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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 is feasible with low mortality and is associated wit
7                                              PDC was modified to account for time to last viral load
8                                              PDC-E2 is a ubiquitous protein present in mitochondria o
9                                              PDC-E2 was found to localize unmodified within apoptotic
10               Three peptides, PDC-E2145-159, PDC-E2(249-263), and PDC-E2(629-643), elicited high-affi
11            Mean adherence was 0.77 +/- 0.28 (PDC +/- SD) at the patient level and 0.78 +/- 0.05 at th
12  and functions, though little is known about PDC-NK cell interactions during these infections.
13 -methyl-D-tryptophan significantly abrogates PDC-driven inducible Treg generation and suppressor cell
14 or, trans-pyrrolidine-2,4-dicarboxylic acid (PDC) for 3 weeks, or a higher level (50 muM) for 48 h, f
15                           Although activated PDC killed the DR5-expressing HIV-infected Sup-T1 cell l
16                            HFD+DCA activated PDC throughout and restored whole-body CHO use during ex
17 on of PDH by PDH phosphatase (PDP) activates PDC.
18            Only 49% of the patients adhered (PDC >/=80%) to all 3 therapies.
19  as with a mouse monoclonal antibody against PDC-E2 and AMA with an immunoglobulin A isotype.
20 ninsula, C9orf72 expansions do not cause ALS-PDC in Chamorros.
21 ewise, LRRK2 mutations do not cause Guam ALS-PDC.
22                                          ALS/PDC shares neuropathological features found in many neur
23 sclerosis/parkinsonism-dementia complex (ALS/PDC) is a fatal neurodegenerative disease found in the C
24 sclerosis/parkinsonism-dementia complex (ALS/PDC), or Alzheimer's disease, has been identified in mor
25                          Thus, examining ALS/PDC may provide further explanations on how various prot
26                     To identify loci for ALS/PDC, we conducted both genome-wide linkage and associati
27 cant evidence for two regions with novel ALS/PDC loci on chromosome 12 and supportive evidence for th
28      Elucidation of the genetic basis of ALS/PDC should improve our understanding of related neurodeg
29                 Our results suggest that ALS/PDC may be influenced by as many as three loci, while il
30 eptides, PDC-E2145-159, PDC-E2(249-263), and PDC-E2(629-643), elicited high-affinity T cell responses
31 icromolar inhibitor of the class C ADC-7 and PDC-3 beta-lactamases.
32  (11.28%) users were adherent (MPR >=70% and PDC <=1.25), 51 (4.23%) were partly adherent (MPR >=70%
33  (4.23%) were partly adherent (MPR >=70% and PDC = 1.50) and 176 (14.60%) were switchers.
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 ipant demographics, baseline viral load, and PDC were explanatory variables.
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 raction between ash plume, thunderstorm, and PDC transport during this secondary period of observed l
44 l beta-sheet structural conformation in anti-PDC-E2 recognition.
45 mal stoichiometry of this in vitro assembled PDC for E2p:E3BP:E1p:E3 is 40:20:40:20.
46 romatin immunoprecipitation (ChIP) to assess PDC's ability to interact with STAT5 DNA-binding sites.
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                            Furthermore, both PDC xenografts and patient-derived xenografts confirm CD
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 f cells within the piezo dispense capillary (PDC) prior to arraying.
57              The presence of CXCR7+ CCR10low PDC-E2-specific ASCs suggests a mechanistic basis for th
58 fections impair plasmacytoid dendritic cell (PDC) and natural killer (NK) cell subset numbers and fun
59         Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological mal
60 he function of plasmacytoid dendritic cells (PDC) in chronic human immunodeficiency virus type 1 (HIV
61                Plasmacytoid dendritic cells (PDC) represent a distinct immune cell type specialized i
62 rturbations of plasmacytoid dendritic cells (PDC), including diminished frequencies in the peripheral
63 ein 3, Pseudomonas-derived cephalosporinase (PDC), and MurA with ceftazidime-avibactam-fosfomycin, an
64 as the primary-and likely sole-S. cerevisiae PDC phosphatase, closing a key knowledge gap about the r
65 itA sensor domains, and this PhoQ-DcuS-CitA (PDC) sensor fold is seen to be distinct from the superfi
66 ntains an inserted repeat of PhoQ/DcuS/CitA (PDC) domains, and similarity between sequence and struct
67 o, using the pyruvate dehydrogenase complex (PDC) activator, dichloroacetate (DCA), would blunt activ
68 reduction in pyruvate dehydrogenase complex (PDC) activity (P < 0.05), and increased glycogen degrada
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    The human pyruvate dehydrogenase complex (PDC) is a 9.5-megadalton catalytic machine that employs
75          The pyruvate dehydrogenase complex (PDC) is a critical mitochondrial enzyme that catalyzes p
76    Mammalian pyruvate dehydrogenase complex (PDC) is a key multi-enzyme assembly that is responsible
77          The pyruvate dehydrogenase complex (PDC) is a multienzyme assembly that converts pyruvate to
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 ing inhibits pyruvate dehydrogenase complex (PDC)-controlled carbohydrate (CHO) oxidation, which cont
84 lyzed by the pyruvate dehydrogenase complex (PDC).
85 consequently pyruvate dehydrogenase complex (PDC).
86 ition of the pyruvate dehydrogenase complex (PDC).
87 units of the pyruvate dehydrogenase complex (PDC).
88 onent of the pyruvate dehydrogenase complex (PDC-E2), has unique features, including continuous high
89 bunit of the pyruvate dehydrogenase complex (PDC-E2), the major mitochondrial autoantigen of PBC and
90 onent of the pyruvate dehydrogenase complex (PDC-E2).
91 onent of the pyruvate dehydrogenase complex (PDC-E2).
92 sis (ALS) and parkinsonism-dementia complex (PDC) exist in Japanese on the Kii Peninsula of Japan and
93 lerosis (ALS)/parkinsonism dementia complex (PDC) of Guam.
94 ds for inspecting protein-detergent complex (PDC) interfaces require high concentrations of protein a
95  pyruvate dehydrogenase multienzyme complex (PDC) and thereby controls the rate of oxidative decarbox
96  pyruvate dehydrogenase multienzyme complex (PDC) is a key regulatory point in cellular metabolism li
97 ndrial pyruvate dehydrogenase (PDH) complex (PDC) acts as a central metabolic node that mediates pyru
98 ), the pyruvate dehydrogenase (PDH) complex (PDC) links glycolysis and the TCA cycle.
99 lfide bond within the lipoic-acid-conjugated PDC-E2 moiety, i.e., by an electrophilic agent renders P
100 onlinearities in parametric down-conversion (PDC) of X-rays to long wavelength radiation in gallium a
101 age 4.5 years after first visit (converters; PDC).
102 io (MPR) and the Proportion of days covered (PDC) approach.
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 roviral therapy (proportion of days covered [PDC] >=90%) and virally suppressed (HIV RNA <200 copies/
107 (measured as the proportion of days covered [PDC] up to 1 year) and a composite outcome comprising ho
108 ime of a deadly pyroclastic density current (PDC) and thunderstorm.
109 matory functions, and plasmacytoid CD123 DC (PDC), which may have tolerogenic potential, were measure
110 atory functions, and plasmacytoid CD123+ DC (PDC), which may have tolerogenic potential, were measure
111 nisms, the action of pyruvate decarboxylase (PDC) and pyruvate formate lyase (PFL)-enzymes that catal
112 rboxylase (BFDC) and pyruvate decarboxylase (PDC) are both thiamin diphosphate-dependent enzymes.
113                      Pyruvate decarboxylase (PDC) uses thiamine diphosphate as an essential cofactor
114               Plant pyruvate decarboxylases (PDC) catalyze the decarboxylation of pyruvate to form ac
115 a induced Pdk4 gene expression and decreased PDC activity.
116 tability, formation of small PDCs, decreased PDC surface flexibility, and potential to mediate crysta
117 was higher and was associated with decreased PDC frequencies.
118 of the E2 subunit of pyruvate dehydrogenase (PDC-E2) are detected in 95% of patients with primary bil
119  the E2 component of pyruvate dehydrogenase (PDC-E2) involving autoantibody and autoreactive cluster
120 of the E2 subunit of pyruvate dehydrogenase (PDC-E2).
121 A = catechol rhodanine acetic acid) and DHP (PDC = pyridine dicarboxylate) binding sites.
122 le hydrolysis of 2-pyrone-4,6-dicarboxylate (PDC) to 4-oxalomesaconate and 4-carboxy-2-hydroxymuconat
123 umarin analogues by a pyridinium dichromate (PDC)-mediated chemoselective allylic oxidation.
124 ection in vivo and document a lack of direct PDC cytolytic activity against autologous infected or un
125  is correlated across these and other double-PDC sensor proteins.
126 C-NK cell culture experiments, CpG-enhanced, PDC-dependent NK cell activity was cell contact and IFN-
127 her TLR2 ligands, PSA is better at enhancing PDC expression of costimulatory molecules required for p
128                                 We evaluated PDC-dependent NK cell killing and gamma interferon (IFN-
129 antly decreased frequency of pDCs expressing PDC-TREM, a modulator of TLR-mediated IFN production.
130 ontext, different preparative approaches for PDC-NCs as well as some of their properties will be pres
131 ctivates the NF-kappaB pathway essential for PDC survival.
132 strate that the IDO pathway is essential for PDC-driven Treg generation from CD4(+)CD25(-) T cells an
133 phosphorylation (inactivation) at E1 by four PDC kinases (PDKs), and reactivation by two PDC phosphat
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  is the principal isozyme regulating hepatic PDC.
138                              In heterologous PDC-NK cell assays, impaired PDC-NK cell killing activit
139                                       Higher PDC (adjusted odds ratio [AOR], 1.74 per 1-level increas
140                                    The human PDC is organized around a 60-meric dodecahedral core com
141                                    The human PDC is subject to inactivation at E1 by serine phosphory
142 o the immune system of intact immunoreactive PDC-E2 within apoptotic blebs.
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 hase fields for the formation of bedforms in PDC deposits.
147  were no significant differential changes in PDC among beneficiaries with at least 1 prescription fil
148 tulating some clinical symptoms described in PDC-deficient patients.
149  than controls, membrane TRAIL expression in PDC from HIV(+) subjects was increased.
150 ds ratio [AOR], 1.74 per 1-level increase in PDC category [95% confidence interval {CI}, 1.30-2.34])
151  including transcription factors involved in PDC development (SpiB, Irf8) and function (Irf7).
152                     IAV exposure resulted in PDC maturation by upregulation of CD86 expression and IF
153                       PDH kinase inactivates PDC by phosphorylating PDH at specific serine residues,
154                           Exercise increased PDC activation and whole-body CHO use in HFD, but to a l
155 creased ACAT1 activity, leading to increased PDC flux and oxidative phosphorylation with attenuated c
156 cate that during uncontrolled HIV infection, PDC-dependent NK cell function is impaired, which is in
157                       CRP directly inhibited PDC IFNalpha release, promoted PDC differentiation, and
158 the apotope of biliary cells contains intact PDC-E2; this apotope, in a setting that includes granulo
159 that BECs translocate immunologically intact PDC-E2 to apoptotic bodies and create an apotope.
160  years in a single institution with intended PDC.
161 d hexanoic acids and the xenobiotic 6BH into PDC-E2.
162 e to aberrantly incorporate xenobiotics into PDC-E2.
163  structures of human recombinant full-length PDC core (rE2/E3BP), truncated PDC core (tE2/E3BP) and n
164 R5-expressing HIV-infected Sup-T1 cell line, PDC did not lyse primary autologous HIV(+) CD4(+) T cell
165 ly higher MDC counts and significantly lower PDC frequencies (P=0.017) during the 1- to 60-day time p
166                    The activity of mammalian PDC is regulated through reversible phosphorylation gove
167 ross-sectional subjects revealed that an MDC:PDC ratio more than or equal to 1.78 was associated with
168             We conclude that an elevated MDC:PDC ratio associates with early small bowel allograft re
169             We conclude that an elevated MDC:PDC ratio associates with liver graft rejection, which o
170  Among rejectors, a significantly higher MDC:PDC ratio (P=0.004) was associated with numerically high
171 s analysis showed a significantly higher MDC:PDC ratio (P=0.043, F-test) among rejectors, compared wi
172 ng characteristic analysis revealed that MDC:PDC ratio more than or equal to 1.52 was associated with
173 tudinal and cross-sectional cohorts, the MDC:PDC ratio was higher and was associated with decreased P
174 1-0.9 percentage points; or 0.6% of the mean PDC [78.2%], P = .01 for both).
175 1-0.5 percentage points; or 0.4% of the mean PDC [82.3%], P = .003) and for metformin in the 2012 and
176 by a corresponding decrease in mitochondrial PDC levels, suggesting a translocation from the mitochon
177       Dynamic translocation of mitochondrial PDC to the nucleus provides a pathway for nuclear acetyl
178 70-fold lower than that of Zymomonas mobilis PDC.
179 tion that AMAs recognize xenobiotic modified PDC-E2 with higher titers than native PDC-E2 raises the
180             E2-2 directly activated multiple PDC-enriched genes, including transcription factors invo
181                       We found that multiple PDC subunits interact with hormone-activated STAT5A in a
182                                       Muscle PDC activity was the same at 2 h and 6 h, but was 65% lo
183 and cathepsin-L activity, and reduced muscle PDC activity.
184 i.e. polymer-derived ceramic nanocomposites (PDC-NCs), which have been shown to be promising material
185 dified PDC-E2 with higher titers than native PDC-E2 raises the possibility that the earliest events i
186  gait (lower pace) deviates from that of non-PDC approximately 4 years prior to diagnosis.
187 95% CI: 1.54 to 1.76) for being nonadherent (PDC <80%) to all 3 therapies.
188                                      Nuclear PDC levels increased in a cell-cycle-dependent manner an
189                        Inhibition of nuclear PDC decreased acetylation of specific lysine residues on
190           We found that knockdown of nuclear PDC in isolated functional nuclei decreased the de novo
191 pically localizes to the cytosol or nucleus, PDC normally resides within the mitochondrial matrix whe
192 tested whether pharmacological activation of PDC overrides these diet-induced changes.
193          Also, pharmacological activation of PDC restores HFD-mediated inhibition of CHO oxidation du
194  and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvas
195                                  Activity of PDC is inhibited by phosphorylation via the pyruvate deh
196 e data strongly suggest that the activity of PDC is regulated by different isozymes in different tiss
197                         However, addition of PDC to SOD1 mutant slices resulted in substantial MN inj
198        The origin and lineage affiliation of PDC have been controversial, partly because PDC show fea
199 lucidate the cellular and molecular basis of PDC development.
200 t normally binds the lipoic acid cofactor of PDC-E2, reacts as well or better to PBC sera than native
201  concert to control molecular composition of PDC and contribute to the Warburg effect.
202 any individual lipoyl domains or the core of PDC.
203 A) forestall binding of the lipoyl domain of PDC to these mutants, analogous to wild-type PDK2 in the
204 lar homology with the inner lipoyl domain of PDC-E2; such chemicals have been proposed as potential e
205  major histocompatibility class I epitope of PDC-E2.
206 ency significantly reduced the expression of PDC-TREM on pDCs from both NZM2410 and C57BL/6 mice.
207 underlie the distinct 'lymphoid' features of PDC.
208       The C-8 and C-11 carboxylate groups of PDC are coordinated within the active site via ion pair
209  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
210 s determined by conducting the hydrolysis of PDC in (18)O-labeled water and subsequent (13)C nuclear
211 e must be deprotonated for the hydrolysis of PDC.
212 colysis and the TCA cycle by inactivation of PDC has only minor effects on cell replication.
213 fect on the overall rates of inactivation of PDC in kinase reaction.
214  was largely responsible for inactivation of PDC in tissues of muscle origin and brown adipose tissue
215                                 Incidence of PDC characterized by prostate weight of more than 1 g wa
216 PDCs, preventing glucocorticoid induction of PDC death and the consequent reduction of systemic IFN-a
217 eron (IFN-alpha) production and induction of PDC-dependent tumor necrosis factor (TNF)-related apopto
218 d muscle PDK4 upregulation and inhibition of PDC and CHO oxidation in humans.
219 nhibits muscle CHO oxidation at the level of PDC during prolonged contraction, and is paralleled by t
220 t of carbohydrate oxidation, at the level of PDC, and up-regulation of muscle protein degradation, in
221 e the integrity and specific localization of PDC-E2 during induced apoptosis.
222 ationship between the nano/microstructure of PDC-NCs and their properties will be highlighted.
223 rrently, there are two conflicting models of PDC (E2+E3BP) core organisation: the 'addition' model (6
224 ge commitment and gene expression program of PDC.
225 rincipally responsible for the regulation of PDC activity in that tissue.
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 derived cell lines (PDCs) of stromal and one PDC of tumorigenic origin were generated from breast or
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           Deciphering which kinase regulates PDC in organisms at specific times or places has been ch
247 isozymes to explore their role in regulating PDC activity.
248 ety, i.e., by an electrophilic agent renders PDC-E2 immunogenic in a genetically susceptible host.
249 orylation of PDH by PDH phosphatase restores PDC activity.
250 NA lowers PDHalpha phosphorylation, restores PDC activity, reverts the Warburg metabolic phenotype, d
251 tilized a mouse model of hepatocyte-specific PDC inactivation to determine the need for this metaboli
252 d GTP, with the formation of 6BH-substituted PDC-E2 predominating in an ATP-rich environment.
253 al therapy (ART) interruption and by testing PDC cytolytic function against autologous HIV-infected C
254  and histological subtype and is better than PDC without- MCR.
255         Sutendra et al. now demonstrate that PDC can translocate from the mitochondria to the nucleus
256                     We also demonstrate that PDC inhibition in cancer cells is associated with normox
257              There is previous evidence that PDC localizes to cancer cell nuclei where it plays a rol
258  challenge the long standing hypothesis that PDC is involved in BCAA-derived aldehyde formation in fr
259 these previous findings, we hypothesize that PDC may modulate STAT5's ability to regulate gene expres
260 er difference (STD) titrations indicate that PDC induces a more dramatic conformational change than N
261 unofluorescence microscopy, we observed that PDC-E2 is present within the adipocyte nucleus where it
262                 These analyses revealed that PDC-E2 is bound to a STAT5-binding site in the promoter
263 hosphatase(s) responsible for activating the PDC in S. cerevisiae has not been conclusively defined.
264 al activities that are not stimulated by the PDC core.
265 vels of other PDK isoforms stimulated by the PDC core.
266               A central issue concerning the PDC structure is the subunit stoichiometry of the E2p/E3
267 nly demonstrate additional functions for the PDC enzyme, but also challenge the long standing hypothe
268 ept for slight differential increases in the PDC for beta-blockers in the 2012 entry cohort (adjusted
269  largely focused on specific residues in the PDC-E2 lipoyl domain critical in maintaining the lipoyl
270  To directly determine the regulation of the PDC by phosphorylation, we developed a complete set of p
271 basal activity of PDK4 in the absence of the PDC core.
272                       Phosphorylation of the PDC E1 subunit was identified as a key inhibitory modifi
273 itate a massively parallel assessment of the PDC interfacial interactions under a fairly broad range
274 ion profile and impaired IFN response of the PDC.
275 a identify E4F1 as a master regulator of the PDC.
276 pithelial cells (BECs) uniquely preserve the PDC-E2 epitope following apoptosis.
277  which specifically tethers E3 dimers to the PDC.
278 re, it appears that the overall flux through PDC in a given tissue largely reflects the properties of
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 SOD1 mutant animals that were not exposed to PDC.
284  phosphocreatine (PCr) concentrations) or to PDC inhibition, whereas after 24 h, muscle lactate accum
285 yl acetyltransferase (E2) to recruit PDP1 to PDC.
286  shifted from extra-pleural pneumonectomy to PDC with the goal of MCR.
287 light the importance of loss of tolerance to PDC-E2 as well as a critical role for the interleukin (I
288 s-pyrrolidine-2,4-dicarboxylic acid (l-trans-PDC) or by partial suppression of GLAST using siRNA inte
289 t full-length PDC core (rE2/E3BP), truncated PDC core (tE2/E3BP) and native bovine heart PDC core (bE
290  PDC kinases (PDKs), and reactivation by two PDC phosphatases.
291       5-year survival of patients undergoing PDC with MCR in multi-modality setting is approaching 25
292 acellular mechanism or mechanisms underlying PDC-induced Treg generation are unknown.
293  roles in cellular metabolism, understanding PDC regulation is pivotal to understanding the larger me
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 ntify potentially antigenic sequences within PDC-E2 (an important hepatic autoantigen) that contain a

 
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