ライフサイエンスコーパス: GDH

1 GDH activity is subject to complex regulation by negativ

2 GDH activity was similarly decreased in HINT2-silenced H

3 GDH enzyme kinetics of hadh(-/-) islets showed an increa

4 GDH is a mitochondrial matrix enzyme that catalyzes the

5 GDH is known to promote the metabolism of glutamate and

6 GDH may also be the form of glycine that comes to Earth

7 GDH screening detected all culture-positive specimens.

8 GDH specifically clips H3 in its free as well as chromat

9 GDH transgenic mice were generated to express the human

10 GDH, mtDNA, and nDNA fragments were measured in serum fr

11 GDH-HI mutations impair GDH sensitivity to GTP inhibitio

12 le testing, 171 GDH antigen positive and 171 GDH antigen negative, were selected for the study.

13 Of 171 GDH antigen-negative samples, none were positive by PCR.

14 Of 171 GDH-positive samples, 4 were excluded (from patients on

15 ted for diagnostic C. difficile testing, 171 GDH antigen positive and 171 GDH antigen negative, were

16 le testing, 200 GDH antigen positive and 200 GDH antigen negative, were selected for analysis.

17 Of 200 GDH-negative samples, 3 were positive by PCR only.

18 re as an independent "gold standard." Of 200 GDH-positive samples, 71 were positive by the Tox A/B II

19 ted for diagnostic C. difficile testing, 200 GDH antigen positive and 200 GDH antigen negative, were

20 igenic C. difficile was found in 1.9% of 211 GDH-Q-negative specimens.

21 l samples were tested by the C. Diff Chek-60 GDH antigen and cytotoxin neutralization assays, the Tox

22 Diff Chek-60 GDH antigen assay, cytotoxin neutralization, and Simplex

23 l samples were tested by the C. Diff Chek-60 GDH antigen assay, cytotoxin neutralization, and Simplex

24 In conclusion, we generated a GDH-HI disease mouse model that has a hypoglycemia pheno

25 Loss of SIRT4 in insulinoma cells activates GDH, thereby upregulating amino acid-stimulated insulin

26 tochondrial pyruvate carrier (MPC) activates GDH and reroutes glutamine metabolism to generate both o

27 the dark, AMPS-Succ-BP reversibly activates GDH.

28 As such, in children with activating GDH mutations of HI/HA, this insulin-independent glucago

29 root companion cells, where all three active GDH enzyme proteins were shown to be present.

30 This complex regulation allows GDH activity to be modulated by changes in energy state

31 p algorithm in which DPCR is used to analyze GDH EIA-positive, toxin EIA-negative specimens provides

32 4%) and decreased activities of CS (15%) and GDH (34%).

33 nsitivities and specificities of GDH-CYT and GDH-Xpert PCR were 57% and 97% and 100% and 97%, respect

34 c stacking interactions between the drug and GDH as well as between the drug molecules themselves.

35 affected by strain type compared to EIA and GDH-based methods.

36 High glucose inhibited both glutaminase and GDH flux, and leucine could not override this inhibition

37 inhibited flux through both glutaminase and GDH, and leucine was unable to override this inhibition.

38 minolysis through activating glutaminase and GDH.

39 GS and GDH were present in oligodendrocytes in normal and non-M

40 Concomitant administration of MPC and GDH inhibitors significantly impaired tumor growth compa

41 ioaffinity interactions between the NAD+ and GDH were secured by cross-linking the system with the gl

42 thesis, IS studies were performed in rat and GDH-HI mouse models.

43 otein-protein interactions between SCHAD and GDH.

44 associated protein 1), citrate synthase, and GDH (glutamate dehydrogenase 1), are substrates of PARP-

45 However, only animal GDH utilizes both NAD(H) or NADP(H) with comparable effi

46 experiments with SCHAD, anti-SCHAD, or anti-GDH antibodies showed protein-protein interactions betwe

47 Complete's glutamate dehydrogenase antigen (GDH) and toxin A/B (CDT) tests in two algorithmic approa

48 etic group for apoglucose dehydrogenase (apo-GDH), is loaded into poly(methyl methacrylate) (PMMA) na

49 alyzes a color change in the presence of apo-GDH, glucose, and the redox dye 1,6-dichlorophenol indop

50 cetonitrile is capable of reconstituting apo-GDH and triggers the enzymatic reaction with excess gluc

51 In phase 2, the agreement between GDH-CYT and Xpert PCR alone was 95%.

52 )) inhibit GDH in vitro and that EGCG blocks GDH-mediated insulin secretion in wild type rat islets.

53 sented here are the structures of apo bovine GDH, bovine GDH complexed with ADP, and the R463A mutant

54 are the structures of apo bovine GDH, bovine GDH complexed with ADP, and the R463A mutant form of hum

55 Compared to the structures of bovine GDH that were complexed with coenzyme and substrate, the

56 tabolism of glutamine and related analogs by GDH in the L cell may explain why GLP-1 secretion, but n

57 lin secretion, a process that is mediated by GDH, under conditions where GDH is no longer inhibited b

58 cond phase, all stool samples were tested by GDH and Xpert PCR.

59 GTP-dependent signal generated via beta-cell GDH that inhibits alpha-cells.

60 e was 60.0%, and the sensitivity of combined GDH algorithms was 72.9%; both were significantly lower

61 , were as follows for an algorithm combining GDH-Q, AB-Q, and DPCR: 83.8%, 99.7%, 97.1%, and 97.9%.

62 vin reductase active-site domain a conserved GDH motif, which is believed to be responsible for the e

63 linism/hyperammonemia syndrome by decreasing GDH sensitivity to the inhibitor, GTP.

64 g the model system of glucose dehydrogenase (GDH) and its nicotinamide adenine dinucleotide cofactor

65 gold (NPG) supported glucose dehydrogenase (GDH) bioanode, immobilised with the assistance of conduc

66 ovalent attachment of glucose dehydrogenase (GDH) enzyme and safranin O to amine-derivative multiwall

67 covalently immobilize glucose dehydrogenase (GDH) in the CNT-CHIT films using glutaric dialdehyde (GD

68 otide (FAD) dependent glucose dehydrogenase (GDH) is a thermostable, oxygen insensitive redox enzyme

69 ntly regenerated by a glucose dehydrogenase (GDH) using only 1.2 equiv of glucose.

70 Glucose dehydrogenase (GDH) was thus efficiently immobilized in the electrogene

71 cose oxidase (GOx) or glucose dehydrogenase (GDH) were immobilized on bioanode and oxidize glucose wh

72 oup of the apo-enzyme glucose dehydrogenase (GDH), are used as the label to probe for bound target DN

73 roup of the apoenzyme glucose dehydrogenase (GDH), are used to detect membrane permeabilization by th

74 sitive mutations in glutamate dehydrogenase (GDH(H454Y)) result in fasting and amino acid-induced hyp

75 te and downregulate glutamate dehydrogenase (GDH) activity.

76 he presence of both glutamate dehydrogenase (GDH) and C. difficile toxins A and B, was evaluated for

77 synthetase (GS) and glutamate dehydrogenase (GDH) and the ammonium-evolving periplasmic enzymes gluta

78 ostridium difficile glutamate dehydrogenase (GDH) and toxin A/B antigens against a standard that comb

79 ium difficile using glutamate dehydrogenase (GDH) and toxin immunoassays combined with tcdB PCR.

80 ifficile-associated glutamate dehydrogenase (GDH) antigen and, if positive, tested for toxin by a dir

81 s a C. Diff Chek-60 glutamate dehydrogenase (GDH) antigen assay followed by cytotoxin neutralization.

82 Diff Chek-60 glutamate dehydrogenase (GDH) antigen assay followed by cytotoxin neutralization.

83 the C. Diff Chek-60 glutamate dehydrogenase (GDH) antigen assay followed by cytotoxin neutralization.

84 a novel activity of glutamate dehydrogenase (GDH) as a histone H3-specific protease in chicken liver

85 ts were tested by a glutamate dehydrogenase (GDH) assay, a toxin A and B enzyme immunoassay (EIA), th

86 ve for C. difficile glutamate dehydrogenase (GDH) by Wampole C Diff Quik Chek EIA (GDH-Q) and negativ

87 Glutamate dehydrogenase (GDH) catalyzes the oxidative deamination of L-glutamate

88 The glutamate dehydrogenase (GDH) enzymes of 19 Streptococcus suis serotype 2 strains

89 yme immunoassay for glutamate dehydrogenase (GDH) followed by the cytotoxin neutralization test (CYT)

90 mutations affecting glutamate dehydrogenase (GDH) formation (gdh-1 and rev-2) had been isolated at a

91 e that contains the glutamate dehydrogenase (GDH) gene and a portion of a second open reading frame e

92 structure of human glutamate dehydrogenase (GDH) has been determined in the absence of active site a

93 Glutamate dehydrogenase (GDH) has been shown to play a regulatory role in insulin

94 Glutamate dehydrogenase (GDH) has been shown to play a regulatory role in this pr

95 latory mutations of glutamate dehydrogenase (GDH) in a form of congenital hyperinsulinism (GDH-HI) is

96 Mammalian glutamate dehydrogenase (GDH) is a homohexameric enzyme that catalyzes the revers

97 Glutamate dehydrogenase (GDH) is found in all organisms and catalyzes the oxidati

98 Glutamate dehydrogenase (GDH) is found in all organisms and catalyzes the reversi

99 Glutamate dehydrogenase (GDH) is regulated by both positive (leucine and ADP) and

100 creatic beta-cells, glutamate dehydrogenase (GDH) modulates insulin secretion, although its function

101 econd occurring via glutamate dehydrogenase (GDH) or transaminases.

102 Glutamate dehydrogenase (GDH) plays an important role in insulin secretion as evi

103 ep algorithms using glutamate dehydrogenase (GDH) screening followed by either EIA or EIA and an in-h

104 e of NADH-dependent glutamate dehydrogenase (GDH) was investigated by studying the physiological impa

105 ighly conserved and glutamate dehydrogenase (GDH) was readily expressed in vitro by all 77 Clostridiu

106 ereas activation of glutamate dehydrogenase (GDH) was required to stimulate insulin secretion from IN

107 ase short chain and glutamate dehydrogenase (GDH) were decreased by 68% and 60%, respectively, withou

108 ate this here using glutamate dehydrogenase (GDH), a 336-kDa metabolic enzyme that catalyzes the oxid

109 or the detection of glutamate dehydrogenase (GDH), and culture of C. difficile.

110 eviously shown that glutamate dehydrogenase (GDH), mitochondrial DNA (mtDNA), and nuclear DNA (nDNA)

111 odes one subunit of glutamate dehydrogenase (GDH), was chosen for further studies for its role in tri

112 ic NAD(+)-dependent glutamate dehydrogenase (GDH), which converts l-glutamate, the product of the AST

113 2-step testing, all glutamate dehydrogenase (GDH)-positive specimens, regardless of fecal toxin resul

114 metabolism through glutamate dehydrogenase (GDH).

115 in the activity of glutamate dehydrogenase (GDH).

116 nthase (GOGAT), and glutamate dehydrogenase (GDH).

117 tic sources; and 3) glutamate dehydrogenase (GDH).

118 teric activation of glutamate dehydrogenase (GDH).

119 amine downstream of glutamate dehydrogenase (GDH).

120 rosis by activating glutamate dehydrogenase (GDH).

121 obody, lateral-flow glutamate dehydrogenase (GDH)/odPCR generated 831 true-positive results and cost

122 nation catalyzed by glutamate dehydrogenase (GDH); secondary reactions enabled other amino acids, suc

123 utamate metabolism (glutamate dehydrogenase [GDH] and glutamine synthetase [GS]), axonal damage (SMI

124 tochondrial damage (glutamate dehydrogenase [GDH] and mitochondrial DNA [mtDNA]) and nuclear DNA frag

125 prepared hybrid system of GC/MWCNTs-NH2/Den/GDH/Safranin as anode in a membraneless enzyme-based glu

126 synthase (GltBD) and anabolic NADP-dependent GDH (GdhA) in cell extracts of strain PAO1, and this rep

127 reactive in assays that detect C. difficile GDH.

128 ied this elusive phase as glycine dihydrate (GDH), representing the first report on the structure of

129 assay (CCNA) for adjudication of discrepant GDH-positive/CDT-negative results.

130 Results showing dual GDH and toxin A/B antigen positives and negatives can be

131 response to glutamine caused by dysregulated GDH is blocked by the addition of EGCG.

132 enase (GDH) by Wampole C Diff Quik Chek EIA (GDH-Q) and negative for toxins A and B by Wampole Tox A/

133 Energy deprivation enhanced GDH-mediated IS, and H454Y mice were hypoglycemic, subst

134 plification (LAMP), and algorithm 2 entailed GDH/CDT followed by cytotoxicity neutralization assay (C

135 costs and <2 transmissions, if lateral-flow GDH diagnostic sensitivity was >93%, or if the symptomat

136 resolutions ranging from 3.2 A to 3.6 A for GDH complexes, including complexes for which crystal str

137 A spectrophotometric activity assay for GDH did not show significant differences between the gro

138 f and that animals evolved new functions for GDH through the addition of allosteric regulation.

139 defined by gdh-1 is the structural gene for GDH.

140 Specimens with discrepant results for GDH and toxins A/B, which comprised 13.2% of the specime

141 were hypoglycemic, substantiating roles for GDH and its regulation by the phosphate potential in bas

142 se current studies, we extend our search for GDH inhibitors using high throughput methods to pan thro

143 Clinically, serum nDNA fragments, GDH, and mtDNA could be useful as part of a panel of bio

144 curve analyses revealed that nDNA fragments, GDH, and mtDNA were predictive of outcome (area under th

145 Furthermore, GDH from SIRT4-deficient or CR mice is insensitive to ph

146 ility and sensitivity of the GC/CNT-CHIT-GDI-GDH biosensor allowed for the interference-free determin

147 se to glutamine alone and had 2-fold greater GDH flux.

148 H454Y GDH transgenic islets were more sensitive to leucine- an

149 Stimulation of insulin release by the H454Y GDH mutation or by leucine activation is associated with

150 The H454Y GDH transgenic mice had hypoglycemia with normal growth

151 In the GDH-HI mouse study, the H454Y GDH-HI mutation driven by the rat insulin promoter was c

152 Comparison with the yet smaller hexameric GDH (protomeric mass of 48 to 55 kDa) of other prokaryot

153 with ADP, and the R463A mutant form of human GDH (huGDH) that is insensitive to ADP activation.

154 of the ADP-resistant, R463A mutant of human GDH is identical to native GDH with the exception of the

155 enna from the Ciliates is spliced onto human GDH, it was found to fully communicate all aspects of ma

156 nic mice were generated to express the human GDH-HI H454Y mutation and human wild-type GDH in islets

157 re new leads in the treatment of hyperactive GDH but also are useful in dissecting the complex allost

158 DH) in a form of congenital hyperinsulinism (GDH-HI) is providing a model for basal insulin secretion

159 GDH-HI mutations impair GDH sensitivity to GTP inhibition, leading to fasting hy

160 e forms a ring around the internal cavity in GDH through aromatic stacking interactions between the d

161 ence or absence of toxigenic C. difficile in GDH-positive/CDT-negative specimens.

162 ate from alpha-ketoglutarate was impaired in GDH-deficient islets.

163 cs of hadh(-/-) islets showed an increase in GDH affinity for its substrate, alpha-ketoglutarate.

164 Gain of function mutations in GDH that abrogate GTP inhibition cause the hyperinsulini

165 cation and allosteric regulation observed in GDH.

166 nsgene expression was confirmed by increased GDH enzyme activity in islets and decreased sensitivity

167 ing, which facilitates glycolysis, increased GDH activity whereas overexpression of Akt suppressed it

168 cted on solid medium suggests that increased GDH expression is the key for rescue of the growth defec

169 EGCG) and epicatechin gallate (ECG)) inhibit GDH in vitro and that EGCG blocks GDH-mediated insulin s

170 nd epicatechin gallate were found to inhibit GDH with nanomolar ED(50) values and were therefore foun

171 itochondrial-localized sirtuin that inhibits GDH.

172 n the presence of purified sirtuin 3, latent GDH activity was recovered (126% in Hint2(-/-) versus 83

173 Unlike GDH from bacteria, mammalian GDH exhibits negative cooperativity with respect to coen

174 rparts from other animal kingdoms, mammalian GDH is regulated by a host of ligands.

175 cemia highlights a central role of the mtGTP-GDH-glucagon axis in glucose homeostasis.

176 The mutant GDH enzyme shows impaired responses to GTP inhibition.

177 ted islets from mice that express the mutant GDH in pancreatic beta cells show an increased rate of g

178 Electron conductive films of such CHIT-NAD+-GDH-GDI-CHIT macrocomplexes (MC) were prepared on glassy

179 NAD-GDH activity was subject to allosteric control by argini

180 NAD-GDH from this organism differs from previously character

181 NAD-GDH was induced 27-fold by exogenous arginine and only 3

182 AD(+)-dependent glutamate dehydrogenase (NAD-GDH) from Pseudomonas aeruginosa PAO1 was purified, and

183 rom the derived sequence for the encoded NAD-GDH was 182.6 kDa, in close agreement with that determin

184 king studies established that the native NAD-GDH is a tetramer of equal subunits.

185 was observed with the smaller tetrameric NAD-GDH (protomeric mass of 110 kDa) from Saccharomyces cere

186 that the main physiological function of NADH-GDH is to provide 2-oxoglutarate for the tricarboxylic a

187 nt subunit of the Chlorella sorokiniana NADP-GDH isozymes were constructed and expressed in Escherich

188 properties of the Chlorella sorokiniana NADP-GDH isozymes were retained after their synthesis in a he

189 A mutant of human GDH is identical to native GDH with the exception of the truncated side chain on th

190 The absence of GDH in islets isolated from betaGlud1(-/-) mice resulted

191 leucine (and its analogue BCH) activation of GDH to stimulation of insulin secretion.

192 ency causes hyperinsulinism by activation of GDH via loss of inhibitory regulation of GDH by SCHAD.

193 strate that EGCG, much like the activator of GDH (BCH), can facilitate dissecting the complex regulat

194 cell mitochondria to repress the activity of GDH by ADP-ribosylation, thereby downregulating insulin

195 s indicated that the deamination activity of GDH might regenerate 2-oxoglutarate, which is a cosubstr

196 entify an unexpected proteolytic activity of GDH specific to histone H3 that is regulated by redox st

197 or that inhibits the H3-clipping activity of GDH.

198 From alignment of GDH from various sources, it is likely that the antenna

199 Pharmacological blockade of GDH elicited largely cytostatic effects in culture, but

200 The internal core of GDH contracts when the catalytic cleft closes during enz

201 Dysregulation of GDH leads to a variety of metabolic and neurologic disor

202 pharmacologically modulating the effects of GDH.

203 ansgenic mice expressing a human HHS form of GDH demonstrate that the hyperresponse to glutamine caus

204 and hyperinsulinemia/hyperammonemia forms of GDH are inhibited by the green tea polyphenols, epigallo

205 ne is therefore proposed to be a function of GDH activation.

206 d hypoglycemia, indicating the importance of GDH in basal secretion and AASIS.

207 The importance of GDH regulation has been highlighted by the discovery of

208 The importance of GDH was underscored by features of hyperinsulinemia/hype

209 ed that the loss of allosteric inhibition of GDH by GTP causes excessive secretion of insulin.

210 Thus, inhibition of GDH converted these glutamine-addicted cells to glucose-

211 Acute pharmacologic inhibition of GDH restored both insulin and glucagon secretion and nor

212 DP are activators and GTP is an inhibitor of GDH.

213 erases, could not compensate for the lack of GDH.

214 of enzymatic assays showed that the level of GDH during anoxia-reoxygenation decreased in the ethylen

215 The clinical manifestations of GDH-HI and related animal studies suggest that GDH regul

216 tion for hypoglycemia caused by mutations of GDH in children.

217 of GDH via loss of inhibitory regulation of GDH by SCHAD.

218 rates or stimuli indicate that regulation of GDH by the beta-cell phosphate potential plays a critica

219 Reintroduction of GDH in betaGlud1(-/-) islets fully restored the secretor

220 1 allele showed no auxotrophy, repression of GDH expression by the nitrogen assimilation control prot

221 This study investigated the role of GDH using a beta-cell-specific GDH knockout mouse model,

222 Fisher's exact test), and the sensitivity of GDH algorithms for ribotypes other than 027 was lower th

223 The sensitivities and specificities of GDH-CYT and GDH-Xpert PCR were 57% and 97% and 100% and

224 The structure of GDH has important implications for the state of glycine

225 Shown here are the structures of GDH complexed with these three compounds.

226 Suppression of GDH activity with RNA interference or an inhibitor showe

227 hat is more than 3 times higher than that of GDH and 5 to 7 times higher catalytic currents with an o

228 Pharmacological inhibition in vivo of GDH blocked secretion of GLP-1 in response to DMG.

229 d model for glutaminolysis in IS is based on GDH providing NADH and alpha-ketoglutarate (alpha-KG) to

230 The effect on GDH resulted from the loss of glycolysis because it coul

231 port the effects of green tea polyphenols on GDH and insulin secretion.

232 d, on average, 2 days to complete testing on GDH-positive results, while testing by the Xpert C. diff

233 Only GDH-positive stools were further tested by CYT.

234 In the first phase of the study, only GDH-positive stool samples were tested by both CYT and X

235 s expressing elevated levels of either GS or GDH are more acid tolerant than the wild type, exhibit e

236 The first suppressor overexpressed GDH, and the second also had a partially impaired glutam

237 Peak GDH activity and mtDNA concentration were increased in p

238 uinone dependent glucose dehydrogenase ((PQQ)GDH) has been immobilized on [poly(3-aminobenzoic acid-c

239 quinoline quinone glucose dehydrogenase (PQQ-GDH) and bilirubin oxidase (BOD) at anode and cathode, r

240 quinoline quinone glucose dehydrogenase (PQQ-GDH) and laccase functioning as the anodic and cathodic

241 the PQQ-dependent glucose dehydrogenase (PQQ-GDH) through the specific binding of its pyrroloquinolin

242 ectroscopic detection of the homogeneous PQQ-GDH reconstitution.

243 t responses of the surface-reconstituted PQQ-GDH and determination of the PQQ equilibrium binding (Kb

244 Like previously reported proteases, GDH too may have the potential to regulate/modulate post

245 the previous proposal that purines regulate GDH activity by altering the dynamics of the NAD binding

246 ustrate the essential role of EIN3-regulated GDH activity in metabolic adjustment during anoxia-reoxy

247 it, suggesting that Akt indirectly regulates GDH through its effects on glucose metabolism.

248 d the role of GDH using a beta-cell-specific GDH knockout mouse model, called betaGlud1(-/-).

249 (class II aaRS homolog) and an NAD-specific GDH-like enzyme (class I aaRS homolog) via its sense and

250 glutamine to the perfusion media stimulated GDH flux approximately 6-fold at both glucose concentrat

251 In summary, GDH-based algorithms detected C. difficile infections wi

252 of pyruvate into the mitochondria suppresses GDH and glutamine-dependent acetyl-CoA formation.

253 ts who died, compared to those who survived (GDH: 450 +/- 73 vs. 930 +/- 145 U/L; mtDNA: 21 +/- 6 vs.

254 e a hyperinsulinism-hyperammonemia syndrome (GDH-HI) and sensitize beta-cells to leucine stimulation.

255 CNA or positivity by LAMP plus another test (GDH, CDT, or the Premier C. difficile toxin A and B enzy

256 lucose-stimulated insulin secretion and that GDH plays an indispensable role in this process.

257 We conclude that GDH is an excellent screening test and that culture with

258 inism-hyperammonemia syndrome indicates that GDH-catalyzed glutamate metabolism plays important roles

259 H-HI and related animal studies suggest that GDH regulates basal IS and AASIS.

260 This study suggests that GDH functions predominantly in the direction of glutamat

261 This suggests that GDH may represent a new and novel drug target to control

262 The GDH-EIA-CCCN procedure required, on average, 2 days to c

263 in-negative/PCR-positive (21 mug/ml) and the GDH-negative groups (13 mug/ml).

264 1, the agreement between the GDH-CYT and the GDH-Xpert PCR was 72%.

265 enzyme cascade consisting of the ATHase, the GDH, a monoamine oxidase, and a catalase leads to the pr

266 In phase 1, the agreement between the GDH-CYT and the GDH-Xpert PCR was 72%.

267 positive by PCR, and 96 were positive by the GDH antigen assay only.

268 Seventy-nine were positive by the GDH antigen assay only.

269 fficile was detection of C. difficile by the GDH screen or by culture and toxin production by direct

270 We characterized the GDH promoter by transfecting Giardia with DNA constructs

271 Combining the GDH and Xpert C. difficile assays lowered both the sensi

272 In the GDH-HI mouse study, the H454Y GDH-HI mutation driven by

273 toxin-positive group (79 mug/ml) than in the GDH-positive/toxin-negative/PCR-positive (21 mug/ml) and

274 Lactoferrin levels were higher in the GDH-positive/toxin-positive group (79 mug/ml) than in th

275 e motifs within a 50-base pair region of the GDH upstream sequence.

276 of the Xpert PCR was higher than that of the GDH-CYT.

277 performed to evaluate the sensitivity of the GDH-Q as a screening test, and toxigenic C. difficile wa

278 These results suggest that the GDH ETs and sequence types may serve as useful markers i

279 P, <0.001 by Fisher's exact test) and to the GDH-EIA-CCCN algorithm (P, 0.0363).

280 ng Giardia with DNA constructs that used the GDH upstream sequence to drive the expression of a lucif

281 An algorithm using the GDH assay and the EIA (plus the CCCN if the EIA was nega

282 estriction of glutamine catabolism via these GDH inhibitors can be useful in treating various tumors.

283 nducted following the discovery that a third GDH gene is expressed in the mitochondria of the root co

284 Mutation of the His140 in this GDH motif to alanine reduced FRD(Aa) activity to <3%.

285 sed directly to generate amino acids through GDH activity.

286 n in beta-cells and that anaplerosis through GDH does not play a major role in this process.

287 Leucine increased the flux through GDH 3-fold compared with controls while causing insulin

288 P(i) and thereby decreasing the flux through GDH and glutaminase.

289 ake via GLS, suggesting that, in addition to GDH, mTORC1 could regulate GLS.

290 essive IS from H454Y islets upon exposure to GDH substrates or stimuli indicate that regulation of GD

291 an GDH-HI H454Y mutation and human wild-type GDH in islets driven by the rat insulin promoter.

292 Unlike GDH from bacteria, mammalian GDH exhibits negative coope

293 otic entry of glutamine to the TCA cycle via GDH.

294 The fluxes via GDH and glutaminase were measured by tracing 15N flux fr

295 eased oxidative deamination of glutamate via GDH.

296 al of 1447 of 12772 (11%) fecal samples were GDH positive, 866 of 1447 (60%) contained toxigenic C. d

297 t is mediated by GDH, under conditions where GDH is no longer inhibited by high energy metabolites.

298 secretion under high energy conditions where GDH is probably fully inhibited.

299 chitosan (CHIT) and allowed to interact with GDH in an aqueous solution.

300 n: algorithm 1 entailed initial testing with GDH/CDT followed by loop-mediated isothermal amplificati