ライフサイエンスコーパス: PDC

1 PDC activation abolished statin myopathy in rodent skele

2 PDC binds cooperatively (Hill coefficient = 2), while NA

3 PDC catalyzes the conversion of pyruvate to acetyl-CoA a

4 PDC depletion had an immediate impact on the activation

5 PDC flux depends on catalytic activity of the most impor

6 PDC inhibition occurs via enhanced expression of pyruvat

7 PDC-E2 is a ubiquitous protein present in mitochondria o

8 PDC-E2 was found to localize unmodified within apoptotic

9 PDC-stimulated NK lysis of HIV-1-infected autologous CD4

10 PDC-stimulated NK lysis was dependent upon MHC class I (

11 Three peptides, PDC-E2145-159, PDC-E2(249-263), and PDC-E2(629-643), elicited high-affi

12 Mean adherence was 0.77 +/- 0.28 (PDC +/- SD) at the patient level and 0.78 +/- 0.05 at th

13 and functions, though little is known about PDC-NK cell interactions during these infections.

14 -methyl-D-tryptophan significantly abrogates PDC-driven inducible Treg generation and suppressor cell

15 or, trans-pyrrolidine-2,4-dicarboxylic acid (PDC) for 3 weeks, or a higher level (50 muM) for 48 h, f

16 ate transport with l-transdicarboxylic acid (PDC) reduced EPSCs, possibly through a mechanism of AMPA

17 Although activated PDC killed the DR5-expressing HIV-infected Sup-T1 cell l

18 HFD+DCA activated PDC throughout and restored whole-body CHO use during ex

19 on of PDH by PDH phosphatase (PDP) activates PDC.

20 Only 49% of the patients adhered (PDC >/=80%) to all 3 therapies.

21 as with a mouse monoclonal antibody against PDC-E2 and AMA with an immunoglobulin A isotype.

22 ninsula, C9orf72 expansions do not cause ALS-PDC in Chamorros.

23 ewise, LRRK2 mutations do not cause Guam ALS-PDC.

24 ALS/PDC shares neuropathological features found in many neur

25 sclerosis/parkinsonism-dementia complex (ALS/PDC) is a fatal neurodegenerative disease found in the C

26 sclerosis/parkinsonism-dementia complex (ALS/PDC), or Alzheimer's disease, has been identified in mor

27 Thus, examining ALS/PDC may provide further explanations on how various prot

28 To identify loci for ALS/PDC, we conducted both genome-wide linkage and associati

29 cant evidence for two regions with novel ALS/PDC loci on chromosome 12 and supportive evidence for th

30 Elucidation of the genetic basis of ALS/PDC should improve our understanding of related neurodeg

31 Our results suggest that ALS/PDC may be influenced by as many as three loci, while il

32 eptides, PDC-E2145-159, PDC-E2(249-263), and PDC-E2(629-643), elicited high-affinity T cell responses

33 icromolar inhibitor of the class C ADC-7 and PDC-3 beta-lactamases.

34 All Chamorro participants with ALS and PDC and control subjects had normal repeats, ranging fro

35 s PDHK1 kinase activity by promoting ATP and PDC binding.

36 en tacrolimus whole blood concentrations and PDC frequencies (Spearman r=-0.370, P=0.005) in 48 cross

37 g to Escherichia coli DHPR: NADH or CRAA and PDC (stable analog of DHP).

38 ligand was observed to enhance both MDC and PDC activation of naive CD4 T cells.

39 ues indicate little synergy between NADH and PDC, (1)H- (15)N HSQC chemical shift perturbation and sa

40 a compelling interaction between STAT5A and PDC subunits in adipocytes under physiological condition

41 validate the interaction between STAT5A and PDC subunits in murine and human cultured adipocytes, as

42 iated by inhibition of both PDC survival and PDC function.

43 l beta-sheet structural conformation in anti-PDC-E2 recognition.

44 mal stoichiometry of this in vitro assembled PDC for E2p:E3BP:E1p:E3 is 40:20:40:20.

45 romatin immunoprecipitation (ChIP) to assess PDC's ability to interact with STAT5 DNA-binding sites.

46 e with the three mitochondrial autoantigens, PDC-E2, BCOADC-E2, and OGDC-E2.

47 The average PDC was 77% for patients in the generic group and 71% fo

48 PDC have been controversial, partly because PDC show features of both lymphocytes and dendritic cell

49 contain a similar characteristic alpha/beta PDC (PhoQ-DcuS-CitA) sensor-domain fold and display simi

50 vo, an effect mediated by inhibition of both PDC survival and PDC function.

51 -producing activity was attributable to both PDC and NK cell defects.

52 ncer, while PDKs may be further activated by PDC by binding to the E2.E3BP core.

53 ignificantly reduced IFN-alpha production by PDC in vitro in response to CpG A ligands or inactivated

54 production of type I interferons in vitro by PDC from HIV-1-infected patients may not represent dimin

55 not late-stage poorly differentiated cancer (PDC).

56 The presence of CXCR7+ CCR10low PDC-E2-specific ASCs suggests a mechanistic basis for th

57 fections impair plasmacytoid dendritic cell (PDC) and natural killer (NK) cell subset numbers and fun

58 Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological mal

59 he function of plasmacytoid dendritic cells (PDC) in chronic human immunodeficiency virus type 1 (HIV

60 Plasmacytoid dendritic cells (PDC) represent a distinct immune cell type specialized i

61 stimulation of plasmacytoid dendritic cells (PDC) with the TLR9 agonist, CpG ODN 2216, triggered NK l

62 rturbations of plasmacytoid dendritic cells (PDC), including diminished frequencies in the peripheral

63 as the primary-and likely sole-S. cerevisiae PDC phosphatase, closing a key knowledge gap about the r

64 itA sensor domains, and this PhoQ-DcuS-CitA (PDC) sensor fold is seen to be distinct from the superfi

65 ntains an inserted repeat of PhoQ/DcuS/CitA (PDC) domains, and similarity between sequence and struct

66 o, using the pyruvate dehydrogenase complex (PDC) activator, dichloroacetate (DCA), would blunt activ

67 reduction in pyruvate dehydrogenase complex (PDC) activity (P < 0.05), and increased glycogen degrada

68 nhibition of pyruvate dehydrogenase complex (PDC) activity contributes to the Warburg metabolic and m

69 itochondrial pyruvate dehydrogenase complex (PDC) are also present and functional in the nucleus of m

70 1) regulates pyruvate dehydrogenase complex (PDC) by acetylating pyruvate dehydrogenase (PDH) and PDH

71 The pyruvate dehydrogenase complex (PDC) catalyzes the conversion of pyruvate into acetyl-Co

72 The human pyruvate dehydrogenase complex (PDC) comprises four multidomain components, E1, E3, E2 a

73 nhibition of pyruvate dehydrogenase complex (PDC) in cancer cells.

74 tion between pyruvate dehydrogenase complex (PDC) inhibition and lactate accumulation in the extensor

75 The human pyruvate dehydrogenase complex (PDC) is a 9.5-megadalton catalytic machine that employs

76 The pyruvate dehydrogenase complex (PDC) is a critical mitochondrial enzyme that catalyzes p

77 Mammalian pyruvate dehydrogenase complex (PDC) is a key multi-enzyme assembly that is responsible

78 itochondrial pyruvate dehydrogenase complex (PDC) is crucial for glucose homeostasis in mammalian cel

79 itochondrial pyruvate dehydrogenase complex (PDC) is down-regulated by phosphorylation catalyzed by p

80 Human pyruvate dehydrogenase complex (PDC) is down-regulated by pyruvate dehydrogenase kinase

81 The pyruvate dehydrogenase complex (PDC) is the primary metabolic checkpoint connecting glyc

82 itochondrial pyruvate dehydrogenase complex (PDC) plays a crucial role in regulation of glucose homoe

83 gral part of pyruvate dehydrogenase complex (PDC) to which it is anchored primarily through the inner

84 ing inhibits pyruvate dehydrogenase complex (PDC)-controlled carbohydrate (CHO) oxidation, which cont

85 ich inhibits pyruvate dehydrogenase complex (PDC)-dependent carbohydrate (CHO) oxidation, would negat

86 lyzed by the pyruvate dehydrogenase complex (PDC).

87 consequently pyruvate dehydrogenase complex (PDC).

88 ition of the pyruvate dehydrogenase complex (PDC).

89 units of the pyruvate dehydrogenase complex (PDC).

90 component of pyruvate dehydrogenase complex (PDC-E2) are targets for autoreactive immune responses in

91 onent of the pyruvate dehydrogenase complex (PDC-E2), has unique features, including continuous high

92 bunit of the pyruvate dehydrogenase complex (PDC-E2), the major mitochondrial autoantigen of PBC and

93 onent of the pyruvate dehydrogenase complex (PDC-E2).

94 onent of the pyruvate dehydrogenase complex (PDC-E2).

95 sis (ALS) and parkinsonism-dementia complex (PDC) exist in Japanese on the Kii Peninsula of Japan and

96 lerosis (ALS)/parkinsonism dementia complex (PDC) of Guam.

97 ds for inspecting protein-detergent complex (PDC) interfaces require high concentrations of protein a

98 pyruvate dehydrogenase multienzyme complex (PDC) and thereby controls the rate of oxidative decarbox

99 pyruvate dehydrogenase multienzyme complex (PDC) is a key regulatory point in cellular metabolism li

100 pyruvate dehydrogenase multienzyme complex (PDC).

101 ndrial pyruvate dehydrogenase (PDH) complex (PDC) acts as a central metabolic node that mediates pyru

102 lfide bond within the lipoic-acid-conjugated PDC-E2 moiety, i.e., by an electrophilic agent renders P

103 was measured by proportion of days covered (PDC) during 180 days following hospital discharge.

104 iption fill) and proportion of days covered (PDC), a standard claims-based measure of adherence, asse

105 measured by the proportion of days covered (PDC).

106 (measured as the proportion of days covered [PDC] up to 1 year) and a composite outcome comprising ho

107 matory functions, and plasmacytoid CD123 DC (PDC), which may have tolerogenic potential, were measure

108 atory functions, and plasmacytoid CD123+ DC (PDC), which may have tolerogenic potential, were measure

109 nisms, the action of pyruvate decarboxylase (PDC) and pyruvate formate lyase (PFL)-enzymes that catal

110 rboxylase (BFDC) and pyruvate decarboxylase (PDC) are both thiamin diphosphate-dependent enzymes.

111 Pyruvate decarboxylase (PDC) uses thiamine diphosphate as an essential cofactor

112 a induced Pdk4 gene expression and decreased PDC activity.

113 tability, formation of small PDCs, decreased PDC surface flexibility, and potential to mediate crysta

114 was higher and was associated with decreased PDC frequencies.

115 of the E2 subunit of pyruvate dehydrogenase (PDC-E2) are detected in 95% of patients with primary bil

116 the E2 component of pyruvate dehydrogenase (PDC-E2) involving autoantibody and autoreactive cluster

117 of the E2 subunit of pyruvate dehydrogenase (PDC-E2).

118 e, the E2 subunit of pyruvate dehydrogenase (PDC-E2).

119 A = catechol rhodanine acetic acid) and DHP (PDC = pyridine dicarboxylate) binding sites.

120 le hydrolysis of 2-pyrone-4,6-dicarboxylate (PDC) to 4-oxalomesaconate and 4-carboxy-2-hydroxymuconat

121 umarin analogues by a pyridinium dichromate (PDC)-mediated chemoselective allylic oxidation.

122 ection in vivo and document a lack of direct PDC cytolytic activity against autologous infected or un

123 is correlated across these and other double-PDC sensor proteins.

124 C-NK cell culture experiments, CpG-enhanced, PDC-dependent NK cell activity was cell contact and IFN-

125 her TLR2 ligands, PSA is better at enhancing PDC expression of costimulatory molecules required for p

126 We evaluated PDC-dependent NK cell killing and gamma interferon (IFN-

127 s a model biligand: (a) if one fragment (ex. PDC) must induce a large structural change before the ot

128 antly decreased frequency of pDCs expressing PDC-TREM, a modulator of TLR-mediated IFN production.

129 ontext, different preparative approaches for PDC-NCs as well as some of their properties will be pres

130 ctivates the NF-kappaB pathway essential for PDC survival.

131 strate that the IDO pathway is essential for PDC-driven Treg generation from CD4(+)CD25(-) T cells an

132 phosphorylation (inactivation) at E1 by four PDC kinases (PDKs), and reactivation by two PDC phosphat

133 d that exogenous NK stimulation derived from PDC can trigger NK cytotoxicity against HIV-1-infected a

134 e accumulation appears to have resulted from PDC activation status limiting pyruvate flux, most proba

135 Functional PDC can form in mitochondria outside of the matrix in so

136 PDC core (tE2/E3BP) and native bovine heart PDC core (bE2/E3BP) obtained by small-angle X-ray scatte

137 In heterologous PDC-NK cell assays, impaired PDC-NK cell killing activit

138 However, PDC activity could be restored in cells from this patien

139 The human PDC is organized around a 60-meric dodecahedral core com

140 The human PDC is subject to inactivation at E1 by serine phosphory

141 o the immune system of intact immunoreactive PDC-E2 within apoptotic blebs.

142 These data indicate that an impaired PDC responsiveness to TLR ligation may play an important

143 In heterologous PDC-NK cell assays, impaired PDC-NK cell killing activity was largely attributable to

144 butable to an NK cell defect, while impaired PDC-NK cell IFN-gamma-producing activity was attributabl

145 In PDC "knockout" (KO) animals, the long-term regenerative

146 were no significant differential changes in PDC among beneficiaries with at least 1 prescription fil

147 lts show that frontal and temporal cortex in PDC is distinguished from AD and PSP by its accumulation

148 tulating some clinical symptoms described in PDC-deficient patients.

149 than controls, membrane TRAIL expression in PDC from HIV(+) subjects was increased.

150 ransferase (E2), which is also integrated in PDC.

151 including transcription factors involved in PDC development (SpiB, Irf8) and function (Irf7).

152 uclein (SNCA) as a major abnormal protein in PDC but not AD.

153 itin, and apolipoprotein E in AD, and tau in PDC, we identified alpha-synuclein (SNCA) as a major abn

154 PDH kinase inactivates PDC by phosphorylating PDH at specific serine residues,

155 Exercise increased PDC activation and whole-body CHO use in HFD, but to a l

156 creased ACAT1 activity, leading to increased PDC flux and oxidative phosphorylation with attenuated c

157 cate that during uncontrolled HIV infection, PDC-dependent NK cell function is impaired, which is in

158 CRP directly inhibited PDC IFNalpha release, promoted PDC differentiation, and

159 the apotope of biliary cells contains intact PDC-E2; this apotope, in a setting that includes granulo

160 that BECs translocate immunologically intact PDC-E2 to apoptotic bodies and create an apotope.

161 d hexanoic acids and the xenobiotic 6BH into PDC-E2.

162 mportant xenobiotic can be incorporated into PDC in place of lipoic acid by the exogenous lipoylation

163 e to aberrantly incorporate xenobiotics into PDC-E2.

164 ulative effects on activity (eg, "total" LAD PDC activity was 21.9+/-3.1 versus 42.8+/-1.9 mU, P<0.05

165 structures of human recombinant full-length PDC core (rE2/E3BP), truncated PDC core (tE2/E3BP) and n

166 R5-expressing HIV-infected Sup-T1 cell line, PDC did not lyse primary autologous HIV(+) CD4(+) T cell

167 ly higher MDC counts and significantly lower PDC frequencies (P=0.017) during the 1- to 60-day time p

168 ross-sectional subjects revealed that an MDC:PDC ratio more than or equal to 1.78 was associated with

169 We conclude that an elevated MDC:PDC ratio associates with early small bowel allograft re

170 We conclude that an elevated MDC:PDC ratio associates with liver graft rejection, which o

171 Among rejectors, a significantly higher MDC:PDC ratio (P=0.004) was associated with numerically high

172 s analysis showed a significantly higher MDC:PDC ratio (P=0.043, F-test) among rejectors, compared wi

173 ng characteristic analysis revealed that MDC:PDC ratio more than or equal to 1.52 was associated with

174 tudinal and cross-sectional cohorts, the MDC:PDC ratio was higher and was associated with decreased P

175 1-0.9 percentage points; or 0.6% of the mean PDC [78.2%], P = .01 for both).

176 1-0.5 percentage points; or 0.4% of the mean PDC [82.3%], P = .003) and for metformin in the 2012 and

177 by a corresponding decrease in mitochondrial PDC levels, suggesting a translocation from the mitochon

178 Dynamic translocation of mitochondrial PDC to the nucleus provides a pathway for nuclear acetyl

179 70-fold lower than that of Zymomonas mobilis PDC.

180 tion that AMAs recognize xenobiotic modified PDC-E2 with higher titers than native PDC-E2 raises the

181 E2-2 directly activated multiple PDC-enriched genes, including transcription factors invo

182 We found that multiple PDC subunits interact with hormone-activated STAT5A in a

183 Muscle PDC activity was the same at 2 h and 6 h, but was 65% lo

184 During contraction, the rate of muscle PDC activation was significantly lower at 100 mg (kg bm)

185 and cathepsin-L activity, and reduced muscle PDC activity.

186 i.e. polymer-derived ceramic nanocomposites (PDC-NCs), which have been shown to be promising material

187 dified PDC-E2 with higher titers than native PDC-E2 raises the possibility that the earliest events i

188 95% CI: 1.54 to 1.76) for being nonadherent (PDC <80%) to all 3 therapies.

189 ers were selectively increased in AD but not PDC or PSP.

190 Nuclear PDC levels increased in a cell-cycle-dependent manner an

191 Inhibition of nuclear PDC decreased acetylation of specific lysine residues on

192 We found that knockdown of nuclear PDC in isolated functional nuclei decreased the de novo

193 pically localizes to the cytosol or nucleus, PDC normally resides within the mitochondrial matrix whe

194 tested whether pharmacological activation of PDC overrides these diet-induced changes.

195 Also, pharmacological activation of PDC restores HFD-mediated inhibition of CHO oxidation du

196 and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvas

197 Activity of PDC is inhibited by phosphorylation via the pyruvate deh

198 However, addition of PDC to SOD1 mutant slices resulted in substantial MN inj

199 The origin and lineage affiliation of PDC have been controversial, partly because PDC show fea

200 lucidate the cellular and molecular basis of PDC development.

201 t normally binds the lipoic acid cofactor of PDC-E2, reacts as well or better to PBC sera than native

202 PDHK2 is an integral component of PDC tightly bound to the inner lipoyl-bearing domains (L

203 concert to control molecular composition of PDC and contribute to the Warburg effect.

204 The molecular control of PDC lineage specification has been poorly understood.

205 any individual lipoyl domains or the core of PDC.

206 A) forestall binding of the lipoyl domain of PDC to these mutants, analogous to wild-type PDK2 in the

207 lar homology with the inner lipoyl domain of PDC-E2; such chemicals have been proposed as potential e

208 hydrolipoyl transacetylase component (E2) of PDC.

209 major histocompatibility class I epitope of PDC-E2.

210 ency significantly reduced the expression of PDC-TREM on pDCs from both NZM2410 and C57BL/6 mice.

211 underlie the distinct 'lymphoid' features of PDC.

212 The C-8 and C-11 carboxylate groups of PDC are coordinated within the active site via ion pair

213 The kinetic constants for the hydrolysis of PDC are 340 s(-1) and 9.8 x 10(6) M(-1) s(-1) (k(cat) an

214 s determined by conducting the hydrolysis of PDC in (18)O-labeled water and subsequent (13)C nuclear

215 e must be deprotonated for the hydrolysis of PDC.

216 Incidence of PDC characterized by prostate weight of more than 1 g wa

217 PDCs, preventing glucocorticoid induction of PDC death and the consequent reduction of systemic IFN-a

218 eron (IFN-alpha) production and induction of PDC-dependent tumor necrosis factor (TNF)-related apopto

219 d muscle PDK4 upregulation and inhibition of PDC and CHO oxidation in humans.

220 nhibits muscle CHO oxidation at the level of PDC during prolonged contraction, and is paralleled by t

221 t of carbohydrate oxidation, at the level of PDC, and up-regulation of muscle protein degradation, in

222 e the integrity and specific localization of PDC-E2 during induced apoptosis.

223 ationship between the nano/microstructure of PDC-NCs and their properties will be highlighted.

224 rrently, there are two conflicting models of PDC (E2+E3BP) core organisation: the 'addition' model (6

225 ge commitment and gene expression program of PDC.

226 nsive analysis of the amino acid residues of PDC-E2 lipoyl beta-sheet with AMA specificity is lacking

227 pha production was reduced responsiveness of PDC to de novo stimulation, not diminished per cell IFN-

228 velopmental origin and genetic similarity of PDC and classical antigen-presenting DC have been establ

229 A second crystal structure of PDC in complex with fluoride shows that the ion organize

230 The current understanding of PDC regulation involves inhibitory serine phosphorylatio

231 tudy was to investigate the effect of CRP on PDC and monocyte responses to nucleoprotein autoantigens

232 -gamma and granzyme B activity (dependent on PDC and NK cells) were impaired in viremic HIV infection

233 om patients with Alzheimer's disease (AD) or PDC and their matched controls using isobaric tags for r

234 he 2-oxo-dehydrogenase pathway, particularly PDC-E2.

235 Three peptides, PDC-E2145-159, PDC-E2(249-263), and PDC-E2(629-643), eli

236 biochemistry, we define Ptc6p as the primary PDC phosphatase in S. cerevisiae Our analyses further su

237 tly inhibited PDC IFNalpha release, promoted PDC differentiation, and increased late endosome localiz

238 In purified PDC-NK cell culture experiments, CpG-enhanced, PDC-depen

239 Real-time PCR analysis of purified PDC from patients prior to and during treatment interrup

240 ated bovine serum albumin (BSA), recombinant PDC-E2 (rPDC-E2) or BSA alone.

241 Here, using an in vitro reconstituted PDC, we provide densitometry, isothermal titration calor

242 on factor alpha (PPARalpha) mRNA and reduced PDC activation.

243 ession of PDK isoforms and therefore reduced PDC activity prevails in cancer and diabetes.

244 mechanisms, which act in concert to regulate PDC activity and promote the Warburg effect.

245 essibility, which act in concert to regulate PDC activity and promote the Warburg effect.

246 ety, i.e., by an electrophilic agent renders PDC-E2 immunogenic in a genetically susceptible host.

247 he 1-methyl-D-tryptophan effect and restores PDC-driven Treg generation.

248 orylation of PDH by PDH phosphatase restores PDC activity.

249 NA lowers PDHalpha phosphorylation, restores PDC activity, reverts the Warburg metabolic phenotype, d

250 tilized a mouse model of hepatocyte-specific PDC inactivation to determine the need for this metaboli

251 d GTP, with the formation of 6BH-substituted PDC-E2 predominating in an ATP-rich environment.

252 al therapy (ART) interruption and by testing PDC cytolytic function against autologous HIV-infected C

253 Sutendra et al. now demonstrate that PDC can translocate from the mitochondria to the nucleus

254 We also demonstrate that PDC inhibition in cancer cells is associated with normox

255 There is previous evidence that PDC localizes to cancer cell nuclei where it plays a rol

256 these previous findings, we hypothesize that PDC may modulate STAT5's ability to regulate gene expres

257 er difference (STD) titrations indicate that PDC induces a more dramatic conformational change than N

258 unofluorescence microscopy, we observed that PDC-E2 is present within the adipocyte nucleus where it

259 These analyses revealed that PDC-E2 is bound to a STAT5-binding site in the promoter

260 cumulation of abnormal SNCA and suggest that PDC be considered a synucleinopathy as well as a tauopat

261 hosphatase(s) responsible for activating the PDC in S. cerevisiae has not been conclusively defined.

262 al activities that are not stimulated by the PDC core.

263 vels of other PDK isoforms stimulated by the PDC core.

264 A central issue concerning the PDC structure is the subunit stoichiometry of the E2p/E3

265 ept for slight differential increases in the PDC for beta-blockers in the 2012 entry cohort (adjusted

266 he maintenance of PDHK2 functionality in the PDC-bound state, the molecular mechanisms responsible fo

267 largely focused on specific residues in the PDC-E2 lipoyl domain critical in maintaining the lipoyl

268 To directly determine the regulation of the PDC by phosphorylation, we developed a complete set of p

269 basal activity of PDK4 in the absence of the PDC core.

270 Phosphorylation of the PDC E1 subunit was identified as a key inhibitory modifi

271 itate a massively parallel assessment of the PDC interfacial interactions under a fairly broad range

272 a specific transcriptional regulator of the PDC lineage in mice and humans and reveal a key function

273 ion profile and impaired IFN response of the PDC.

274 a identify E4F1 as a master regulator of the PDC.

275 cycle of PDHK and its translocation over the PDC surface is thought to be mediated by the "symmetric"

276 pithelial cells (BECs) uniquely preserve the PDC-E2 epitope following apoptosis.

277 which specifically tethers E3 dimers to the PDC.

278 efine its functional specificity towards the PDC.

279 Pyruvate flux through PDC is regulated via phosphorylation (inactivation) at E

280 IRT3 and recruits acetyltransferase ACAT1 to PDC, resulting in increased inhibitory lysine acetylatio

281 PDP1 dissociates SIRT3 and recruits ACAT1 to PDC.

282 e mice, by measuring levels of antibodies to PDC-E2, immunohistology of liver, and expression of Gal-

283 sions as well as appearance of antibodies to PDC-E2, serum levels of tumor necrosis factor-alpha and

284 SOD1 mutant animals that were not exposed to PDC.

285 phosphocreatine (PCr) concentrations) or to PDC inhibition, whereas after 24 h, muscle lactate accum

286 yl acetyltransferase (E2) to recruit PDP1 to PDC.

287 wy bodies that was quantitatively similar to PDC.

288 embly are discussed, using CRAA tethering to PDC as a model biligand: (a) if one fragment (ex. PDC) m

289 light the importance of loss of tolerance to PDC-E2 as well as a critical role for the interleukin (I

290 s-pyrrolidine-2,4-dicarboxylic acid (l-trans-PDC) or by partial suppression of GLAST using siRNA inte

291 t full-length PDC core (rE2/E3BP), truncated PDC core (tE2/E3BP) and native bovine heart PDC core (bE

292 PDC kinases (PDKs), and reactivation by two PDC phosphatases.

293 acellular mechanism or mechanisms underlying PDC-induced Treg generation are unknown.

294 n of exercise were used to estimate CHO use, PDC activation, and mRNAs associated with insulin, fat,

295 While PDC from HIV-infected subjects expressed less interferon

296 remely limited activity with pyruvate, while PDC has no activity with benzoylformate.

297 ith BBr3 and oxidized to the o-quinones with PDC.

298 e fact that AMA-containing sera reacted with PDC-E2 on apoptotic BECs without a requirement for perme

299 blast population were uniquely reactive with PDC-E2, detected in the CXCR7+ CCR10low plasmablast popu

300 ce an immune response that cross-reacts with PDC-E2.

301 ntify potentially antigenic sequences within PDC-E2 (an important hepatic autoantigen) that contain a