Glutamic acid decarboxylase

If a substance is to be a NT it should be possible to demonstrate appropriate enzymes for its synthesis from a precursor at its site of action, although peptides are transported to their sites of location and action after synthesis in the axon or distal neuronal cell body. The specificity of any enzyme system must also be established, especially if they are to be modified to manipulate the levels of a particular NT, or used as markers for it. Thus choline acetyltransferase (ChAT) may be taken as indicative of ACh and glutamic acid decarboxylase (GAD) of GABA but some of the synthesising enzymes for the monoamines lack such specificity. 

Asada, H, Kawamura, Y, Maruyama, K, Kume, H, Ding, RG, Kanbara, N, Kuzume, H, Sanbo, M, Yagi, T and Obata, K (1997) Cleft palate and decreased brain y-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase. Proc. Natl. Acad. Sci. USA 94 6496-6499. 

Fig. 45. GABAergic neurone synapse. GAD, glutamic acid decarboxylase M, mito-chodria G, GABA. 

Majumdar, S. Mallick, B. N. (2003). Increased levels of tyrosine hydroxylase and glutamic acid decarboxylase in locus coeruleus neurons after rapid eye movement sleep deprivation in rats. Neurosci. Lett. 338, 193-6. 

Human glutamic acid decarboxylase (hGAD) CaMVenhanced 35S promoter/ TEV 5 UTR/nos terminator Low alkaloid tobacco Solanum tuberosum 0.4% ofTSP of leaves or tuber 12... 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Glutamic acid decarboxylase Mitochondrial Phosphate-activated glutaminaset... 

CREM CRE-modulatory protein GAD glutamic acid decarboxylase... 

Diabetes (type 1) 192 48% Islet IA-2, glutamic acid decarboxylase Infectious agents, ultraviolet radiation/vitamin D... 

Ji, F., Kanbara, N., and Obata, K. (1999) GABA and histogenesis in fetal and neonatal mouse brain lacking both the isoforms of glutamic acid decarboxylase. Neurosci. Res. 33, 187-194. 

Peat, M. A., and Gibb, J. W. (1983) The effects of phencyclidine on glutamic acid decarboxylase activity in several regions of the rat brain. Neurosci. Lett., 35 301-306. 

This situation is largely due to the rise of type 2 DM which now accounts for 85-90% of all cases of DM type 1 DM in which antibodies directed at the enzyme glutamic acid decarboxylase (GAD) attack and destroy the insulin-producing (3 cells... 

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