteur . - 2008 . - p.3-40.
Langues : Anglais (eng)
Mots-clés : Engrailed 2 Neurodéveloppement Modelage; Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=703 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire Engrailed2 modulates cerebellar granule neuron precursor proliferation, differentiation and insulin-like growth factor 1 signaling during postnatal development / Ian ROSSMAN in Molecular Autism, (February 2014)
[article]
Titre : Engrailed2 modulates cerebellar granule neuron precursor proliferation, differentiation and insulin-like growth factor 1 signaling during postnatal development Type de document : Texte imprimé et/ou numérique Auteurs : Ian ROSSMAN, Auteur ; Lulu LIN, Auteur ; Katherine MORGAN, Auteur ; Marissa DIGIOVINE, Auteur ; Elise VAN BUSKIRK, Auteur ; Silky KAMDAR, Auteur ; James MILLONIG, Auteur ; Emanuel DICICCO-BLOOM, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The homeobox transcription factor Engrailed2 (En2) has been studied extensively in neurodevelopment, particularly in the midbrain/hindbrain region and cerebellum, where it exhibits dynamic patterns of expression and regulates cell patterning and morphogenesis. Because of its roles in regulating cerebellar development and evidence of cerebellar pathology in autism spectrum disorder (ASD), we previously examined an ENGRAILED2 association and found evidence to support EN2 as a susceptibility gene, a finding replicated by several other investigators. However, its functions at the cell biological level remain undefined. In the mouse, En2 gene is expressed in granule neuron precursors (GNPs) just as they exit the cell cycle and begin to differentiate, raising the possibility that En2 may modulate these developmental processes. To define En2 functions, we examined proliferation, differentiation and signaling pathway activation in En2 knockout (KO) and wild-type (WT) GNPs in response to a variety of extracellular growth factors and following En2 cDNA overexpression in cell culture. In vivo analyses of cerebellar GNP proliferation as well as responses to insulin-like growth factor-1 (IGF1) treatment were also conducted. Proliferation markers were increased in KO GNPs in vivo and in 24-h cultures, suggesting En2 normally serves to promote cell cycle exit. Significantly, IGF1 stimulated greater DNA synthesis in KO than WT cells in culture, a finding associated with markedly increased phospho-S6 kinase activation. Similarly, there was three-fold greater DNA synthesis in the KO cerebellum in response to IGF1 in vivo. On the other hand, KO GNPs exhibited reduced neurite outgrowth and differentiation. Conversely, En2 overexpression increased cell cycle exit and promoted neuronal differentiation. In aggregate, our observations suggest that the ASD-associated gene En2 promotes GNP cell cycle exit and differentiation, and modulates IGF1 activity during postnatal cerebellar development. Thus, genetic/epigenetic alterations of EN2 expression may impact proliferation, differentiation and IGF1 signaling as possible mechanisms that may contribute to ASD pathogenesis. En ligne : http://dx.doi.org/10.1186/2040-2392-5-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227
in Molecular Autism > (February 2014)[article] Engrailed2 modulates cerebellar granule neuron precursor proliferation, differentiation and insulin-like growth factor 1 signaling during postnatal development [Texte imprimé et/ou numérique] / Ian ROSSMAN, Auteur ; Lulu LIN, Auteur ; Katherine MORGAN, Auteur ; Marissa DIGIOVINE, Auteur ; Elise VAN BUSKIRK, Auteur ; Silky KAMDAR, Auteur ; James MILLONIG, Auteur ; Emanuel DICICCO-BLOOM, Auteur.
Langues : Anglais (eng)
in Molecular Autism > (February 2014)
Index. décimale : PER Périodiques Résumé : The homeobox transcription factor Engrailed2 (En2) has been studied extensively in neurodevelopment, particularly in the midbrain/hindbrain region and cerebellum, where it exhibits dynamic patterns of expression and regulates cell patterning and morphogenesis. Because of its roles in regulating cerebellar development and evidence of cerebellar pathology in autism spectrum disorder (ASD), we previously examined an ENGRAILED2 association and found evidence to support EN2 as a susceptibility gene, a finding replicated by several other investigators. However, its functions at the cell biological level remain undefined. In the mouse, En2 gene is expressed in granule neuron precursors (GNPs) just as they exit the cell cycle and begin to differentiate, raising the possibility that En2 may modulate these developmental processes. To define En2 functions, we examined proliferation, differentiation and signaling pathway activation in En2 knockout (KO) and wild-type (WT) GNPs in response to a variety of extracellular growth factors and following En2 cDNA overexpression in cell culture. In vivo analyses of cerebellar GNP proliferation as well as responses to insulin-like growth factor-1 (IGF1) treatment were also conducted. Proliferation markers were increased in KO GNPs in vivo and in 24-h cultures, suggesting En2 normally serves to promote cell cycle exit. Significantly, IGF1 stimulated greater DNA synthesis in KO than WT cells in culture, a finding associated with markedly increased phospho-S6 kinase activation. Similarly, there was three-fold greater DNA synthesis in the KO cerebellum in response to IGF1 in vivo. On the other hand, KO GNPs exhibited reduced neurite outgrowth and differentiation. Conversely, En2 overexpression increased cell cycle exit and promoted neuronal differentiation. In aggregate, our observations suggest that the ASD-associated gene En2 promotes GNP cell cycle exit and differentiation, and modulates IGF1 activity during postnatal cerebellar development. Thus, genetic/epigenetic alterations of EN2 expression may impact proliferation, differentiation and IGF1 signaling as possible mechanisms that may contribute to ASD pathogenesis. En ligne : http://dx.doi.org/10.1186/2040-2392-5-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 Gaps in Current Autism Research: The Thoughts of the Autism Research Editorial Board and Associate Editors / David G. AMARAL in Autism Research, 12-5 (May 2019)
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Titre : Gaps in Current Autism Research: The Thoughts of the Autism Research Editorial Board and Associate Editors Type de document : Texte imprimé et/ou numérique Auteurs : David G. AMARAL, Auteur ; George M. ANDERSON, Auteur ; A. BAILEY, Auteur ; Raphael BERNIER, Auteur ; Somer L. BISHOP, Auteur ; Gene J. BLATT, Auteur ; Ricardo CANAL-BEDIA, Auteur ; Tony CHARMAN, Auteur ; G. DAWSON, Auteur ; P. J. DE VRIES, Auteur ; Emanuel DICICCO-BLOOM, Auteur ; Cheryl DISSANAYAKE, Auteur ; Y. KAMIO, Auteur ; R. KANA, Auteur ; N. Z. KHAN, Auteur ; A. KNOLL, Auteur ; F. KOOY, Auteur ; J. LAINHART, Auteur ; P. LEVITT, Auteur ; K. LOVELAND, Auteur ; N. MINSHEW, Auteur ; R. A. MUELLER, Auteur ; D. MURPHY, Auteur ; Peter C. MUNDY, Auteur ; S. PALENCIA, Auteur ; J. PINTO-MARTIN, Auteur ; A. RATTAZZI, Auteur ; S. ROGERS, Auteur ; W. L. STONE, Auteur ; S. J. WEBB, Auteur ; Andrew J. O. WHITEHOUSE, Auteur Article en page(s) : p.700-714 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.2101 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=397
in Autism Research > 12-5 (May 2019) . - p.700-714[article] Gaps in Current Autism Research: The Thoughts of the Autism Research Editorial Board and Associate Editors [Texte imprimé et/ou numérique] / David G. AMARAL, Auteur ; George M. ANDERSON, Auteur ; A. BAILEY, Auteur ; Raphael BERNIER, Auteur ; Somer L. BISHOP, Auteur ; Gene J. BLATT, Auteur ; Ricardo CANAL-BEDIA, Auteur ; Tony CHARMAN, Auteur ; G. DAWSON, Auteur ; P. J. DE VRIES, Auteur ; Emanuel DICICCO-BLOOM, Auteur ; Cheryl DISSANAYAKE, Auteur ; Y. KAMIO, Auteur ; R. KANA, Auteur ; N. Z. KHAN, Auteur ; A. KNOLL, Auteur ; F. KOOY, Auteur ; J. LAINHART, Auteur ; P. LEVITT, Auteur ; K. LOVELAND, Auteur ; N. MINSHEW, Auteur ; R. A. MUELLER, Auteur ; D. MURPHY, Auteur ; Peter C. MUNDY, Auteur ; S. PALENCIA, Auteur ; J. PINTO-MARTIN, Auteur ; A. RATTAZZI, Auteur ; S. ROGERS, Auteur ; W. L. STONE, Auteur ; S. J. WEBB, Auteur ; Andrew J. O. WHITEHOUSE, Auteur . - p.700-714.
Langues : Anglais (eng)
in Autism Research > 12-5 (May 2019) . - p.700-714
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.2101 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=397