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Gene Review

Gad1  -  glutamate decarboxylase 1

Mus musculus

Synonyms: 67 kDa glutamic acid decarboxylase, EP10, GAD-67, GAD25, GAD44, ...
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Disease relevance of Gad1


Psychiatry related information on Gad1

  • Those containing glutamate decarboxylase terminate in the superficial dorsal horn and are likely to be involved in antinociception, whereas those containing peptides terminate principally in motor nuclei and are likely to modulate motor activity [6].

High impact information on Gad1


Chemical compound and disease context of Gad1

  • Glutamatergic or GABAergic neuron-specific, long-term expression in neocortical neurons from helper virus-free HSV-1 vectors containing the phosphate-activated glutaminase, vesicular glutamate transporter-1, or glutamic acid decarboxylase promoter [5].
  • We report the transcriptional initiation sites and promoter sequences important for expression in islet beta-cells and C6 glioma cells, and demonstrate that the GAD67 promoter harbors elements that are responsive to glucose in primary islet cells [11].

Biological context of Gad1


Anatomical context of Gad1

  • Building on these results we show that Gad1-lacZ "knockin" reporter ES cell lines can be used to easily monitor Gad1 expression patterns and expression levels during ES differentiation [17].
  • The objective of this study was to define additional structures outside of the central nervous system that express Gad1, indicating those structures that may require its function for normal development [18].
  • 5. Tissues expressing Gad1 included the tail bud mesenchyme, the pharyngeal pouches and arches, the ectodermal placodes of the developing vibrissae, and the apical ectodermal ridge (AER), mesenchyme and ectoderm of the limb buds [18].
  • Reelin and glutamic acid decarboxylase (GAD)67 expressed by cortical gamma-aminobutyric acid-ergic interneurons are down-regulated in schizophrenia [13].
  • GAD activities and GABA contents were reduced to 20% and 7%, respectively, in the cerebral cortex of the newborn GAD67 -/- mice [2].

Associations of Gad1 with chemical compounds

  • Therefore, these results do not support the hypothesis of an involvement of Gad1 or Gad2 in the pathophysiology of acute ethanol withdrawal severity and the other ethanol related traits [19].
  • The dynamic expression of Gad1 in such tissues suggests a wider role for GABA signaling in development than was previously appreciated [18].
  • Protracted l-methionine (6.6 mmolkg for 15 days, twice a day) treatment in mice elicited in brain an increase of S-adenosyl-homocysteine, the processing product of the methyl donor S-adenosyl-methionine, and a marked decrease of reelin and GAD67 mRNAs in both WT and heterozygous reeler mice [13].
  • Furthermore, in GAD65-/- mouse brain, GAD67, which no longer partitions into the Triton X-114 detergent phase, still anchors to membranes at similar levels as in wild-type mice [14].
  • In brain extracts, almost all GAD67 is in an active holoenzyme form, saturated with its cofactor, pyridoxal phosphate [20].

Physical interactions of Gad1


Co-localisations of Gad1


Regulatory relationships of Gad1


Other interactions of Gad1


Analytical, diagnostic and therapeutic context of Gad1


  1. Conserved function of Caenorhabditis elegans UNC-30 and mouse Pitx2 in controlling GABAergic neuron differentiation. Westmoreland, J.J., McEwen, J., Moore, B.A., Jin, Y., Condie, B.G. J. Neurosci. (2001) [Pubmed]
  2. Cleft palate and decreased brain gamma-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase. Asada, H., Kawamura, Y., Maruyama, K., Kume, H., Ding, R.G., Kanbara, N., Kuzume, H., Sanbo, M., Yagi, T., Obata, K. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  3. Localization and quantitation of expression of two glutamate decarboxylase genes in pancreatic beta-cells and other peripheral tissues of mouse and rat. Faulkner-Jones, B.E., Cram, D.S., Kun, J., Harrison, L.C. Endocrinology (1993) [Pubmed]
  4. CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. Tarbell, K.V., Lee, M., Ranheim, E., Chao, C.C., Sanna, M., Kim, S.K., Dickie, P., Teyton, L., Davis, M., McDevitt, H. J. Exp. Med. (2002) [Pubmed]
  5. Glutamatergic or GABAergic neuron-specific, long-term expression in neocortical neurons from helper virus-free HSV-1 vectors containing the phosphate-activated glutaminase, vesicular glutamate transporter-1, or glutamic acid decarboxylase promoter. Rasmussen, M., Kong, L., Zhang, G.R., Liu, M., Wang, X., Szabo, G., Curthoys, N.P., Geller, A.I. Brain Res. (2007) [Pubmed]
  6. A confocal microscopic survey of serotoninergic axons in the lumbar spinal cord of the rat: co-localization with glutamate decarboxylase and neuropeptides. Maxwell, L., Maxwell, D.J., Neilson, M., Kerr, R. Neuroscience (1996) [Pubmed]
  7. Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice. Tisch, R., Yang, X.D., Singer, S.M., Liblau, R.S., Fugger, L., McDevitt, H.O. Nature (1993) [Pubmed]
  8. Cytotoxic T cells specific for glutamic acid decarboxylase in autoimmune diabetes. Panina-Bordignon, P., Lang, R., van Endert, P.M., Benazzi, E., Felix, A.M., Pastore, R.M., Spinas, G.A., Sinigaglia, F. J. Exp. Med. (1995) [Pubmed]
  9. Cerebellar granule cell neurogenesis is regulated by cell-cell interactions in vitro. Gao, W.O., Heintz, N., Hatten, M.E. Neuron (1991) [Pubmed]
  10. Neogenesis of cerebellar Purkinje neurons from gene-marked bone marrow cells in vivo. Priller, J., Persons, D.A., Klett, F.F., Kempermann, G., Kreutzberg, G.W., Dirnagl, U. J. Cell Biol. (2001) [Pubmed]
  11. Characterization of the rat GAD67 gene promoter reveals elements important for basal transcription and glucose responsiveness. Pedersen, A.A., Videbaek, N., Skak, K., Petersen, H.V., Michelsen, B.K. DNA Seq. (2001) [Pubmed]
  12. Quantitative trait loci involved in genetic predisposition to acute alcohol withdrawal in mice. Buck, K.J., Metten, P., Belknap, J.K., Crabbe, J.C. J. Neurosci. (1997) [Pubmed]
  13. An epigenetic mouse model for molecular and behavioral neuropathologies related to schizophrenia vulnerability. Tremolizzo, L., Carboni, G., Ruzicka, W.B., Mitchell, C.P., Sugaya, I., Tueting, P., Sharma, R., Grayson, D.R., Costa, E., Guidotti, A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  14. The hydrophilic isoform of glutamate decarboxylase, GAD67, is targeted to membranes and nerve terminals independent of dimerization with the hydrophobic membrane-anchored isoform, GAD65. Kanaani, J., Lissin, D., Kash, S.F., Baekkeskov, S. J. Biol. Chem. (1999) [Pubmed]
  15. Ontogeny of glutamic acid decarboxylase gene expression in the mouse pancreas. Pleau, J.M., Throsby, M., Esling, A., Dardenne, M. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  16. Reelin and glutamic acid decarboxylase67 promoter remodeling in an epigenetic methionine-induced mouse model of schizophrenia. Dong, E., Agis-Balboa, R.C., Simonini, M.V., Grayson, D.R., Costa, E., Guidotti, A. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  17. Neuronal development of embryonic stem cells: a model of GABAergic neuron differentiation. Westmoreland, J.J., Hancock, C.R., Condie, B.G. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  18. Dynamic expression of a glutamate decarboxylase gene in multiple non-neural tissues during mouse development. Maddox, D.M., Condie, B.G. BMC Dev. Biol. (2001) [Pubmed]
  19. Evaluation of the glutamate decarboxylase genes Gad1 and Gad2 as candidate genes for acute ethanol withdrawal severity in mice. Fehr, C., Rademacher, B.L., Buck, K.J. Prog. Neuropsychopharmacol. Biol. Psychiatry (2003) [Pubmed]
  20. Two forms of the gamma-aminobutyric acid synthetic enzyme glutamate decarboxylase have distinct intraneuronal distributions and cofactor interactions. Kaufman, D.L., Houser, C.R., Tobin, A.J. J. Neurochem. (1991) [Pubmed]
  21. The Cav2.1/alpha1A (P/Q-type) voltage-dependent calcium channel mediates inhibitory neurotransmission onto mouse cerebellar Purkinje cells. Stephens, G.J., Morris, N.P., Fyffe, R.E., Robertson, B. Eur. J. Neurosci. (2001) [Pubmed]
  22. Ectopic expression of the Dlx genes induces glutamic acid decarboxylase and Dlx expression. Stühmer, T., Anderson, S.A., Ekker, M., Rubenstein, J.L. Development (2002) [Pubmed]
  23. Developmental profile of ErbB receptors in murine central nervous system: implications for functional interactions. Fox, I.J., Kornblum, H.I. J. Neurosci. Res. (2005) [Pubmed]
  24. Cholinergic properties of neurons differentiated from an embryonal carcinoma cell-line (P19). Parnas, D., Linial, M. Int. J. Dev. Neurosci. (1995) [Pubmed]
  25. DNA methyltransferase 1 regulates reelin mRNA expression in mouse primary cortical cultures. Noh, J.S., Sharma, R.P., Veldic, M., Salvacion, A.A., Jia, X., Chen, Y., Costa, E., Guidotti, A., Grayson, D.R. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  26. Reelin down-regulation in mice and psychosis endophenotypes. Tueting, P., Doueiri, M.S., Guidotti, A., Davis, J.M., Costa, E. Neuroscience and biobehavioral reviews (2006) [Pubmed]
  27. Epilepsy in mice deficient in the 65-kDa isoform of glutamic acid decarboxylase. Kash, S.F., Johnson, R.S., Tecott, L.H., Noebels, J.L., Mayfield, R.D., Hanahan, D., Baekkeskov, S. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  28. Dark-rearing-induced reduction of GABA and GAD and prevention of the effect by BDNF in the mouse retina. Lee, E.J., Gibo, T.L., Grzywacz, N.M. Eur. J. Neurosci. (2006) [Pubmed]
  29. Pancreatic hormone and glutamic acid decarboxylase expression in the mouse thymus: a real-time PCR study. Pléau, J.M., Esling, A., Geutkens, S., Dardenne, M., Homo-Delarche, F. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
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