ライフサイエンスコーパス: PDH

1 t-the Procedural circuit Deficit Hypothesis (PDH).

2 egulates the pyruvate dehydrogenase complex (PDH).

3 ant enzyme component pyruvate dehydrogenase (PDH).

4 vate via the pyruvate dehydrogenase complex (PDH).

5 cated in the mitochondria and interacts with PDH.

6 ges an endogenous octanoate pool to activate PDH.

7 ], which results in constitutively activated PDH.

8 n which rapidly discharges hydrogen from the PdH.

9 lycosylated and glycosylated (gPDH) forms of PDH.

10 osis was sevenfold greater than flux through PDH.

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

12 s, Plasmodium parasites lack a mitochondrial PDH.

13 eukaryotes, Plasmodium lacks a mitochondrial PDH.

14 % of stationary-phase populations expressing pdh.

15 , leading to an increase in dephosphorylated PDH.

16 g energies of key intermediates on supported PdH.

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

18 is dependent on the phosphorylation state of PDH.

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

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

21 g the interactions between the encapsulated [PdH(2) ](2-) unit and its Cu(14) bicapped icosahedral ca

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

23 ngs indicate that CL is required for optimal PDH activation, generation of acetyl-CoA, and TCA cycle

24 yruvate dehydrogenase kinase (PDK) inhibitor/PDH activator dichloroacetate (DCA) normalizes HPMC meta

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

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

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

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

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

30 We find that increasing PDH activity impairs cell proliferation by reducing the

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

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

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

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

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

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

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

38 bilized TAZ-KO mitochondria with CL restored PDH activity to WT levels.

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

40 PDH activity was monitored in these cells by hyperpolari

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

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

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

44 dehydrogenase (PDH), dramatically increased PDH activity, and an impaired response to mitochondrial

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

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

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

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

49 Furthermore, mitochondrial MITF regulates PDH activity.

50 mportant physiological control mechanisms of PDH activity.

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

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

53 lysine acetyltransferase (DLAT), diminishing PDH activity.

54 e mitochondria and involved in regulation of PDH activity.

55 roblasts had reduced pyruvate dehydrogenase (PDH) activity and elevated intracellular lactate:pyruvat

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

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

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

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

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

61 o a ~50% decrease in pyruvate dehydrogenase (PDH) activity, which was observed in both TAZ-KO cells a

62 (P5CS) and decreasing proline dehydrogenase (PDH) activity, while Si reversed these effects caused by

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

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

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

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

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

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

69 eting of both leader and follower cells with PDH and GLUT1 inhibitors, respectively, inhibits cell gr

70 pack and provides rationale for co-targeting PDH and GLUT1 to inhibit collective invasion.

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

72 Blocking E1alpha phosphorylation activated PDH and reduced intracellular lactate concentrations.

73 us aspects of language, and then present the PDH and relevant evidence across language-related disord

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

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

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

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

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

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

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

81 nzymatic activity of pyruvate dehydrogenase (PDH), and increased production of lactate compared to HP

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

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

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

85 e extracts confirmed that flux rates through PDH, as well as pyruvate carboxylase and pyruvate cyclin

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

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

88 by stimulating the PDPhosphatase-phosphoPDH-PDH axis.

89 tein-lipid overlay experiments revealed that PDH binds to CL, and supplementing digitonin-solubilized

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

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

92 Phosphorylation of PDH by one of the pyruvate dehydrogenase kinases 1-4 (PD

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

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

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

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

97 The PDH bypass and the GABA shunt serve to maintain mainline

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

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

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

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

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

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

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

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

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

107 The PDH complex catalyses the conversion of pyruvate to acet

108 The PDH complex catalyzes the conversion of pyruvate to acet

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

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

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

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

113 tyl-CoA (AcCoA), the pyruvate dehydrogenase (PDH) complex (PDC) links glycolysis and the TCA cycle.

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

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

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

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

118 of the mitochondrial pyruvate dehydrogenase (PDH) complex.

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

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

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

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

123 The pyruvate dehydrogenase complex (PDH) critically regulates carbohydrate metabolism.

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

125 pression of the LonP1-P761L variant leads to PDH deficiency and energy metabolism dysfunction, which

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

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

128 We define a pyruvate dehydrogenase (PDH) dependency in leader cells that can be therapeutica

129 ssion affected some of these parameters in a PDH-dependent manner.

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

131 hosphatase (PDP) and pyruvate dehydrogenase (PDH), dramatically increased PDH activity, and an impair

132 onstrated that in the siblings' fibroblasts, PDH dysfunction was caused by increased levels of the ph

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

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

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

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

137 e parallels decreased phosphorylation of the PDH E1alpha subunit (pE1alpha) in liver tissue.

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

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

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

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

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

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

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

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

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

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

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

149 ng its phosphorylation leading to suppressed PDH enzymatic activity.

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

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

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

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

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

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

156 (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

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

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

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

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

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

162 maging tools for noninvasive measurements of PDH flux in rodent models.

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

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

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

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

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

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

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

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

171 e states and developing therapies to improve PDH flux.

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

173 Wistar rats, we used pyruvate dehydrogenase (PDH) flux studies to demonstrate changes in carbohydrate

174 and a nearly threefold rise in flux through PDH (from 0.182 +/- 0.114 to 0.486 +/- 0.139, P = .002),

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

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

177 The PDH has substantial explanatory power, and both basic re

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

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

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

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

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

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

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

185 the therapeutic perspective, reactivation of PDH in cancer cells that were weakly sensitive for reovi

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

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

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

189 -ray diffraction identifies the formation of PdH in Pd/NbN and Pd/C under CO(2) RR conditions, wherea

190 Conditional deletion of PDH in SMSCs affects cell divisions generating myocytes

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

192 e pyruvate away from pyruvate dehydrogenase (PDH) in an NO-dependent and hypoxia-inducible factor 1al

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

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

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

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

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

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

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

200 PDH interaction with MITF was measured before and after

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

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

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

204 PDH is essential for immunologically mediated degranulat

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

206 After activation, PDH is serine dephosphorylated.

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

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

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

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

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

212 eakly sensitive for reovirus, either through PDH kinase (PDK) inhibitors dichloroacetate and AZD7545

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

214 PDH kinase 1, highly expressed under hypoxia, is down-re

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

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

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

218 PDH kinase inactivates PDC by phosphorylating PDH at spe

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

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

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

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

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

224 osphorylated pyruvate dehydrogenase pPDH and PDH-kinase.

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

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

227 We report here that CRISPR/Cas9-generated PDH-knockout (PDH-KO) rat fibroblasts reprogrammed their

228 PDH-KO cells had increased oxygen consumption rates in r

229 We conclude that PDH-KO cells maintain proliferative capacity by utilizin

230 PDH-KO cells replicated normally but produced surprising

231 In addition, PDH-KO cells showed altered cytoplasmic and mitochondria

232 ere that CRISPR/Cas9-generated PDH-knockout (PDH-KO) rat fibroblasts reprogrammed their metabolism an

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

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

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

236 ells exhibited an increase in phosphorylated PDH, levels of which were reduced in the presence of sup

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

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

239 PDH-mediated metabolic flow is critical for skeletal mus

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

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

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

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

244 ized *HOCO and weakened *CO intermediates on PdH/NbN are critical to achieving higher CO(2) RR activi

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

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

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

248 /VN is not fully transformed into the active PdH phase.

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

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

251 acetylating pyruvate dehydrogenase (PDH) and PDH phosphatase.

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

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

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

255 , and expression of UCP3, AAC1, or AAC2, and PDH phosphorylation status did not differ between the ni

256 iated with impaired TBC1D4 S341 and elevated PDH phosphorylation.

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

258 from glycolysis to the TCA cycle mediated by PDH plays a pivotal role in the differentiation of SMSCs

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

260 The PDH posits that abnormalities of brain structures underl

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

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

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

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

265 wnstream metabolism of [1-(13)C]pyruvate via PDH (pyruvate dehydrogenase, [(13)C]bicarbonate), lactat

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

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

268 Therefore, PDH represents a metabolic intervention point that might

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

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

271 1 T338 phosphorylation levels correlate with PDH S293 inactivating phosphorylation levels and poor pr

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

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

274 PDH synthesizes acetyl-CoA; acetate supplementation allo

275 se morphology affects transformations in the PdH system.

276 y phosphorylation of pyruvate dehydrogenase (PDH) that impaired the routing of pyruvate into the tric

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

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

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

280 tivating the pyruvate dehydrogenase complex (PDH) to increase pyruvate oxidation at the expense of fe

281 nfirm the transformation of Pd into hydride (PdH) under the CO(2) RR environment.

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

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

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

285 gnificant increase in metabolic flux through PDH was observed after the oral glucose challenge (P<0.0

286 Metabolic flux through cardiac PDH was significantly reduced in the people with T2DM (F

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

288 AAC) 1 and AAC2, and pyruvate dehydrogenase (PDH) were assessed by respirometry and Western blotting.

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

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

291 nuclear pyruvate and pyruvate dehydrogenase (PDH), which induced histone acetylation and subsequently

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

293 ion or activation of pyruvate dehydrogenase (PDH), which mediates opening of the gateway from glycoly

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

295 els of the phosphorylated E1alpha subunit of PDH, which inhibits enzyme activity.

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

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

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

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

300 A solid proton reservoir layer, PdH(x), also serves as the gate terminal.