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1 quirement for H(2) suggests that its role is anaplerotic.
4 ycolytic pathway for glucose catabolism, and anaplerotic activity is high to replenish the TCA cycle
5 lysis enabled the resolution of the involved anaplerotic activity of the microorganism using only one
8 ificantly reduced levels of intermediate and anaplerotic acyl-coenzyme A (CoA) species incorporated i
10 li diet are consistent with a rebalancing of anaplerotic and cataplerotic reactions and enhanced inte
13 cycle therefore represents a key pathway for anaplerotic carbon fixation into nitrogenous compounds t
14 ly essential" amino acid glutamine (Q) as an anaplerotic carbon source for TCA cycle intermediates an
15 ly essential' amino acid glutamine (Q) as an anaplerotic carbon source for TCA cycle intermediates.
17 5% of mitochondrial oxaloacetate arises from anaplerotic carboxylation of pyruvate, while in the anae
18 he cytosolic oxaloacetate is synthesized via anaplerotic carboxylation of pyruvate; (d) the malic enz
20 lin resistant through high-fat (HF) feeding; anaplerotic, cataplerotic, and oxidative metabolic fluxe
21 at induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backe
22 se organelles also accommodate high-capacity anaplerotic/cataplerotic pathways that are essential to
23 tegrated to remodel pathways associated with anaplerotic central metabolism, lipid anabolism and the
25 enes for Sec-like protein secretion systems, anaplerotic CO(2) incorporation, and phosphorus and sulf
26 , carbon acquisition pathways shifted toward anaplerotic CO2 fixation in the light, contributing 31 +
27 hermore, loss of muscle PDH induces adaptive anaplerotic compensation by increasing pyruvate-alanine
31 way has been shown previously to promote the anaplerotic entry of glutamine to the TCA cycle via GDH.
32 in level, and relative mRNA level of the key anaplerotic enzyme pyruvate carboxylase (PC) were 80-90%
34 itrate and malate and higher capacity of key anaplerotic enzymes, notably the mitochondrial NAD-depen
36 xtracts was used to indirectly calculate the anaplerotic flux (0.90 +/- 0.07 x citrate synthase flux)
37 icarboxylic acid (TCA) cycle flux (VTCA) and anaplerotic flux (VANA) to be 0.43 +/- 0.04 mumol g(-1)
41 a of palmitate-treated hepatocytes activates anaplerotic flux from glutamine to alpha-ketoglutarate (
42 ction of second messengers through increased anaplerotic flux has been shown to be critical for coupl
43 ring muscle contraction, (2) higher relative anaplerotic flux in oxidative (soleus) versus glycolytic
46 ertrophied rats displayed an 83% increase in anaplerotic flux into the tricarboxylic acid cycle (P<0.
47 ted with pyruvate carboxylase (PC)-catalyzed anaplerotic flux into the tricarboxylic acid cycle and s
48 be 0.08 +/- 0.039 in brain, indicating that anaplerotic flux is significant and should be considered
52 tion, which indicates that absolute rates of anaplerotic flux rise in proportion to increased oxidati
53 ated with a approximately 4-fold increase in anaplerotic flux that could mostly be attributed to an i
54 ruvate oxidation in ssTnI during TAC reduced anaplerotic flux, ameliorating inefficiencies in glucose
59 ith thioredoxin in particular enable the Pck anaplerotic function under fermentative growth condition
60 e TCA cycle in the tumors and tumors utilize anaplerotic glutamine to a greater extent than adjacent
62 alic enzyme (ME), producing malate, enables "anaplerotic" influx of carbon into the citric acid cycle
65 iable activation of glycolysis, cataplerotic/anaplerotic Krebs cycle including reductive carboxylatio
67 d cells revealed induction of a compensatory anaplerotic mechanism catalyzed by pyruvate carboxylase
68 osed that induction of the PhoPR regulon and anaplerotic metabolism, in concert with the restricted u
70 , pyruvate carboxylation was suppressed, and anaplerotic oxaloacetate was derived from glutamine.
71 ating acetate and pyruvate through the CO(2)-anaplerotic pathway and pyruvate synthesis from acetyl-C
73 e by succinyl-CoA synthetase (SCS-GTP) to an anaplerotic pathway producing phosphoenolpyruvate (PEP).
74 ate:ferredoxin oxidoreductase, and the CO(2)-anaplerotic pathway via phosphoenolpyruvate carboxylase.
76 reliance of proliferating cells on different anaplerotic pathways depends on the relative availabilit
78 umber of studies underline the importance of anaplerotic pathways for hepatic biosynthetic functions
80 ever, the regulation of flux through various anaplerotic pathways in response to combinations of phys
82 sults demonstrate: (1) relative flux through anaplerotic pathways is 15-41 % of TCA cycle flux at res
83 g contraction, and (3) relative flux through anaplerotic pathways is maintained in all muscle fibre t
85 enables calculation of Y (flux rate through anaplerotic pathways relative to tricarboxylic acid (TCA
87 r biosynthesis, and they must be replaced by anaplerotic pathways that regenerate these intermediates
88 Therefore, targeting fatty acid oxidation or anaplerotic pathways that support fatty acid oxidation m
89 wn at early disease stages and activation of anaplerotic pathways to regenerate energy equivalents to
90 A cycle, fatty acid, and gluconeogenesis and anaplerotic pathways were expressed differently between
91 uvate:ferredoxin oxidoreductase reaction and anaplerotic pathways) and Re-citrate synthase (Ccar_0615
93 omer analysis to quantify flux through three anaplerotic pathways: 1) pyruvate carboxylase of pyruvat
94 somal activities and metabolite-restoration (anaplerotic) pathways that would mitigate the loss of a
97 al control of respiratory CO2 refixation and anaplerotic photosynthate partitioning in support of sto
99 and protein of ATP citrate lyase, which uses anaplerotic products in the cytosol, were 60-75% lower i
100 in fatty acids (precursors of acetyl-CoA and anaplerotic propionyl-CoA) would restore energy producti
101 malate and aspartate indicated high rates of anaplerotic pyruvate carboxylase activity and incomplete
103 gnificantly, Q deprivation or suppression of anaplerotic Q utilization created synthetic lethality to
107 et of rapamycin signaling regulates specific anaplerotic reactions by coupling nitrogen quality to th
108 s, a fuel switch caused by the activation of anaplerotic reactions driven by AMP deaminase 3 (Ampd3)
109 Rebalancing nitrogen metabolism requires anaplerotic reactions that resemble at least parts of a
110 by the TCA cycle that must be replenished by anaplerotic reactions to maintain the respiratory compet
111 Glutamate oxaloacetate transaminase enables anaplerotic refilling of TCA cycle intermediates in stro
113 vate carboxylase, the predominant enzyme for anaplerotic replenishing of the TCA cycle, was elevated
114 of a range of components that debilitate an anaplerotic role for mitochondria in cellular carbon met
115 ylate cycle genes in metazoa and suggests an anaplerotic role of purine degradation in early eukaryot
116 is converted via pyruvate carboxylase as an anaplerotic route at a rate more than sufficient to comp
117 n-traditional ways, while utilizing multiple anaplerotic routes into a canonical tricarboxylic acid (
120 utamine as a source of nitrogen and as a key anaplerotic source to provide metabolites to the tricarb
124 the cell contents of Gln, glutamate, and the anaplerotic substrate 2-oxoglutarate, inhibiting MM cell
125 vely, of acetyl-coenzyme A while the rate of anaplerotic substrate entry was 7 +/- 3, 25 +/- 8, and 1
126 ctivates the mechanisms needed to switch the anaplerotic substrate from glucose to glutamine to accom
127 lts demonstrate that MDV infection activates anaplerotic substrate from glucose to glutamine to provi
128 ndicates that DC 8 is chain shortened to the anaplerotic substrate succinate and that peroxisomal FAO
129 re that cardiac glycogen does indeed provide anaplerotic substrate to facilitate beta-hydroxybutyrate
130 cer cells in culture rely on glutamine as an anaplerotic substrate to replenish tricarboxylic acid (T
132 armacological anaplerotic therapy when other anaplerotic substrates are impractical or contraindicate
136 diates; therefore their utilisation requires anaplerotic supplementation, and intra-myocardial glycog
137 luble DODA in nutritional or pharmacological anaplerotic therapy when other anaplerotic substrates ar
138 ng three heptanoate chains, is thought to be anaplerotic through production of propionyl- and acetyl-
139 Results include a rapid increase in ATP/ADP, anaplerotic tricarboxylic acid cycle flux, and increases
140 ween growing and mature leaves, with greater anaplerotic, tricarboxylic acid cycle and mitochondrial
141 P production and have a notable addiction to anaplerotic use of glutamine for macromolecular synthesi