Littérature scientifique sur le sujet « GAD67 gene »
Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres
Sommaire
Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « GAD67 gene ».
À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.
Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.
Articles de revues sur le sujet "GAD67 gene"
SCHMIDLI, Robert S., Beverly E. FAULKNER-JONES, Leonard C. HARRISON, Roger F. L. JAMES et Henry J. DeAIZPURUA. « Cytokine regulation of glutamate decarboxylase biosynthesis in isolated rat islets of Langerhans ». Biochemical Journal 317, no 3 (1 août 1996) : 713–19. http://dx.doi.org/10.1042/bj3170713.
Texte intégralYANAGAWA, Yuchio, Takashi KOBAYASHI, Takashi KAMEI, Kenji ISHII, Michiharu NISHIJIMA, Akira TAKAKU, Takayasu KOBAYASHI et Shinri TAMURA. « Structure and alternative promoters of the mouse glutamic acid decarboxylase 67 gene ». Biochemical Journal 326, no 2 (1 septembre 1997) : 573–78. http://dx.doi.org/10.1042/bj3260573.
Texte intégralPedersen, Anette Amstrup, Helle Vestergaard Petersen, Nicoline Videbæk, Kresten Skak et Birgitte Koch Michelsen. « PDX-1 mediates glucose responsiveness of GAD67, but not GAD65, gene transcription in islets of Langerhans ». Biochemical and Biophysical Research Communications 295, no 2 (juillet 2002) : 243–48. http://dx.doi.org/10.1016/s0006-291x(02)00674-5.
Texte intégralBen David, Gil, Yam Amir, Kuldeep Tripathi, Lital Sharvit, Amir Benhos, Rachel Anunu, Gal Richter-Levin et Gil Atzmon. « Exposure to Juvenile Stress Induces Epigenetic Alterations in the GABAergic System in Rats ». Genes 14, no 3 (23 février 2023) : 565. http://dx.doi.org/10.3390/genes14030565.
Texte intégralLariviere, K., L. MacEachern, V. Greco, G. Majchrzak, S. Chiu, G. Drouin et V. L. Trudeau. « GAD65 and GAD67 Isoforms of the Glutamic Acid Decarboxylase Gene Originated Before the Divergence of Cartilaginous Fishes ». Molecular Biology and Evolution 19, no 12 (1 décembre 2002) : 2325–29. http://dx.doi.org/10.1093/oxfordjournals.molbev.a004057.
Texte intégralZhu, Xiya, Patricia J. Ward et Arthur W. English. « Selective Requirement for Maintenance of Synaptic Contacts onto Motoneurons by Target-Derived trkB Receptors ». Neural Plasticity 2016 (2016) : 1–11. http://dx.doi.org/10.1155/2016/2371893.
Texte intégralPöstyéni, Etelka, Andrea Kovács-Valasek, Péter Urbán, Lilla Czuni, György Sétáló, Csaba Fekete et Robert Gabriel. « Profile of miR-23 Expression and Possible Role in Regulation of Glutamic Acid Decarboxylase during Postnatal Retinal Development ». International Journal of Molecular Sciences 22, no 13 (30 juin 2021) : 7078. http://dx.doi.org/10.3390/ijms22137078.
Texte intégralSoghomonian, Jean-Jacques, et Nathalie Laprade. « Glutamate decarboxylase (GAD67 and GAD65) gene expression is increased in a subpopulation of neurons in the putamen of parkinsonian monkeys ». Synapse 27, no 2 (octobre 1997) : 122–32. http://dx.doi.org/10.1002/(sici)1098-2396(199710)27:2<122 ::aid-syn3>3.0.co;2-g.
Texte intégralKhalifa, D., H. Gabr, H. Fathy, H. Abdou et M. Batrawy. « Cognitive Impairment and the correlation with genetic Expression of GAD67, Gad65 and GABA beta2 Using Human Induced Pluripotent Stem Cells ». European Psychiatry 65, S1 (juin 2022) : S314. http://dx.doi.org/10.1192/j.eurpsy.2022.801.
Texte intégralGass, P., D. Inta, A. Luoni et M. A. Riva. « Differential Effects of MGluR5 Receptor Blockade on Behavior, Schizophrenia-relevant Gene Expression and Neuronal Activation Patterns from Development to Aging Mice ». European Psychiatry 41, S1 (avril 2017) : S165. http://dx.doi.org/10.1016/j.eurpsy.2017.01.2048.
Texte intégralThèses sur le sujet "GAD67 gene"
Djebbara-Hannas, Zahia. « Utilisation de vecteurs plasmidiques et d'oligonucléotides antisens pour exprimer et/ou inhiber le gène de la glutamate décarboxylase dans le système nerveux central ». Lyon 1, 1997. http://www.theses.fr/1997LYO1T166.
Texte intégralTUCCI, Marianna. « GAD67 gene and alcoholism. An association study between single nucleotide polymorphism and alcohol dependence ». Doctoral thesis, 2009. http://hdl.handle.net/11562/337346.
Texte intégralAlcoholism is one of the major social, economic and public health problems facing the world today. Social drinking can be associated with development of alcohol tolerance, leading in turn to abuse and dependence. Primary features of alcoholism include loss of control over consumption, obsessional thoughts about the next drink, and continuation of abuse despite negative health effects and social consequences. Epidemiologically alcoholism is defined as a heterogeneous, complex disorder with both genetic and environmental influences. A meta-analysis of twin studies has shown that the genetic influence of all addictive substances ranges from 40–70% and the heritability of alcoholism, derived from nearly 10000 twin pairs, is found to be 50%, showing that genetic and environmental risk factors for alcoholism are almost equally important although they may differ in the different populations. Additionally alcoholism is a disease with an underlying complex of biochemical pathophysiology. Unlike other addictive drugs, alcohol has widespread effects throughout the brain; it acts at a variety of targets within cell membranes and in the intracellular signal transduction, inducing effects on neurotransmitter and neurohormone membrane receptors and receptor-gated and voltage-activated ion channels. In the central nervous system, ethanol alters the activity of several neurotransmitters including monoamines and gamma-aminobutyric acid 2 (GABA). Genetic vulnerability to alcoholism is therefore likely due to a number of genes of small varying degrees in many neurotransmitter systems and signal transduction pathways. In particular, several studies suggest that GABA may be involved in alcohol withdrawal and tolerance; the genes encoding for glutamate decarboxylase (GAD), the rate-limiting enzyme in GABA synthesis, are of potential interest for their association to ethanol consumption and alcohol dependence. In our project we evaluated, in a case-control association study, the relationship between the GAD gene and alcohol use disorder. Specifically, the total cohort analyzed was 283 male individuals, 107 of which were alcohol dependent subjects and 176 controls. As a whole, in all experiments carried out a total of 26 single nucleotide polymorphisms (SNPs) localized in the promoter, exonic and intronic regions of the GAD 67 gene by using GenomeLab SNPStream Genotyping System technology were analyzed. Our results showed a significant difference in genotype distribution of one SNP (rs 11542313) localized in the exon 3 of the GAD 67 gene that is responsible for a silent mutation (His-His).
Alsamkari, Afraa Awad. « Gene expression in neurological disease : autism and Parkinson's disease ». Thesis, 2016. https://hdl.handle.net/2144/19182.
Texte intégral