Glutamate decarboxylase
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| Identifiers | |
| Symbol | GAD1 |
| Alt. Symbols | GLUTAMATE DECARBOXYLASE, BRAIN, 67-KD; GAD67 |
| Entrez | 2571 |
| HUGO | 4092 |
| OMIM | 605363 |
| UniProt | Q99259 |
| Other data | |
| EC number | 4.1.1.15 |
| Locus | Chr. 2 q31 |
| Identifiers | |
| Symbol | GAD2 |
| Entrez | 2572 |
| HUGO | 11284 |
| OMIM | 4093 |
| PDB | 1ES0 |
| UniProt | Q05329 |
| Other data | |
| EC number | 4.1.1.15 |
| Locus | Chr. 10 p11.23 |
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Overview
Glutamate decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2. GAD uses PLP as a cofactor. The reaction proceeds as follows:
HOOC-CH2-CH2-CH(NH2)-COOH → CO2 + HOOC-CH2-CH2-CH2NH2
In mammals, GAD exists in two isoforms encoded by two different genes - Gad1 and Gad2. These isoforms are GAD67 and GAD65 with molecular weights of 67 and 65 kDa, respectively.[1] GAD1 and GAD2 are expressed in the brain where GABA is used as a neurotransmitter, GAD2 is also expressed in the pancreas.
Role in pathology
Diabetes
Both GAD67 and GAD65 are targets of autoantibodies in people who later develop insulin-dependent diabetes mellitus.[2] [3] Injections with GAD65 has been shown to preserve some insulin production for 30 months in humans with type 1 diabetes.[4]
Schizophrenia and Bipolar disorder
Substantial dysregulation of GAD mRNA expression, coupled with downregulation of reelin, is observed in schizophrenia and bipolar disorder.[5] The most pronounced downregulation of GAD67 was found in hippocampal stratum oriens layer in both disorders and in other layers and structures of hippocampus with varying degrees.[6]
References
- ↑ Erlander MG, Tillakaratne NJ, Feldblum S, Patel N, Tobin AJ (1991). "Two genes encode distinct glutamate decarboxylases". Neuron 7 (1): 91–100. doi:10.1016/0896-6273(91)90077-D. PMID 2069816.
- ↑ Baekkeskov S, Aanstoot HJ, Christgau S, Reetz A, Solimena M, Cascalho M, Folli F, Richter-Olesen H, De Camilli P, Camilli PD (1990). "Identification of the 64K autoantigen in insulin-dependent diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase". Nature 347 (6289): 151–6. doi:10.1038/347151a0. PMID 1697648.
- ↑ Kaufman DL, Erlander MG, Clare-Salzler M, Atkinson MA, Maclaren NK, Tobin AJ (1992). "Autoimmunity to two forms of glutamate decarboxylase in insulin-dependent diabetes mellitus". J. Clin. Invest. 89 (1): 283–92. PMID 1370298.
- ↑ Diamyd press release
- ↑ Woo TU, Walsh JP, Benes FM (2004). "Density of glutamic acid decarboxylase 67 messenger RNA-containing neurons that express the N-methyl-D-aspartate receptor subunit NR2A in the anterior cingulate cortex in schizophrenia and bipolar disorder". Arch. Gen. Psychiatry 61 (7): 649–57. doi:10.1001/archpsyc.61.7.649. PMID 15237077.
- ↑ Benes FM, Lim B, Matzilevich D, Walsh JP, Subburaju S, Minns M (2007). "Regulation of the GABA cell phenotype in hippocampus of schizophrenics and bipolars". Proc. Natl. Acad. Sci. U.S.A. 104 (24): 10164–9. doi:10.1073/pnas.0703806104. PMID 17553960.
External links
- Genetics, Expression Profiling Support GABA Deficits in Schizophrenia - Schizophrenia Research Forum, 25 June 2007.
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
