ライフサイエンスコーパス: glutamic acid decarboxylase

1 ter enzyme inhibition (monoamine oxidase and glutamic acid decarboxylase).

2 ve for GABA and the GABA-synthesizing enzyme glutamic acid decarboxylase.

3 sporters or is synthesized from glutamate by glutamic acid decarboxylase.

4 choline acetlytransferase, substance P, and glutamic acid decarboxylase.

5 5 has the ability to inhibit the activity of glutamic acid decarboxylase.

6 and there were always some Th1 responses to glutamic acid decarboxylase.

7 actin-2, GlyR, D1R, D2R, AMPAR, GABA(B)R and glutamic acid decarboxylase.

8 , consistent with a presynaptic reduction in glutamic acid decarboxylase 1 (Gad1) and glutamic acid d

9 ext, we produced conditional null alleles of Glutamic acid decarboxylase 1 (Gad1) and Resistant to di

10 nerated transgenic mouse lines that suppress glutamic acid decarboxylase 1 (GAD1) in either cholecyst

11 Levels of gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase 1 (GAD1), the enzyme that sy

12 NA levels for somatostatin, parvalbumin, and glutamic acid decarboxylase 1.

13 in glutamic acid decarboxylase 1 (Gad1) and glutamic acid decarboxylase 2 (Gad2) levels, and GABA im

14 hether E(2) directly regulates expression of glutamic acid decarboxylase 2 (gad2), the enzyme primari

15 hypothalamus activated a small population of glutamic acid decarboxylase 2 (GAD2)-expressing neurons

16 The glutamic acid decarboxylase 2 but not the parvalbumin su

17 In contrast, the silencing of glutamic acid decarboxylase 2-positive interneurons, whi

18 x/klox) mice exhibited reduced expression of glutamic acid decarboxylase 65 (a GABA synthase), increa

19 n of T1D-related autoantigens [proinsulin or glutamic acid decarboxylase 65 (GAD)] delayed T1D onset,

20 Several lines of evidence implicate the glutamic acid decarboxylase 65 (GAD-65) peptide, p524-54

21 tis Abs as well as thyroperoxidase (TPO) and glutamic acid decarboxylase 65 (GAD65) Abs.

22 Glutamic acid decarboxylase 65 (GAD65) and autoantibodie

23 during early embryonic ages (E12-E16), both glutamic acid decarboxylase 65 (GAD65) and GABA were exp

24 l groups, as identified by the expression of glutamic acid decarboxylase 65 (GAD65) and type 2 vesicu

25 Glutamic acid decarboxylase 65 (GAD65) appears to be an

26 r the development of insulin autoantibodies, glutamic acid decarboxylase 65 (GAD65) autoantibodies, i

27 diabetic patients the B cell response to the glutamic acid decarboxylase 65 (GAD65) autoantigen is ex

28 been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their

29 ain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription th

30 Glutamic acid decarboxylase 65 (GAD65)- and Doublecortin

31 pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD

32 ecipient mice immunized with pDNA encoding a glutamic acid decarboxylase 65 (GAD65)-IgFc fusion prote

33 OFQ neurons (approximately 50-60%) expressed glutamic acid decarboxylase 65 and 67 mRNAs, markers for

34 gic knowledge on cerebellar ataxia (CA) with glutamic acid decarboxylase 65 antibodies (GAD65-Abs) is

35 Although this 12-mer glutamic acid decarboxylase 65 fragment is only slightly

36 etic (NOD) mice and BALB/c mice treated with glutamic acid decarboxylase 65 peptides (p206 and p221).

37 cell populations could be identified for two glutamic acid decarboxylase 65 peptides, but tetramers w

38 with syndromes associated with antibodies to glutamic acid decarboxylase 65 were used as controls.

39 e responsive to an immunodominant epitope of glutamic acid decarboxylase 65(555-567), which is identi

40 /HuD (Hu-antigen C/Hu-antigen D), and GAD65 (glutamic acid decarboxylase 65), as well as the oligoden

41 ice lacking the GABA synthetic enzyme GAD65 (glutamic acid decarboxylase 65).

42 id, beta-lactoglobulin, and the autoantigens glutamic acid decarboxylase 65, heat shock protein 60, a

43 globulin) and diabetes-related autoantigens (glutamic acid decarboxylase 65, insulin, heat shock prot

44 t the type 1 diabetes-associated autoantigen glutamic acid decarboxylase 65, the melanocyte different

45 Serologic study results revealed glutamic acid decarboxylase 65-IgG in all cases (median

46 man syndrome (4 classic; 5 variant; 66% were glutamic acid decarboxylase 65-IgG positive) and 1 with

47 brane protein (PMP) antibody positivity; and glutamic acid decarboxylase 65-kDa isoform (GAD65) antib

48 atus of the second GABA-synthesizing enzyme, glutamic acid decarboxylase 65-kDa isoform (GAD65), rema

49 (vesicular GABA transporter), and GAD65/67 (glutamic acid decarboxylase 65/67) in interneurons withi

50 f the enzyme responsible for GABA synthesis, glutamic acid decarboxylase (65+67), in the ventromedial

51 ved DC were pulsed with preproinsulin (PPI), glutamic acid decarboxylase (65-kDa isoform; GAD65), and

52 ted autoantigen from the human islet antigen glutamic acid decarboxylase, 65-kDa isoform (GAD65), by

53 pus, as shown by decreased immunolabeling of glutamic acid decarboxylase-65 (GAD65), GAD67, and GABA

54 nced the immunohistochemical localization of glutamic acid decarboxylase-65 (GAD65), the rate-limitin

55 PMCA2a also did not colocalize with glutamic acid decarboxylase-65, a marker of GABA-ergic t

56 A receptor activation, or levels of punctate glutamic acid decarboxylase-65/67 immunoreactivity.

57 fluorescent protein under the control of the glutamic acid decarboxylase 65kDa (GAD65) promoter.

58 Reelin and glutamic acid decarboxylase 67 (GAD(67)) expression down

59 erences is strongly correlated with that for glutamic acid decarboxylase 67 (GAD(67)) mRNA, a synthes

60 They exhibit, (i) a down-regulation of glutamic acid decarboxylase 67 (GAD(67))-positive neuron

61 in the subset of presynaptic cells that lack glutamic acid decarboxylase 67 (GAD).

62 tors contained GABA and stained positive for glutamic acid decarboxylase 67 (GAD-67) as shown by immu

63 (A) receptors with the GABA synthetic enzyme glutamic acid decarboxylase 67 (GAD67) also resulted in

64 1 receptor (CB1R) in CCK(b) cells, and lower glutamic acid decarboxylase 67 (GAD67) and increased mu

65 lation of the corresponding mRNAs, including glutamic acid decarboxylase 67 (GAD67) and reelin (RELN)

66 The expression of GABAergic marker glutamic acid decarboxylase 67 (GAD67) and the number of

67 in the cortex of schizophrenia (SZ) brains, glutamic acid decarboxylase 67 (GAD67) expression is dow

68 pendent expression levels of parvalbumin and glutamic acid decarboxylase 67 (GAD67) in schizophrenia

69 eased levels of the GABA-synthesizing enzyme glutamic acid decarboxylase 67 (GAD67) in the mPFC for u

70 The enzyme glutamic acid decarboxylase 67 (GAD67) is critical for G

71 dies have consistently found lower levels of glutamic acid decarboxylase 67 (GAD67) messenger RNA (mR

72 hat this treatment down-regulated reelin and glutamic acid decarboxylase 67 (GAD67) mRNA expression b

73 Reelin and glutamic acid decarboxylase 67 (GAD67) mRNAs and protein

74 histochemistry with immunohistochemistry for glutamic acid decarboxylase 67 (GAD67) or calcium/calmod

75 expressing green fluorescent protein at the glutamic acid decarboxylase 67 (GAD67) promoter.

76 ents, these interneurons show reduced PV and glutamic acid decarboxylase 67 (GAD67), an enzyme that s

77 ter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons

78 rojecting to the PVN were immunoreactive for glutamic acid decarboxylase 67 (GAD67), NPY, and beta-en

79 cGMPir was also found in association with glutamic acid decarboxylase 67 (GAD67)- and vesicular gl

80 were significantly correlated with those in glutamic acid decarboxylase 67 and cholecystokinin mRNA

81 Reduced expression of glutamic acid decarboxylase 67 and parvalbumin was accom

82 eurons positively stained with antibodies to glutamic acid decarboxylase 67 was also reduced in the d

83 ss GFP (green fluorescent protein) in GAD67 (glutamic acid decarboxylase 67)-synthesizing cells, we i

84 ion of brain-derived neurotrophic factor and glutamic acid decarboxylase 67, an increased expression

85 staining for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase 67, calretinin and/or calbin

86 of DNMT1 to psychiatric candidate promoters (glutamic acid decarboxylase 67, Reelin, and brain-derive

87 We used glutamic acid decarboxylase 67-kDa isoform (GAD67) and p

88 Levels of the GABA-synthesizing enzyme glutamic acid decarboxylase 67-kDa isoform (GAD67) in th

89 n the same neurons that coexpress reelin and glutamic acid decarboxylase 67.

90 Using glutamic acid decarboxylase 67/65 antibodies to mark GAB

91 by using in situ hybridization combined with glutamic acid decarboxylase 67/65, vesicular glutamate t

92 ression for the synthesizing enzyme of GABA, glutamic acid decarboxylase(67), in the same subjects.

93 g N-methyl-D-aspartate receptor subunits and glutamic acid decarboxylase, 67 kDa isoform protein leve

94 gamma-aminobutyric acid-related inhibition (glutamic acid decarboxylase, 67 kDa isoform) in the BLA

95 ergic, gamma-aminobutyric acid (GABA)-ergic (glutamic acid decarboxylase, 67 kDa isoform; GAD-67), an

96 ex, a quantitative analysis of reelin and of glutamic acid decarboxylase-67 (GAD(67)) mRNA-positive n

97 nsive cells were GABAergic as illustrated by glutamic acid decarboxylase-67 (GAD67) immunostaining.

98 nel of immunocytochemical markers, including glutamic acid decarboxylase-67 (GAD67), somatostatin, an

99 Here, we used transgenic glutamic acid decarboxylase-67 (GAD67)-GFP expressing mi

100 transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67).

101 With glutamic acid decarboxylase-67 and gamma-aminobutyric ac

102 rated through reduced expression of mRNA for glutamic acid decarboxylase-67 and micro-opioid receptor

103 OFC), reduced gray matter volume and reduced glutamic acid decarboxylase 67kDa isoform (GAD67) messen

104 Few (11.33%) terminals contain glutamic acid decarboxylase (a marker for GABAergic axon

105 orn, and most apoptotic cells also expressed glutamic acid decarboxylase, a key enzyme for the synthe

106 f an adenoassociated virus vector expressing glutamic acid decarboxylase (AAV-GAD).

107 ences in phosphate-activated glutaminase and glutamic acid decarboxylase activities in equivalent spe

108 Glutamic acid decarboxylase activities were twofold grea

109 Greater phosphate-activated glutaminase and glutamic acid decarboxylase activities, specific to schi

110 um of Stiff-person syndrome/muscle rigidity (glutamic acid decarboxylase, amphiphysin, GABA(A)-recept

111 c factor receptor) and a transmitter enzyme (glutamic acid decarboxylase and aromatic acid decarboxyl

112 nd the neurotransmitter-synthesizing enzymes glutamic acid decarboxylase and aromatic amino acid deca

113 In situ hybridization for glutamic acid decarboxylase and immunocytochemistry for

114 g NE cells and foci of NED in human CaP, (b) glutamic acid decarboxylase and its product (gamma-amino

115 antibodies against the GABA synthetic enzyme glutamic acid decarboxylase and synaptophysin support th

116 pothalamic glutamatergic neurons, as well as glutamic acid decarboxylase and vesicular GABA transport

117 d unc-47 encode the GABA biosynthetic enzyme glutamic acid decarboxylase and vesicular transporter, r

118 did not contain the GABA-synthesizing enzyme glutamic acid decarboxylase and were therefore glycinerg

119 (Hu, Yo, Ri, CV2, Tr, amphiphysin, and Ma2), glutamic acid decarboxylase, and mGluR1 antibodies.

120 Autoantibodies to insulin, glutamic acid decarboxylase, and the insulinoma-associat

121 Four patients also had high glutamic acid decarboxylase antibodies (>1000 U/ml), and

122 ms of pathology, many patients with SPS have glutamic acid decarboxylase antibodies (GAD-ab), but the

123 Little is known of glutamic acid decarboxylase antibodies (GAD-abs) in the

124 tions of SPS despite the persistence of anti-glutamic acid decarboxylase antibodies following auto-HS

125 riodontal conditions, retinopathy, and serum glutamic acid decarboxylase antibody (GADA) titers in re

126 Two anti-glutamic acid decarboxylase antibody-positive patients w

127 els or N-methyl-D-aspartate receptors, or to glutamic acid decarboxylase, are found in patients with

128 ln3-knockout mice have decreased activity of glutamic acid decarboxylase as a result of the inhibitio

129 We investigated the association of glutamic acid decarboxylase autoantibodies (GADA) and in

130 balanced for age, sex, disease duration, and glutamic acid decarboxylase autoantibody titers.

131 s for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoan

132 No significant differences in glutamic acid decarboxylase-bouton densities were found

133 activity to the neuronal marker NeuN, and to glutamic acid decarboxylase, but not to glial fibrillary

134 kers of PGCs including tyrosine hydroxylase, glutamic acid decarboxylase, calbindin, or calretinin, a

135 When receiving GABAergic innervation from glutamic acid decarboxylase-containing interneurons, pyr

136 ain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert

137 axon terminals in these synapses coexpressed glutamic acid decarboxylase, findings that are of functi

138 minotransferase, aspartate aminotransferase, glutamic acid decarboxylase, GABA-transaminase, and succ

139 hydroxylase (TH), DA transporter (DAT), and glutamic acid decarboxylase (GAD 65/67), over 17 days in

140 of GABA, its rate-limiting synthetic enzyme glutamic acid decarboxylase (GAD(65) and GAD(67) isoform

141 s visualized with ICC for the 67-kDa form of glutamic acid decarboxylase (GAD(67)) and in situ hybrid

142 tu hybridization to localize mRNA for 67-kDa glutamic acid decarboxylase (GAD(67)) and related to the

143 aminobutyric acid (GABA)-synthesizing enzyme glutamic acid decarboxylase (GAD(67)) in the visual syst

144 gamma-aminobutyric acid synthesizing enzyme glutamic acid decarboxylase (GAD(67)) with digoxigenin.

145 rodents, METH induces apoptosis of striatal glutamic acid decarboxylase (GAD) -containing neurons.

146 zation of NOD mice with autoantigens such as glutamic acid decarboxylase (GAD) 221-235 peptide (p221)

147 DMH-NPY neurons expressed Glutamic Acid Decarboxylase (GAD) 65 and 67, suggesting

148 A levels of the following GABAergic markers: glutamic acid decarboxylase (GAD) 65 and 67; GABA plasma

149 High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observ

150 Glutamic acid decarboxylase (GAD) 65 is one of the major

151 horn levels of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD) 65 kDa ipsilateral to

152 ent protein (GFP) driven by the promoter for glutamic acid decarboxylase (GAD) 65 kDa, 67 kDa, or tyr

153 Basal expression of glutamic acid decarboxylase (GAD) 65 mRNA was increased

154 colocalization of VGLUT1 or VGLUT2 mRNAs in glutamic acid decarboxylase (GAD) 65-positive neurons, i

155 the SHRP, this study assessed expression of glutamic acid decarboxylase (GAD) 67 in key stress-regul

156 A down-regulation of reelin and glutamic acid decarboxylase (GAD) 67 mRNAs was detected

157 on of genes encoding GABA receptor subunits, glutamic acid decarboxylase (GAD) and a GABA transporter

158 gamma aminobutyric acid synthesizing enzyme glutamic acid decarboxylase (GAD) and choline acetyltran

159 ys an important role in regulating soluble l-glutamic acid decarboxylase (GAD) and membrane-associate

160 Gene transfer of glutamic acid decarboxylase (GAD) and other methods that

161 talytic subunit-related protein, insulin, or glutamic acid decarboxylase (GAD) are believed to play i

162 High levels of antibodies against glutamic acid decarboxylase (GAD) are observed in patien

163 High titers of autoantibodies to glutamic acid decarboxylase (GAD) are well documented in

164 or DR4, and 29.5% positive for either IA2 or glutamic acid decarboxylase (GAD) autoantibodies.

165 In this study a glutamic acid decarboxylase (GAD) diabetogenic epitope w

166 l-Glutamic acid decarboxylase (GAD) exists as both membran

167 sporter (GLYT2) for glycinergic neurons, and glutamic acid decarboxylase (GAD) for GABAergic neurons.

168 ility, and potential efficacy of transfer of glutamic acid decarboxylase (GAD) gene with adeno-associ

169 is is controlled by enzymes derived from two glutamic acid decarboxylase (GAD) genes, GAD1 and GAD2,

170 Antibodies to glutamic acid decarboxylase (GAD) have been associated w

171 Antibodies to glutamic acid decarboxylase (GAD) have been found in pat

172 iabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in beta cells have sug

173 fiber terminals (MFTs) are known to express glutamic acid decarboxylase (GAD) in early postnatal dev

174 atment group, there was higher expression of glutamic acid decarboxylase (GAD) in layer V of cortex a

175 f the rate-limiting GABA-synthesizing enzyme glutamic acid decarboxylase (GAD) is decreased in Brodma

176 Glutamic acid decarboxylase (GAD) is the rate-limiting e

177 of activation (Fos) of GABAergic neurons and glutamic acid decarboxylase (GAD) mRNA expression in the

178 nthesized from L-glutamic acid by the enzyme glutamic acid decarboxylase (GAD) of which there are two

179 umerically compares cortical and hippocampal glutamic acid decarboxylase (GAD) positive neurons betwe

180 probe for imaging the activity of the enzyme glutamic acid decarboxylase (GAD) present in neurons.

181 Glutamic acid decarboxylase (GAD) produces GABA; the two

182 icacy of immunohistochemical localization of glutamic acid decarboxylase (GAD) protein, specifically

183 Glutamic acid decarboxylase (GAD) sequence 206-220 (desi

184 bnormalities, including decreased reelin and glutamic acid decarboxylase (GAD)(67) expression, decrea

185 d transection at approximately T12 increases glutamic acid decarboxylase (GAD)(67) in both the dorsal

186 ctive neurons (IRNs) in these nuclei contain glutamic acid decarboxylase (GAD), a marker of GABAergic

187 pocampal slices and activity measurements of glutamic acid decarboxylase (GAD), a PLP-dependent enzym

188 ry for calbindin (CALB), parvalbumin (PARV), glutamic acid decarboxylase (GAD), and choline transport

189 dinucleotide phosphate-diaphorase (NADPH-d), glutamic acid decarboxylase (GAD), cytochrome oxidase (C

190 ed whether the expression of two isoforms of glutamic acid decarboxylase (GAD), GAD65 (GAD2) and GAD6

191 itter that is synthesized by two isoforms of glutamic acid decarboxylase (GAD), GAD65 and GAD67.

192 he alpha(1A)-AR colocalized with markers for glutamic acid decarboxylase (GAD), gamma-aminobutyric ac

193 minobutyric acid (GABA)-synthesizing enzyme, glutamic acid decarboxylase (GAD), in the prefrontal cor

194 ied expression of the GABA synthetic enzyme, glutamic acid decarboxylase (GAD), in the VMH of control

195 disorder characterized by autoantibodies to glutamic acid decarboxylase (GAD), the enzyme responsibl

196 ly detect somal immunoreactivity for GABA or glutamic acid decarboxylase (GAD), the enzyme that produ

197 neuronal marker, or to the 67-kDa isoform of glutamic acid decarboxylase (GAD), the rate-limiting enz

198 wholemounts immunostained with antibodies to glutamic acid decarboxylase (GAD), vesicular acetylcholi

199 ficity of these alterations, the activity of glutamic acid decarboxylase (GAD), was also measured in

200 ific changes of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD), with increased GAD-67

201 tions of embryos (E12-15) were processed for glutamic acid decarboxylase (GAD)-65 and L1 immunocytoch

202 the presence of the mRNA for DNPI/VGLUT2 and glutamic acid decarboxylase (GAD)-67 was mutually exclus

203 e and some were parvalbumin-, calbindin-, or glutamic acid decarboxylase (GAD)-67-positive.

204 Dye release is reduced in both glutamic acid decarboxylase (GAD)-immunoreactive and GAD

205 unoreactivity (MOR1-IR) was colocalized with glutamic acid decarboxylase (GAD)-IR in profiles apposin

206 The nAChRs in all mice colocalized with glutamic acid decarboxylase (GAD)-positive interneurons

207 ErbB4, a key NRG1 receptor, is expressed in glutamic acid decarboxylase (GAD)-positive neurons, litt

208 II presentation of the diabetes autoantigen glutamic acid decarboxylase (GAD).

209 staining for c-Fos protein with staining for glutamic acid decarboxylase (GAD).

210 hibitory neurotransmitter, is synthesized by glutamic acid decarboxylase (GAD).

211 -Ig dimers tethered to peptides derived from glutamic acid decarboxylase (GAD)65 (sIA(g7)-pGAD65).

212 d a group of neurons that contained mRNA for glutamic acid decarboxylase (GAD)65 and GAD67 within the

213 the enzymes responsible for GABA synthesis, glutamic acid decarboxylase (GAD)65 and GAD67.

214 nobutyric acid (GABA) transporter (vGAT) and glutamic acid decarboxylase (GAD)65 in the GABAergic con

215 Glutamic acid decarboxylase (GAD)65 is an early and impo

216 Additionally, glutamic acid decarboxylase (GAD)65-loaded tolDCs from w

217 on, with either green fluorescent protein or glutamic acid decarboxylase (GAD)65/67 immunoreactivity

218 t increase in colocalization coefficients of glutamic acid decarboxylase (GAD)65/p38 immunoreactivity

219 Here, we study the distribution of glutamic acid decarboxylase (GAD)67 and GLY transporter

220 Reelin and glutamic acid decarboxylase (GAD)67 expressed by cortica

221 reen fluorescent protein (GFP) driven by the glutamic acid decarboxylase (GAD)67 promoter.

222 uorescent protein (GFP) is controlled by the glutamic acid decarboxylase (GAD)67 promotor.

223 aminobutyric acid (GABA) synthesizing enzyme glutamic acid decarboxylase (GAD)67, labeled with digoxi

224 parvalbumin-positive- and a subpopulation of glutamic acid decarboxylase (GAD)67-positive interneuron

225 is synthesized by two isoforms of the enzyme glutamic acid decarboxylase (GAD): GAD65 and GAD67.

226 ic acid (GABA); the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD); GABA transporter 1; t

227 ic acid (GABA); the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD); GABA transporter 1; t

228 g GABA, two isoforms of its synthetic enzyme glutamic acid decarboxylase (GAD-65 and GAD-67), and the

229 ites were labeled with the 65-kDa isoform of glutamic acid decarboxylase (GAD-65) as presynaptic mark

230 nobutyric acid (GABA), its synthetic enzyme, glutamic acid decarboxylase (GAD-67) and its receptor su

231 -label immunohistochemistry for ER alpha and glutamic acid decarboxylase (GAD; a marker of GABAergic

232 P), or Cre-recombinase in cells that contain glutamic acid decarboxylase (GAD; GAD2-cre).

233 OHDA, was established by their expression of glutamic acid decarboxylase (GAD; the synthesizing enzym

234 Recent in vivo studies on glutamic acid decarboxylase [GAD 65 (-/-)] knock-out mic

235 [TH; a marker for dopamine (DA) neurons] or glutamic acid decarboxylase [GAD; synthesizing enzyme of

236 ced green fluorescent protein [vGluT2-eGFP], glutamic acid decarboxylase [GAD]67-eGFP, and glycine tr

237 e transporter 2; VGluT2) and GABA signaling (glutamic acid decarboxylase; GAD, and vesicular GABA tra

238 y postsynaptic currents or expression of the glutamic acid decarboxylase GAD65.

239 not to the well characterized autoantigens, glutamic acid decarboxylase (GAD65) and insulin.

240 and, in a subset, further characterized with glutamic acid decarboxylase (GAD65) autoantibody and fas

241 we report the presence of an autoantibody to glutamic acid decarboxylase (GAD65) in cln3-knockout mic

242 The 65-kD isoform of glutamic acid decarboxylase (GAD65) is a major autoantig

243 CD4(+) T cell responses to glutamic acid decarboxylase (GAD65) spontaneously arise

244 le spasms, high titers of antibodies against glutamic acid decarboxylase (GAD65), and a frequent asso

245 tibodies against insulin, the 65-kDa form of glutamic acid decarboxylase (GAD65), insulinoma-associat

246 were triple-labeled for the 65 kD isoform of glutamic acid decarboxylase (GAD65), PV and the GABA(A)

247 sporter (GLYT2) for glycinergic neurons, and glutamic acid decarboxylase (GAD65/67) for GABAergic neu

248 sporter 1 (VGLUT1) and the 65 kDa isoform of glutamic acid-decarboxylase (GAD65) as markers of, respe

249 Reduction of prefrontal cortex glutamic acid decarboxylase (GAD67) and reelin (mRNAs an

250 alcium-binding protein, calretinin (CR), and glutamic acid decarboxylase (GAD67) in postmortem brain

251 Gad1 gene-encoded 67-kDa protein isoform of glutamic acid decarboxylase (GAD67) is a hallmark of sch

252 ose proximity to terminals expressing 67-kDa glutamic acid decarboxylase (GAD67) of parvalbumin-expre

253 om the RVLM, were assessed for expression of glutamic acid decarboxylase (GAD67) or preproenkephalin

254 ntain normal levels of the 67 kDa isoform of glutamic acid decarboxylase (GAD67) protein, the enzyme

255 to lower expression of the 67-kDa isoform of glutamic acid decarboxylase (GAD67), a key enzyme for GA

256 to lower expression of the 67 kDa isoform of glutamic acid decarboxylase (GAD67), the major gamma-ami

257 ectively decreased expression of one form of glutamic acid decarboxylase (GAD67).

258 in cells that contain the 67 kDa isoform of glutamic acid decarboxylase (GAD67-GFP), or Cre-recombin

259 n of Dlx2 and Dlx5 induced the expression of glutamic acid decarboxylases (GADs), the enzymes that sy

260 Glutamic acid decarboxylase, glycine transporter-2, and

261 tibodies against GAD65 (Mr 65.000 isoform of glutamic acid decarboxylase), IA-2 (insulinoma-associate

262 oimmune process by treatment at 7-10 wk with glutamic acid decarboxylase-IgG retrovirally transduced

263 ear antigen (NeuN+) and 65/67 kDa isoform of glutamic acid decarboxylase immunopositive (GAD65/67+) n

264 ized with glutamate immunoreactivity but not glutamic acid decarboxylase immunoreactivity.

265 ts, expressing myelin basic protein (MBP) or glutamic acid decarboxylase in B cells, can be used for

266 he presence of the GABA-synthesizing enzyme, glutamic acid decarboxylase in EC were confirmed by immu

267 brillary acidic protein-immunocytochemistry, glutamic acid decarboxylase in situ hybridization, and p

268 ing feature of poor-prognosis NE tumors is a glutamic acid decarboxylase-independent pathway for prod

269 double labeling using antibodies to bNOS and glutamic acid decarboxylase indicate that bNOS is expres

270 H), achieved by chronic microinfusion of the glutamic acid decarboxylase inhibitor L-allylglycine, so

271 .3(high)IKCa1(low) phenotype was not seen in glutamic acid decarboxylase, insulin-peptide or ovalbumi

272 the labeling of the GABA-synthesizing enzyme glutamic acid decarboxylase is also significantly increa

273 Glutamic acid decarboxylase is the rate-limiting enzyme

274 To test this hypothesis, regulation of glutamic acid decarboxylase isoform mRNA was studied in

275 hat specific promoter regulatory elements of glutamic acid decarboxylase isoforms (Gad1 and Gad2), wh

276 originate from interneurons, as indicated by glutamic acid decarboxylase labeling.

277 ransporter 2 mRNA (glutamatergic neurons) or glutamic acid decarboxylase mRNA (GABAergic neurons) wer

278 d these neurons by in situ hybridization for glutamic acid decarboxylase mRNA combined with immunohis

279 clease protection assay, however, EB reduced glutamic acid decarboxylase mRNA expression 42 hr but no

280 IgE responses to insulin, autoantibodies to glutamic acid decarboxylase or insulinoma-associated ant

281 antibodies to intracellular proteins such as glutamic acid decarboxylase or specific ribonuclear prot

282 f IA, defined as being positive for insulin, glutamic acid decarboxylase, or insulinoma-associated an

283 These T cells are specific for the glutamic acid decarboxylase p206-220 peptide and are iso

284 lear layer and in the ganglion cell layer is glutamic acid decarboxylase-positive and shows the morph

285 etween PS and control rats, there were fewer glutamic acid decarboxylase-positive neurons in the form

286 sed to estimate numbers of granule cells and glutamic acid decarboxylase-positive neurons per dentate

287 ctive herpes simplex virus vector coding for glutamic acid decarboxylase (QHGAD67) release GABA to pr

288 o abnormal binding of pyridoxal phosphate to glutamic acid decarboxylase resulting in decreased gamma

289 ria and colocalization of some TH cells with glutamic acid decarboxylase suggest that these cells are

290 re also immunopositive to antibodies against glutamic acid decarboxylase, suggesting that they use ga

291 dehydrogenase, glutamate dehydrogenase, and glutamic acid decarboxylase support a perturbation of BC

292 expression for the 67-kilodalton isoform of glutamic acid decarboxylase, the GABA membrane transport

293 label in situ RNA hybridization for POMC and glutamic acid decarboxylase, the GABA synthetic enzyme,

294 ith SPS have antibodies directed against the glutamic acid decarboxylase, the rate-limiting enzyme fo

295 We also used immunohistochemistry for glutamic acid decarboxylase to distinguish GABAergic fro

296 sted whether transfer of the gene coding for glutamic acid decarboxylase to dorsal root ganglion usin

297 Here we show that unlike tolerance to glutamic acid decarboxylase, tolerance to transgenically

298 ctive herpes simplex virus vector expressing glutamic acid decarboxylase (vector QHGAD67) 7 days afte

299 gic neurons expressing different isoforms of glutamic acid decarboxylase were found to have different

300 Imc neurons contain glutamic acid decarboxylase, which is consistent with Im