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 GDH(+)/toxin(+), 53 GDH(-)/toxin(-), and 124 GDH(+)/toxin(-) samples, of which 39 were CCNA(+) and 85

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

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

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

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

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

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

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

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

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

22 The testing algorithm resulted in 34 GDH(+)/toxin(+), 53 GDH(-)/toxin(-), and 124 GDH(+)/toxi

23 algorithm resulted in 34 GDH(+)/toxin(+), 53 GDH(-)/toxin(-), and 124 GDH(+)/toxin(-) samples, of whi

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

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

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

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

28 reement with a testing algorithm utilizing a GDH-and-toxin EIA and CCNA.

29 ual deidentified stool samples tested with a GDH-and-toxin EIA (C.

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

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

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

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

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

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

36 4%) and decreased activities of CS (15%) and GDH (34%).

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

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

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

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

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

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

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

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

45 otein-protein interactions between SCHAD and GDH.

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

47 Third, the expression levels of XR and GDH are adjusted to maximize tagatose production.

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

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

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

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

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

53 the complexity of allosteric network behind GDH regulation, identifications of allosteric factors an

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

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

56 ow that the binding of GTP to the NADH-bound GDH activates a triangular allosteric network, interlink

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

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

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

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

61 C. difficile status was assessed by GDH EIA and real-time PCR targeting the toxin A (tcdA) a

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

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

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

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

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

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

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

69 reductase (XR) and galactitol dehydrogenase (GDH) are introduced into the Deltagal1 strain.

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

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

72 otide (FAD) dependent glucose dehydrogenase (GDH) complex, to elucidate its characteristic properties

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

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

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

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

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

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

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

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

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

82 te and downregulate glutamate dehydrogenase (GDH) activity.

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

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

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

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

87 A) for detection of glutamate dehydrogenase (GDH) and toxins A and B arbitrated by a semiquantitative

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

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

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

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

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

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

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

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

96 immunoassays (EIA), glutamate dehydrogenase (GDH) detection, and PCR were performed on all samples.

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

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

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

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

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

102 Glutamate dehydrogenase (GDH) is a key enzyme interlinking carbon and nitrogen me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 2-step testing, all glutamate dehydrogenase (GDH)-positive specimens, regardless of fecal toxin resul

120 rosis by activating glutamate dehydrogenase (GDH).

121 metabolism through glutamate dehydrogenase (GDH).

122 in the activity of glutamate dehydrogenase (GDH).

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

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

125 amine downstream of glutamate dehydrogenase (GDH).

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

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

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

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

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

131 reactive in assays that detect C. difficile GDH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 The H454Y GDH transgenic mice had hypoglycemia with normal growth

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

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

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

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

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

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

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

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

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

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

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

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

166 cation and allosteric regulation observed in GDH.

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

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

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

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

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

172 itochondrial-localized sirtuin that inhibits GDH.

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

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

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

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

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

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

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

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

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

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

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

184 designer FADGDH was confirmed to be a novel GDH that possesses electrode DET ability.

185 of GDH(+)/toxin(-)/CCNA(+) samples, 90.0% of GDH(+)/toxin(-)/CCNA(+) (high-positive) samples, and 31.

186 Clarity agreed with 61.5% of GDH(+)/toxin(-)/CCNA(+) samples, 90.0% of GDH(+)/toxin(-

187 CNA(+) (high-positive) samples, and 31.6% of GDH(+)/toxin(-)/CCNA(+) (low-positive) samples.

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

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

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

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

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

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

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

195 nt mutations and consequent over-activity of GDH through alteration of this allosteric communication

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

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

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

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

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

201 pharmacologically modulating the effects of GDH.

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

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

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

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

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

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

208 the inhibitor GTP binding and inhibition of GDH catalytic activity. We further show that the binding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 tive diseases have reinvigorated interest on GDH regulation, which remains poorly understood despite

228 These results shed new light on GDH regulation and may lay new foundation in the design

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

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

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

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

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

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

235 Peak GDH activity and mtDNA concentration were increased in p

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

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

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

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

240 ectroscopic detection of the homogeneous PQQ-GDH reconstitution.

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

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

243 anding of the complex dynamics that regulate GDH enzymatic activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 1, the agreement between the GDH-CYT and the GDH-Xpert PCR was 72%.

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

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

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

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

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

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

268 al transition is a fundamental switch in the GDH enzymatic activity. It introduces a torsional stress

269 hat the cofactor NADH is a key player in the GDH regulation process. Our structural analysis indicate

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

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

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

273 trogen metabolism. Recent discoveries of the GDH specific role in breast cancer, hyperinsulinism/hype

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

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

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

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

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

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

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

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

282 sed directly to generate amino acids through GDH activity.

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

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

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

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

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

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

289 Unlike GDH from bacteria, mammalian GDH exhibits negative coope

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

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

292 eased oxidative deamination of glutamate via GDH.

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

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

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

296 xin(-) samples, 100% positive agreement with GDH(+)/toxin(+) samples, and 95.3% agreement with GDH(+)

297 )/toxin(+) samples, and 95.3% agreement with GDH(+)/toxin(-)/CCNA(-) samples.

298 -) Clarity had 96.2% negative agreement with GDH(-)/toxin(-) samples, 100% positive agreement with GD

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

300 Diff Quik Chek Complete; Techlab), with GDH-and-toxin discordant samples tested with CCNA.

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