Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development / M. MAIRA in Journal of Neurodevelopmental Disorders, 2-1 (March 2010)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.47 Titre : Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development Type de document : Texte imprimé et/ou numérique Auteurs : M. MAIRA, Auteur ; J. E. LONG, Auteur ; A. Y. LEE, Auteur ; J. L. RUBENSTEIN, Auteur ; S. STIFANI, Auteur Article en page(s) : p.47 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development [Texte imprimé et/ou numérique] / M. MAIRA, Auteur ; J. E. LONG, Auteur ; A. Y. LEE, Auteur ; J. L. RUBENSTEIN, Auteur ; S. STIFANI, Auteur . - p.47. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.47 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons / R. MAO in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36 Titre : Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons Type de document : Texte imprimé et/ou numérique Auteurs : R. MAO, Auteur ; Damon T. PAGE, Auteur ; I. MERZLYAK, Auteur ; C. KIM, Auteur ; L. H. TECOTT, Auteur ; P. H. JANAK, Auteur ; J. L. RUBENSTEIN, Auteur ; M. SUR, Auteur Article en page(s) : p.224-36 Langues : Anglais (eng) Mots-clés : Associative learning  Behavior  Calretinin  Fear conditioning  GABAergic  Hyperactivity  Inhibitory  Interneuron  Neuropsychiatric disease  Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons [Texte imprimé et/ou numérique] / R. MAO, Auteur ; Damon T. PAGE, Auteur ; I. MERZLYAK, Auteur ; C. KIM, Auteur ; L. H. TECOTT, Auteur ; P. H. JANAK, Auteur ; J. L. RUBENSTEIN, Auteur ; M. SUR, Auteur . - p.224-36. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36 Mots-clés : Associative learning  Behavior  Calretinin  Fear conditioning  GABAergic  Hyperactivity  Inhibitory  Interneuron  Neuropsychiatric disease  Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development / M. MAIRA in Journal of Neurodevelopmental Disorders, 2-1 (March 2010)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.48-60 Titre : Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development Type de document : Texte imprimé et/ou numérique Auteurs : M. MAIRA, Auteur ; J. E. LONG, Auteur ; A. Y. LEE, Auteur ; J. L. RUBENSTEIN, Auteur ; S. STIFANI, Auteur Article en page(s) : p.48-60 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Signaling mechanisms mediated by the Transforming Growth Factor-beta (TGF-beta) superfamily regulate a variety of developmental processes. Here we show that components of both bone morphogenetic protein/growth differentiation factor and TGF-beta/activin/Nodal branches of TGF-beta superfamily signaling are expressed in the developing subpallium. Furthermore, Smad proteins, transcriptional effectors of TGF-beta signaling, are co-expressed and physically interact in the basal ganglia with Dlx homeodomain transcription factors, which are critical regulators of the differentiation, migration and survival of telencephalic GABAergic neurons. We also show that Dlx and Smad proteins localize to promoters/enhancers of a number of common telencephalic genes in vivo and that Smad proteins co-activate transcription with Dlx family members, except with certain mutated human DLX proteins identified in autistic individuals. In agreement with these observations, expression of dominant-negative Smads in the developing basal ganglia phenocopies the cell migration defects observed in Dlx1/2-deficient mice. Together, these results suggest that TGF-beta superfamily signaling plays a role in telencephalic GABAergic neuron development through functional interactions with Dlx transcription factors. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9035-6) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9035-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development [Texte imprimé et/ou numérique] / M. MAIRA, Auteur ; J. E. LONG, Auteur ; A. Y. LEE, Auteur ; J. L. RUBENSTEIN, Auteur ; S. STIFANI, Auteur . - p.48-60. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.48-60 Index. décimale : PER Périodiques Résumé : Signaling mechanisms mediated by the Transforming Growth Factor-beta (TGF-beta) superfamily regulate a variety of developmental processes. Here we show that components of both bone morphogenetic protein/growth differentiation factor and TGF-beta/activin/Nodal branches of TGF-beta superfamily signaling are expressed in the developing subpallium. Furthermore, Smad proteins, transcriptional effectors of TGF-beta signaling, are co-expressed and physically interact in the basal ganglia with Dlx homeodomain transcription factors, which are critical regulators of the differentiation, migration and survival of telencephalic GABAergic neurons. We also show that Dlx and Smad proteins localize to promoters/enhancers of a number of common telencephalic genes in vivo and that Smad proteins co-activate transcription with Dlx family members, except with certain mutated human DLX proteins identified in autistic individuals. In agreement with these observations, expression of dominant-negative Smads in the developing basal ganglia phenocopies the cell migration defects observed in Dlx1/2-deficient mice. Together, these results suggest that TGF-beta superfamily signaling plays a role in telencephalic GABAergic neuron development through functional interactions with Dlx transcription factors. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9035-6) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9035-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer / J. FORES-MARTOS in Molecular Autism, 10 (2019)  

Public ISBD [article]  inMolecular Autism > 10 (2019) . - 17 p. Titre : Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer Type de document : Texte imprimé et/ou numérique Auteurs : J. FORES-MARTOS, Auteur ; F. CATALA-LOPEZ, Auteur ; J. SANCHEZ-VALLE, Auteur ; K. IBANEZ, Auteur ; H. TEJERO, Auteur ; H. PALMA-GUDIEL, Auteur ; J. CLIMENT, Auteur ; V. PANCALDI, Auteur ; L. FANANAS, Auteur ; C. ARANGO, Auteur ; Mara PARELLADA, Auteur ; A. BAUDOT, Auteur ; D. VOGT, Auteur ; J. L. RUBENSTEIN, Auteur ; A. VALENCIA, Auteur ; R. TABARES-SEISDEDOS, Auteur Article en page(s) : 17 p. Langues : Anglais (eng) Mots-clés : asd  Autism  Cancer  Comorbidity  Gene expression  Meta-analysis  Multimorbidity  Transcriptome Index. décimale : PER Périodiques Résumé : Background: Epidemiological and clinical evidence points to cancer as a comorbidity in people with autism spectrum disorders (ASD). A significant overlap of genes and biological processes between both diseases has also been reported. Methods: Here, for the first time, we compared the gene expression profiles of ASD frontal cortex tissues and 22 cancer types obtained by differential expression meta-analysis and report gene, pathway, and drug set-based overlaps between them. Results: Four cancer types (brain, thyroid, kidney, and pancreatic cancers) presented a significant overlap in gene expression deregulations in the same direction as ASD whereas two cancer types (lung and prostate cancers) showed differential expression profiles significantly deregulated in the opposite direction from ASD. Functional enrichment and LINCS L1000 based drug set enrichment analyses revealed the implication of several biological processes and pathways that were affected jointly in both diseases, including impairments of the immune system, and impairments in oxidative phosphorylation and ATP synthesis among others. Our data also suggest that brain and kidney cancer have patterns of transcriptomic dysregulation in the PI3K/AKT/MTOR axis that are similar to those found in ASD. Conclusions: Comparisons of ASD and cancer differential gene expression meta-analysis results suggest that brain, kidney, thyroid, and pancreatic cancers are candidates for direct comorbid associations with ASD. On the other hand, lung and prostate cancers are candidates for inverse comorbid associations with ASD. Joint perturbations in a set of specific biological processes underlie these associations which include several pathways previously implicated in both cancer and ASD encompassing immune system alterations, impairments of energy metabolism, cell cycle, and signaling through PI3K and G protein-coupled receptors among others. These findings could help to explain epidemiological observations pointing towards direct and inverse comorbid associations between ASD and specific cancer types and depict a complex scenario regarding the molecular patterns of association between ASD and cancer. En ligne : http://dx.doi.org/10.1186/s13229-019-0262-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=398 [article] Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer [Texte imprimé et/ou numérique] / J. FORES-MARTOS, Auteur ; F. CATALA-LOPEZ, Auteur ; J. SANCHEZ-VALLE, Auteur ; K. IBANEZ, Auteur ; H. TEJERO, Auteur ; H. PALMA-GUDIEL, Auteur ; J. CLIMENT, Auteur ; V. PANCALDI, Auteur ; L. FANANAS, Auteur ; C. ARANGO, Auteur ; Mara PARELLADA, Auteur ; A. BAUDOT, Auteur ; D. VOGT, Auteur ; J. L. RUBENSTEIN, Auteur ; A. VALENCIA, Auteur ; R. TABARES-SEISDEDOS, Auteur . - 17 p. Langues : Anglais (eng) in Molecular Autism > 10 (2019) . - 17 p. Mots-clés : asd  Autism  Cancer  Comorbidity  Gene expression  Meta-analysis  Multimorbidity  Transcriptome Index. décimale : PER Périodiques Résumé : Background: Epidemiological and clinical evidence points to cancer as a comorbidity in people with autism spectrum disorders (ASD). A significant overlap of genes and biological processes between both diseases has also been reported. Methods: Here, for the first time, we compared the gene expression profiles of ASD frontal cortex tissues and 22 cancer types obtained by differential expression meta-analysis and report gene, pathway, and drug set-based overlaps between them. Results: Four cancer types (brain, thyroid, kidney, and pancreatic cancers) presented a significant overlap in gene expression deregulations in the same direction as ASD whereas two cancer types (lung and prostate cancers) showed differential expression profiles significantly deregulated in the opposite direction from ASD. Functional enrichment and LINCS L1000 based drug set enrichment analyses revealed the implication of several biological processes and pathways that were affected jointly in both diseases, including impairments of the immune system, and impairments in oxidative phosphorylation and ATP synthesis among others. Our data also suggest that brain and kidney cancer have patterns of transcriptomic dysregulation in the PI3K/AKT/MTOR axis that are similar to those found in ASD. Conclusions: Comparisons of ASD and cancer differential gene expression meta-analysis results suggest that brain, kidney, thyroid, and pancreatic cancers are candidates for direct comorbid associations with ASD. On the other hand, lung and prostate cancers are candidates for inverse comorbid associations with ASD. Joint perturbations in a set of specific biological processes underlie these associations which include several pathways previously implicated in both cancer and ASD encompassing immune system alterations, impairments of energy metabolism, cell cycle, and signaling through PI3K and G protein-coupled receptors among others. These findings could help to explain epidemiological observations pointing towards direct and inverse comorbid associations between ASD and specific cancer types and depict a complex scenario regarding the molecular patterns of association between ASD and cancer. En ligne : http://dx.doi.org/10.1186/s13229-019-0262-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=398

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