ライフサイエンスコーパス: PDH

1 egulates the pyruvate dehydrogenase complex (PDH).

2 ant enzyme component pyruvate dehydrogenase (PDH).

3 vate via the pyruvate dehydrogenase complex (PDH).

4 apicoplast-localized pyruvate dehydrogenase (PDH).

5 mitochondrial enzyme pyruvate dehydrogenase (PDH).

6 ges an endogenous octanoate pool to activate PDH.

7 id, yielding the metabolic protein lipoyl-E2-PDH.

8 ], which results in constitutively activated PDH.

9 n which rapidly discharges hydrogen from the PdH.

10 lycosylated and glycosylated (gPDH) forms of PDH.

11 osis was sevenfold greater than flux through PDH.

12 , or decarboxylation of [1-(13)C]pyruvate by PDH.

13 s, Plasmodium parasites lack a mitochondrial PDH.

14 eukaryotes, Plasmodium lacks a mitochondrial PDH.

15 % of stationary-phase populations expressing pdh.

16 10-fold-higher K(i) for NADH than the native PDH.

17 ipoamide dehydrogenase (LPD), a component of PDH.

18 SOD) as well as the previously characterized PDH.

19 ity in the alpha subunit of alpha(2) beta(2) PDH.

20 and phosphorylation-dependent inhibition of PDH.

21 th phosphorylation of the alphaE1 subunit of PDH.

22 d, DlaT and Lpd join with AceE to constitute PDH.

23 me capable of phosphorylating and inhibiting PDH.

24 is dependent on the phosphorylation state of PDH.

25 cated in the mitochondria and interacts with PDH.

26 erred to here as pigment-dispersing hormone [PDH]).

27 )(OMe)(20)(O(2)CMe)(10)] and [Ga(18)(pd)(12)(pdH)(12)(O(2)CMe)(6)(NO(3))(6)](NO(3))(6).

28 rms, PDK2 and PDK3, culminating in increased PDH activation in mutant cells.

29 reater in HYP than SHAM but was lowered with PDH activation: HYP=1419+/-220 nmol/g dry weight; HYP+DC

30 ck-out (KO) keratinocytes exhibited impaired PDH activity and a redirection of the glycolytic flux to

31 E4F1 dysfunction results in 80% decrease of PDH activity and alterations of pyruvate metabolism.

32 Mutant cells exhibited decreased PDH activity and increased PDH E1alpha phosphorylation/i

33 fibroblasts demonstrated a 55% reduction in PDH activity and markedly decreased immunoreactivity for

34 H kinase isoforms (e.g., PDK3), ameliorating PDH activity and mitochondrial metabolism and further af

35 ndings reveal a novel strategy to manipulate PDH activity by selectively targeting PDK4 content throu

36 Pharmacological stimulation of PDH activity improves recovery in contractile function d

37 There was a trend to increased PDH activity in 1alpha,25(OH)2D3-treated cells (p = 0.09

38 PDH to NADH inhibition apparently increased PDH activity in anaerobic E. coli cultures and created t

39 ediated regulation of DLAT lipoyl levels and PDH activity in cells and in vivo, in mouse liver.

40 ratinocytes and illustrate the importance of PDH activity in skin homeostasis.

41 ed the effect of HDACIs on the regulation of PDH activity in striatal cells derived from HD knock-in

42 Reduced PDH activity in U87 glioblastoma and NHA IDH1 mutant cel

43 The inhibition of PDH activity resulting from reduced levels of Sirt3 indu

44 on in oxidative capacities and the increased PDH activity suggesting that calcium might play a role i

45 of cardiac reperfusion, resulted in loss in PDH activity that was largely attributable to translocat

46 , we show sensitivity of these antibodies to PDH activity using the pyruvate dehydrogenase kinase-spe

47 tant IDH1 neurosphere models, we showed that PDH activity was essential for cell proliferation.

48 PDH activity was monitored in these cells by hyperpolari

49 ed compared to contralateral hemisphere, and PDH activity was not affected.

50 drial localization of MITF and its effect on PDH activity were determined.

51 reby decreasing PDK2 activity and increasing PDH activity, accelerating oxygen consumption, and augme

52 Mitochondrial biogenesis, PDH activity, and mitochondrial complex activity were re

53 GLN addicted cells exhibit reduced PDH activity, increased PDK1 expression, and PDK inhibit

54 sults in viable animals that show low muscle PDH activity, severe endurance defects, and chronic lact

55 mportant physiological control mechanisms of PDH activity.

56 (PDK4) that inhibits PDH, thereby increasing PDH activity.

57 uvate dehydrogenase kinase-1, which inhibits PDH activity.

58 lysine acetyltransferase (DLAT), diminishing PDH activity.

59 e mitochondria and involved in regulation of PDH activity.

60 of this process resulted in full recovery of PDH activity.

61 of energy metabolism, leading to an enhanced PDH activity.

62 Furthermore, mitochondrial MITF regulates PDH activity.

63 As pyruvate dehydrogenase (PDH) activity appears central to the balance of substrat

64 f both glutamate and pyruvate dehydrogenase (PDH) activity have been shown to be affected in U87 glio

65 causes inhibition of pyruvate dehydrogenase (PDH) activity resulting in diminished ox-phos levels.

66 iated with decreased pyruvate dehydrogenase (PDH) activity, accumulation of pyruvate and lactate meta

67 line with decreased pyruvate dehydrogenase (PDH) activity, suggesting impairment of the oxidative ph

68 tb lysates contained pyruvate dehydrogenase (PDH) activity, which was lost when the dlaT gene (former

69 appear once the Pd shells are converted into PdH after hydrogen absorption.

70 ielded AceE, annotated as an E1 component of PDH, along with DlaT and Lpd.

71 of a tyrosine residue Tyr-301 also inhibits PDH alpha 1 (PDHA1) by blocking pyruvate binding through

72 e complexes, such as pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase (KGDH), and the

73 eceptor gamma (ERRgamma), thereby inhibiting PDH and attenuating the flux of glycolytic carbon into m

74 phosphorylates and inactivates mitochondrial PDH and consequently pyruvate dehydrogenase complex (PDC

75 tyl-CoA concentrations, thereby inactivating PDH and decreasing glucose oxidation.

76 r received dichloroacetate (DCA) to activate PDH and increase substrate competition with ME.

77 ly inhibition of neuronal and hepatocellular PDH and KGDH activities, followed by reduced mitochondri

78 Thus, we tested the balance between PDH and ME fluxes in hypertrophied hearts and examined w

79 cid synthetic intermediate, octanoyl-ACP, to PDH and OGDH.

80 degrees C for 24-72 h yielded an increase in PDH and SSHH abundance.

81 ; increased cholesterol content yielded more PDH and SSHH at 60 degrees C.

82 drogenase (PDH) kinase isoforms that inhibit PDH and subsequent glucose oxidation.

83 e is essential for function of the pyruvate (PDH) and 2-oxoglutarate (OGDH) dehydrogenases and thus f

84 e phosphorylation of pyruvate dehydrogenase (PDH) and consequently inhibition of pyruvate dehydrogena

85 (PDC) by acetylating pyruvate dehydrogenase (PDH) and PDH phosphatase.

86 ncreased abundance of parallel double helix (PDH) and single-stranded head-to-head (SSHH) dimers were

87 is, gluconeogenesis, pyruvate dehydrogenase [PDH], and H2O2 levels) in mice subjected to unilateral i

88 oxygen species in mutant cells, emphasizing PDH as an interesting therapeutic target in HD.

89 ugh malic enzyme and pyruvate dehydrogenase (PDH) as well as fatty acid and branched-chain amino acid

90 A Pyruvate dehydrogenase (PDH) assay mechanistically confirmed that these agents t

91 DH kinase inactivates PDC by phosphorylating PDH at specific serine residues, including Ser-293, wher

92 by stimulating the PDPhosphatase-phosphoPDH-PDH axis.

93 .4-fold increase in binding affinity for the PDH-binding domain of dihydrolipoamide acetyltransferase

94 (c) reinsertion of the silyl olefin into the PdH bond of the Heck intermediate followed by beta-Si sy

95 Notably, pharmacological activation of PDH by cell exposure to dichloroacetate (DCA) increased

96 H kinase (PDK), whereas dephosphorylation of PDH by PDH phosphatase (PDP) activates PDC.

97 luding Ser-293, whereas dephosphorylation of PDH by PDH phosphatase restores PDC activity.

98 e phosphorylation of pyruvate dehydrogenase (PDH) by PDH kinase (PDK), whereas dephosphorylation of P

99 cing MICU1 activates pyruvate dehydrogenase (PDH) by stimulating the PDPhosphatase-phosphoPDH-PDH axi

100 n of pyruvate in the mitochondria and on the PDH bypass in the cytosol, which synthesizes acetyl-CoA

101 L-deficient cells as a result of a defective PDH bypass pathway.

102 Consistent with perturbation of the PDH bypass, crd1Delta cells grown on acetate as the sole

103 lation did not compensate for defects in the PDH bypass.

104 However, the additional NADH produced by PDH can be used for conversion of acetyl coenzyme A into

105 e residues carrying carbohydrate moieties in PDH can serve as a solid background for production of re

106 hesis of acetyl-CoA depends primarily on the PDH-catalyzed conversion of pyruvate in the mitochondria

107 the E1alpha or E3 subunit genes of P. yoelii PDH caused no defect in blood stage development, mosquit

108 pha or E3 subunit genes of Plasmodium yoelii PDH caused no defect in blood stage development, mosquit

109 CD(3)OD to 1 forms the hydride species [(P^P)PdH(CH(3)OH)](+)(OTf)(-) (2-CH(3)OH) or the deuteride [(

110 metabolism, such as pyruvate dehydrogenase (PDH), citrate synthase, and acyl-CoA dehydrogenases.

111 accounting for congenital deficiency of the PDH complex and perhaps other inborn errors of metabolis

112 The PDH complex catalyses the conversion of pyruvate to acet

113 The PDH complex catalyzes the conversion of pyruvate to acet

114 n appears regulated by dissociation from the PDH complex dependent on the respiratory state and energ

115 ed into lower sensitivity of the appropriate PDH complex to NADH inhibition.

116 GDH complex at about twice the rate from the PDH complex, four times the rate from the BCKDH complex,

117 the OGDH complex, the BCKDH complex, or the PDH complex.

118 The mitochondrial pyruvate dehydrogenase (PDH) complex (PDC) acts as a central metabolic node that

119 iencies of the human pyruvate dehydrogenase (PDH) complex are considered to be due to loss of functio

120 The pyruvate dehydrogenase (PDH) complex connects the glycolytic flux to the tricarb

121 by showing that the pyruvate dehydrogenase (PDH) complex is a promising therapeutic target.

122 lciparum possesses a pyruvate dehydrogenase (PDH) complex that is localized to the apicoplast, a spec

123 veratrol targets the pyruvate dehydrogenase (PDH) complex, a key mitochondrial gatekeeper of energy m

124 of the mitochondrial pyruvate dehydrogenase (PDH) complex.

125 late and inhibit the pyruvate dehydrogenase (PDH) complex.

126 ion at the level of NADH may be the OGDH and PDH complexes, but these activities may often be misattr

127 in vitro with Km values typical of bacterial PDH complexes.

128 ogenase (BCKDH), and pyruvate dehydrogenase (PDH) complexes are also capable of considerable superoxi

129 Our findings indicate that PDH could arise as a new target for the manipulation of

130 [e.g., beta-pigment-dispersing hormone (beta-PDH), crustacean cardioactive peptide, and red pigment-c

131 by a ketogenic diet, two treatments used for PDH deficiencies.

132 Here we describe a case of PDH deficiency associated with the PDH E1beta subunit (P

133 These data indicate that PDH deficiency in our patient involves a post-translatio

134 atient was consistent with reported cases of PDH deficiency.

135 Although PDH-deficient parasites have no blood-stage growth defec

136 Herein, we analyze PDH-deficient parasites using rapid stable-isotope label

137 rapid stable-isotope labeling and show that PDH does not appreciably contribute to acetyl-CoA synthe

138 that control inhibition and reactivation of PDH during reperfusion were therefore investigated.

139 ormone RPCH) and pigment-dispersing hormone (PDH) during development, as these have roles as neuromod

140 nergetics, including pyruvate dehydrogenase (PDH) dysfunction, have been described in Huntington's di

141 ing a rodent malaria model, we show that the PDH E1 alpha and E3 subunits colocalize with the FAS II

142 alyses of cDNAs corresponding to the patient PDH E1alpha (PDHA1) and PDHB genes revealed no pathologi

143 ing a rodent malaria model, we show that the PDH E1alpha and E3 subunits co-localize with the FAS II

144 hibited decreased PDH activity and increased PDH E1alpha phosphorylation/inactivation, accompanied by

145 sts in vitro induced hyperacetylation of the PDH E1alpha subunit, altering its phosphorylation leadin

146 ipulated to alter the net phosphorylation of PDH E1alpha through reduced kinase expression or enhance

147 deacetylation is the E1alpha subunit of PDH (PDH E1alpha).

148 Thus, PDH-E1alpha expression and covalent regulation, and henc

149 UNSAT decreased PDH-E1alpha protein content and increased inhibitory PDH

150 pha protein content and increased inhibitory PDH-E1alpha Ser(300) phosphorylation and FA oxidation.

151 After CHO, muscle PDH-E1alpha Ser(300) phosphorylation was decreased, and

152 a case of PDH deficiency associated with the PDH E1beta subunit (PDHB) gene.

153 Scavenged lipoate was not attached to the PDH E2 subunit, implying that lipoate scavenging drives

154 rates for the octanoylation of mitochondrial PDH-E2 and GDC H-protein; it shows no reactivity with ba

155 AtLPLA is essential for the octanoylation of PDH-E2, whereas GDC H-protein can optionally also be oct

156 ached to the H-protein to KGDH-E2 but not to PDH-E2, which is exclusively octanoylated by LPLA.

157 The association of mitochondrial MITF with PDH emerges as an important regulator of mast cell funct

158 ng its phosphorylation leading to suppressed PDH enzymatic activity.

159 ls were up-regulated in crd1Delta cells, but PDH enzyme activity was not increased, indicating that P

160 is due to decreased pyruvate dehydrogenase (PDH) enzyme activity related, in turn, to increased expr

161 tes possess a single pyruvate dehydrogenase (PDH) enzyme complex that is localized to the plastid-lik

162 tes possess a single pyruvate dehydrogenase (PDH) enzyme complex that is localized to the plastid-lik

163 We infer that the pdh-expressing subpopulation is able grow and divide and

164 ion between MICU1 and pPDH (inactive form of PDH) expression with poor prognosis.

165 (10.8 +/- 0.7 vs. 8.4 +/- 0.5 mmol/L), lower PDH flux (0.005 +/- 0.001 vs. 0.017 +/- 0.002 s(-1)), an

166 scopy and echocardiography to assess cardiac PDH flux and function, respectively.

167 imed to investigate the relationship between PDH flux and myocardial function in a rodent model of ty

168 Overexpression of ErbB2 maintains PDH flux by suppressing PDK4 expression in an Erk-depend

169 The 3dRH animals decreased PDH flux in both compartments (-75 +/- 20% in astrocytes

170 ent manner, and Erk signaling also regulates PDH flux in ECM-attached cells.

171 ogical intervention, we demonstrate that the PDH flux is an important node for M(LPS) macrophage acti

172 Furthermore, we found that the PDH flux is maintained by unchanged PDK1 abundance, desp

173 cids induce insulin resistance by decreasing PDH flux remains unknown.

174 potent inducer of Erk, positively regulates PDH flux through decreased PDK4 expression.

175 f glucose by controlling PDK4 expression and PDH flux to influence proliferation.

176 s of treatment with dichloroacetate restored PDH flux to normal levels (0.018 +/- 0.002 s(-1)), rever

177 ttached cells, PDK4 overexpression decreases PDH flux, de novo lipogenesis, and cell proliferation.

178 tes and to explore whether or not increasing PDH flux, with dichloroacetate, would restore the balanc

179 : controls decreased pyruvate dehydrogenase (PDH) flux in astrocytes by 64 +/- 20% (P = 0.01), wherea

180 Purification of PDH from Mtb yielded AceE, annotated as an E1 component

181 PDH function is inhibited by PDH kinases (PDHKs).

182 metabolic flexibility in part by regulating PDH function through deacetylation.

183 The mutated forms of the PDH had a 10-fold-higher K(i) for NADH than the native P

184 The pyruvate dehydrogenase complex (PDH) has been hypothesized to link lipid exposure to ske

185 ) transmetalation of the silyl olefin on the PdH Heck intermediate followed by reductive elimination

186 ding NSELINSILGLPKVMNDAamide (authentic beta-PDH; here termed Canpr-beta-PDH I) or NSELINSLLGISRLMNEA

187 nduces SIRT4 lipoamidase activity to inhibit PDH, highlighting SIRT4 as a guardian of cellular metabo

188 ght on the origin and diversification of pdf/pdh homologs in Panarthropoda (Onychophora + Tardigrada

189 a neurohormone in the SG, whereas Canpr-beta-PDH I may function as a local transmitter/modulator.

190 Likewise, only prepro-beta-pdh I mRNA was detected in the somata of the lamina gang

191 cretory sinus gland (SG), whereas Canpr-beta-PDH I was found in all other parts of the eyestalk.

192 (authentic beta-PDH; here termed Canpr-beta-PDH I) or NSELINSLLGISRLMNEAamide (Canpr-beta-PDH II) we

193 ch of the C. productus beta-PDHs; Canpr-beta-PDH II appears to be a neurohormone in the SG, whereas C

194 ct tissue mass spectrometry, only Canpr-beta-PDH II was detected in the neurosecretory sinus gland (S

195 DH I) or NSELINSLLGISRLMNEAamide (Canpr-beta-PDH II) were cloned.

196 ing suggests that Ser-293 phosphorylation of PDH impedes active site accessibility to its substrate p

197 ty acid beta-oxidation-induced inhibition of PDH improve cardiac efficiency and subsequent function d

198 ization of glucose metabolism by stimulating PDH in cancer cells restores their susceptibility to ano

199 solutions the open circuit potential of the PdH in equilibrium between its beta and alpha phases (OC

200 We sought to explore the role played by PDH in mast cell exocytosis and to determine whether MIT

201 However, the role of PDH in mast cell function has not been described.

202 Is, particularly SB, promote the activity of PDH in the HD brain, helping to counteract HD-related de

203 y separated on the chromosome, reconstituted PDH in vitro with Km values typical of bacterial PDH com

204 xidation, other than pyruvate dehydrogenase (PDH), in hypertrophied heart.

205 ration and requires a retinol dehydrogenase, PDH, in retinal pigment cells.

206 ound that depletion of PDK4 or activation of PDH increased mitochondrial respiration and oxidative st

207 The effect of PDH inhibition on mast cell function was examined.

208 at heart model, we observed ischemia-induced PDH inhibition with only partial recovery evident on rep

209 concomitant with increased expression of the PDH inhibitory kinase, PDH kinase 4 (PDK4), and increase

210 ls was associated with relative increases in PDH inhibitory phosphorylation, expression of pyruvate d

211 With regard to their encoding genes (pdf, pdh), insects possess only one, nematodes two, and decap

212 PDH interaction with MITF was measured before and after

213 We demonstrate that lipoyl-E2-PDH is also released by S. aureus and moonlights as a ma

214 n speculated that pyruvate oxidation through PDH is decreased in pro-inflammatory macrophages.

215 rmation of H. capsulatum in regions in which PDH is endemic.

216 PDH is essential for immunologically mediated degranulat

217 Fragmented deglycosylated PDH is formed from the deglycosylated enzyme (dgPDH) whe

218 After activation, PDH is serine dephosphorylated.

219 support the hypothesis that the sole role of PDH is to provide acetyl-CoA for FAS II.

220 filing revealed that pyruvate dehydrogenase (PDH) is a key bifurcation point between T cell glycolyti

221 owever, flux through pyruvate dehydrogenase (PDH) is disproportionally decreased, concomitant with in

222 onditions, an active pyruvate dehydrogenase (PDH) is expected to create a redox imbalance in wild-typ

223 Pyruvate dehydrogenase (PDH) is the main regulator of the Krebs cycle and is loc

224 vo sequenced 23 novel ones (e.g., a new beta-PDH isoform and the first B-type allatostatins identifie

225 u hybridization revealed that these two beta-PDH isoforms are differentially distributed within the e

226 Two beta-pigment-dispersing hormone (beta-PDH) isoforms have been identified in several decapod cr

227 evolution rate was significantly reduced in Pdh, it was hypothesized that the role of PDHC is to pro

228 orylation of pyruvate dehydrogenase (PDH) by PDH kinase (PDK), whereas dephosphorylation of PDH by PD

229 d pyruvate dehydrogenase (PDH) (Ser-293) and PDH kinase 4 (PDK4) decreased in 1alpha,25(OH)2D3-treate

230 sed expression of the PDH inhibitory kinase, PDH kinase 4 (PDK4), and increased carbon secretion.

231 related, in turn, to increased expression of PDH kinase 4 (pdk4).

232 PDH kinase inactivates PDC by phosphorylating PDH at spe

233 decrease the expression of the most abundant PDH kinase isoforms (e.g., PDK3), ameliorating PDH activ

234 Adropin downregulates PDH kinase-4 (PDK4) that inhibits PDH, thereby increasin

235 g gene expression of pyruvate dehydrogenase (PDH) kinase 1 (PDHK1), which phosphorylates and inactiva

236 arkedly upregulating pyruvate dehydrogenase (PDH) kinase 4 (PDK4) through estrogen-related receptor g

237 , which can activate pyruvate dehydrogenase (PDH) kinase isoforms that inhibit PDH and subsequent glu

238 osphorylated pyruvate dehydrogenase pPDH and PDH-kinase.

239 PDH function is inhibited by PDH kinases (PDHKs).

240 n of the three phosphorylation sites by four PDH kinases (PDK1-4) and two PDH phosphatases (PDP1-2) w

241 n, accompanied by enhanced protein levels of PDH kinases 1 and 3 (PDK1 and PDK3).

242 a homogeneous carbonylation catalyst [(dtbpx)PdH(L)](+) by addition of diprotonated diphosphine (dtbp

243 coli MG1655 and a PDHC-deficient derivative (Pdh) led to the identification of the role of PDHC in th

244 AKI decreased PDH levels, potentially limiting pyruvate to acetyl CoA

245 Here we show that the distribution of beta-PDH-like immunoreactivity in the nervous system of C. pr

246 Interestingly, the PDH-like pathway contributes glucose-derived acetyl-CoA

247 t acetyl-CoA demands are supplied through a "PDH-like" enzyme and provide evidence that the branched-

248 This suggests that PDH modulation could be a novel therapy for the treatmen

249 PDH mRNA and protein levels were up-regulated in crd1Del

250 nclusion was supported by the phenotype of a pdh mutant, which grew poorly on electron-rich substrate

251 Three of the four glycosites in PDH: N(75), N(175), and N(252) were assigned using mass

252 attenuated by pharmacological stimulation of PDH or by a ketogenic diet, two treatments used for PDH

253 irt3 deacetylation is the E1alpha subunit of PDH (PDH E1alpha).

254 roadly reactive antibody that recognizes PDF/PDH peptides in numerous species, revealed an elaborate

255 e (PDK), whereas dephosphorylation of PDH by PDH phosphatase (PDP) activates PDC.

256 Ser-293, whereas dephosphorylation of PDH by PDH phosphatase restores PDC activity.

257 acetylating pyruvate dehydrogenase (PDH) and PDH phosphatase.

258 n sites by four PDH kinases (PDK1-4) and two PDH phosphatases (PDP1-2) were investigated by substitut

259 Prior exercise led to higher PDH phosphorylation and activation of glycogen synthase

260 n presented higher mRNA levels of PDK1-3 and PDH phosphorylation and decreased energy levels that wer

261 We go on to use these antibodies to assess PDH phosphorylation in a patient suffering from Leigh's

262 DHK genes, PDHK1 is essential for inhibitory PDH phosphorylation of E1alpha at serine 232, is partial

263 iated with impaired TBC1D4 S341 and elevated PDH phosphorylation.

264 Intralipid enhanced pyruvate dehydrogenase (PDH) phosphorylation and lactate release.

265 Pyruvate dehydrogenase (PDH) plays a well-known metabolic role inside cells.

266 evealed a bimodal expression pattern for the pdh promoter, with less than 1% of stationary-phase popu

267 ration and decreased pyruvate dehydrogenase (PDH) protein level and activity as early as 3 months of

268 ffords the stable and isolable hydride [(P^P)PdH(pyridine)](+)(OTf)(-) (2-pyr).

269 vels in late pregnancy lead to inhibition of PDH (pyruvate dehydrogenase) and pyruvate flux into the

270 zymes, MCAT (malonylCoA:ACP transferase) and PDH (pyruvate dehydrogenase).

271 olic remodeling in the heart at the level of PDH, rather than at the level of insulin signaling.

272 Increasing competition from PDH reduced anaplerosis in HYP+DCA by 18%.

273 Therefore, PDH represents a metabolic intervention point that might

274 Absence of PDH resulted in progressive light-dependent loss of rhod

275 of progressive disseminated histoplasmosis (PDH) results in high mortality rates.

276 1 T338 phosphorylation levels correlate with PDH S293 inactivating phosphorylation levels and poor pr

277 Phosphorylated pyruvate dehydrogenase (PDH) (Ser-293) and PDH kinase 4 (PDK4) decreased in 1alp

278 s, in contrast to inhibition of complex I or PDH, suppression of pyruvate transport induces a form of

279 PDH synthesizes acetyl-CoA; acetate supplementation allo

280 se morphology affects transformations in the PdH system.

281 Pyruvate dehydrogenase (PDH), the first component of the human pyruvate dehydrog

282 nregulates PDH kinase-4 (PDK4) that inhibits PDH, thereby increasing PDH activity.

283 Glucose-derived pyruvate is oxidized via PDH to generate citrate in the mitochondria.

284 The lower sensitivity of PDH to NADH inhibition apparently increased PDH activity

285 and repurposes the lipoylated E2 subunit of PDH to suppress TLR-mediated activation of host macropha

286 activity was not increased, indicating that PDH up-regulation did not compensate for defects in the

287 Regulation of PDH via regulation of the E3 component by the NAD(+)/NAD

288 DK1), which inhibits pyruvate dehydrogenase (PDH) via phosphorylation.

289 f aceE, a subunit of pyruvate dehydrogenase (PDH), was found to increase levels of RpoS by affecting

290 d phosphorylation of pyruvate dehydrogenase (PDH) were observed in kidneys from diabetic mice.

291 thal with mutants in pyruvate dehydrogenase (PDH), which catalyzes the conversion of pyruvate to acet

292 e, adropin activates pyruvate dehydrogenase (PDH), which is rate limiting for glucose oxidation and s

293 PDH, which converts pyruvate to acetyl-CoA, has been kno

294 activity of the three investigated forms of PDH, "wired" to graphite electrodes with two different o

295 ic enzyme complex pyruvate dehydrogenase (E2-PDH) with a fatty acid derivative, lipoic acid, yielding

296 endent inhibition of pyruvate dehydrogenase (PDH) within a single day of feeding mice a high fat diet

297 ld-effect transistor with proton-transparent PdH(x) contacts.

298 or = 1.0% H(2) due to volume expansion upon PdH(x) formation, which leads to a direct connection bet

299 s due to the formation of the more resistive PdH(x) in the presence of H(2).

300 leads to a direct connection between Pd (as PdH(x)) and Electrode 2 through the porous 4-10 nm thick