ライフサイエンスコーパス: anaplerotic

1 quirement for H(2) suggests that its role is anaplerotic.

2 ycolytic pathway for glucose catabolism, and anaplerotic activity is high to replenish the TCA cycle

3 lysis enabled the resolution of the involved anaplerotic activity of the microorganism using only one

4 hat was previously thought to have merely an anaplerotic activity.

5 r hypoxic conditions, also increased the Pck anaplerotic activity.

6 ificantly reduced levels of intermediate and anaplerotic acyl-coenzyme A (CoA) species incorporated i

7 li diet are consistent with a rebalancing of anaplerotic and cataplerotic reactions and enhanced inte

8 in M. smegmatis, pyruvate carboxylase is not anaplerotic but rather gluconeogenic.

9 olytic oligotrophic lifestyle alongside with anaplerotic carbon assimilation.

10 cycle therefore represents a key pathway for anaplerotic carbon fixation into nitrogenous compounds t

11 ly essential" amino acid glutamine (Q) as an anaplerotic carbon source for TCA cycle intermediates an

12 ly essential' amino acid glutamine (Q) as an anaplerotic carbon source for TCA cycle intermediates.

13 5% of mitochondrial oxaloacetate arises from anaplerotic carboxylation of pyruvate, while in the anae

14 he cytosolic oxaloacetate is synthesized via anaplerotic carboxylation of pyruvate; (d) the malic enz

15 at induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backe

16 se organelles also accommodate high-capacity anaplerotic/cataplerotic pathways that are essential to

17 tegrated to remodel pathways associated with anaplerotic central metabolism, lipid anabolism and the

18 The results suggest a role for Cpb in anaplerotic CO(2) fixation reactions by supplying bicarb

19 enes for Sec-like protein secretion systems, anaplerotic CO(2) incorporation, and phosphorus and sulf

20 , carbon acquisition pathways shifted toward anaplerotic CO2 fixation in the light, contributing 31 +

21 also a key nutrient providing a substantial anaplerotic contribution to the TCA cycle.

22 conditions, accelerates the reaction in the anaplerotic direction.

23 way has been shown previously to promote the anaplerotic entry of glutamine to the TCA cycle via GDH.

24 in level, and relative mRNA level of the key anaplerotic enzyme pyruvate carboxylase (PC) were 80-90%

25 ng pyruvate dehydrogenase to compete against anaplerotic enzymes for pyruvate carboxylation.

26 itrate and malate and higher capacity of key anaplerotic enzymes, notably the mitochondrial NAD-depen

27 conditions predicted dependence on specific anaplerotic enzymes.

28 xtracts was used to indirectly calculate the anaplerotic flux (0.90 +/- 0.07 x citrate synthase flux)

29 icarboxylic acid (TCA) cycle flux (VTCA) and anaplerotic flux (VANA) to be 0.43 +/- 0.04 mumol g(-1)

30 irements, promoting macromolecule synthesis, anaplerotic flux and ATP.

31 This mismatch induces increased anaplerotic flux and inefficient glucose metabolism.

32 ction, nor have fibre type-specific rates of anaplerotic flux been studied.

33 ction of second messengers through increased anaplerotic flux has been shown to be critical for coupl

34 ring muscle contraction, (2) higher relative anaplerotic flux in oxidative (soleus) versus glycolytic

35 Anaplerotic flux into the Kreb's cycle is crucial for gl

36 ertrophied rats displayed an 83% increase in anaplerotic flux into the tricarboxylic acid cycle (P<0.

37 ted with pyruvate carboxylase (PC)-catalyzed anaplerotic flux into the tricarboxylic acid cycle and s

38 be 0.08 +/- 0.039 in brain, indicating that anaplerotic flux is significant and should be considered

39 s compartment, consistent with the view that anaplerotic flux occurs primarily in astrocytes.

40 y contributes approximately 50% of the total anaplerotic flux of glutamine into the TCA cycle.

41 At substimulatory glucose, anaplerotic flux rate in the clonal INS-1 832/13 cells w

42 tion, which indicates that absolute rates of anaplerotic flux rise in proportion to increased oxidati

43 ated with a approximately 4-fold increase in anaplerotic flux that could mostly be attributed to an i

44 ruvate oxidation in ssTnI during TAC reduced anaplerotic flux, ameliorating inefficiencies in glucose

45 ase, a key regulator of pyruvate cycling and anaplerotic flux, was also increased.

46 oxylic acid cycle turnover at the expense of anaplerotic flux.

47 Forward and backward directions of anaplerotic fluxes could be distinguished.

48 ith thioredoxin in particular enable the Pck anaplerotic function under fermentative growth condition

49 s the catabolic beta-oxidation cycle and the anaplerotic glyoxylate cycle.

50 alic enzyme (ME), producing malate, enables "anaplerotic" influx of carbon into the citric acid cycle

51 ation of glutamate, tricarboxylic acid (TCA) anaplerotic intermediates and GSH.

52 d cells revealed induction of a compensatory anaplerotic mechanism catalyzed by pyruvate carboxylase

53 , pyruvate carboxylation was suppressed, and anaplerotic oxaloacetate was derived from glutamine.

54 ating acetate and pyruvate through the CO(2)-anaplerotic pathway and pyruvate synthesis from acetyl-C

55 We confirm that the CO(2)-anaplerotic pathway is active during phototrophic growth

56 e by succinyl-CoA synthetase (SCS-GTP) to an anaplerotic pathway producing phosphoenolpyruvate (PEP).

57 ate:ferredoxin oxidoreductase, and the CO(2)-anaplerotic pathway via phosphoenolpyruvate carboxylase.

58 Glutaminolysis, an anaplerotic pathway, replenished aspartate for anabolic

59 try into and exit from the TCA cycle through anaplerotic pathways during contraction.

60 umber of studies underline the importance of anaplerotic pathways for hepatic biosynthetic functions

61 triacylglycerol synthesis, and flux through anaplerotic pathways in mitochondria of human liver.

62 ever, the regulation of flux through various anaplerotic pathways in response to combinations of phys

63 Flux through anaplerotic pathways in skeletal muscle has not been eva

64 sults demonstrate: (1) relative flux through anaplerotic pathways is 15-41 % of TCA cycle flux at res

65 g contraction, and (3) relative flux through anaplerotic pathways is maintained in all muscle fibre t

66 enables calculation of Y (flux rate through anaplerotic pathways relative to tricarboxylic acid (TCA

67 Additionally, flux through anaplerotic pathways relative to tricarboxylic acid cycl

68 Therefore, targeting fatty acid oxidation or anaplerotic pathways that support fatty acid oxidation m

69 A cycle, fatty acid, and gluconeogenesis and anaplerotic pathways were expressed differently between

70 uvate:ferredoxin oxidoreductase reaction and anaplerotic pathways) and Re-citrate synthase (Ccar_0615

71 omer analysis to quantify flux through three anaplerotic pathways: 1) pyruvate carboxylase of pyruvat

72 somal activities and metabolite-restoration (anaplerotic) pathways that would mitigate the loss of a

73 mtGTP synthesis with insulin release through anaplerotic PEP cycling.

74 We found that in respiring root tips, anaplerotic phosphoenolpyruvate carboxylase activity was

75 al control of respiratory CO2 refixation and anaplerotic photosynthate partitioning in support of sto

76 n coordinating ammonia assimilation with the anaplerotic production of carbon skeletons.

77 and protein of ATP citrate lyase, which uses anaplerotic products in the cytosol, were 60-75% lower i

78 in fatty acids (precursors of acetyl-CoA and anaplerotic propionyl-CoA) would restore energy producti

79 malate and aspartate indicated high rates of anaplerotic pyruvate carboxylase activity and incomplete

80 hancing oxidative pyruvate dehydrogenase and anaplerotic pyruvate carboxylase fluxes.

81 gnificantly, Q deprivation or suppression of anaplerotic Q utilization created synthetic lethality to

82 This anaplerotic rate in the awake rat brain was severalfold

83 on of pyruvate to oxaloacetate, an important anaplerotic reaction in mammalian tissues.

84 ed factors influencing the gluconeogenic and anaplerotic reaction kinetics.

85 et of rapamycin signaling regulates specific anaplerotic reactions by coupling nitrogen quality to th

86 s, a fuel switch caused by the activation of anaplerotic reactions driven by AMP deaminase 3 (Ampd3)

87 Rebalancing nitrogen metabolism requires anaplerotic reactions that resemble at least parts of a

88 by the TCA cycle that must be replenished by anaplerotic reactions to maintain the respiratory compet

89 Glutamate oxaloacetate transaminase enables anaplerotic refilling of TCA cycle intermediates in stro

90 GOT overexpression increased anaplerotic refilling of tricarboxylic acid cycle interm

91 of a range of components that debilitate an anaplerotic role for mitochondria in cellular carbon met

92 n-traditional ways, while utilizing multiple anaplerotic routes into a canonical tricarboxylic acid (

93 utamine as a source of nitrogen and as a key anaplerotic source to provide metabolites to the tricarb

94 The major anaplerotic sources are pyruvate and glutamine, which re

95 c acid cycle activity by providing alternate anaplerotic sources of biosynthetic precursors.

96 The combination of these specific anaplerotic steps can support energy demand despite HIFs

97 the cell contents of Gln, glutamate, and the anaplerotic substrate 2-oxoglutarate, inhibiting MM cell

98 vely, of acetyl-coenzyme A while the rate of anaplerotic substrate entry was 7 +/- 3, 25 +/- 8, and 1

99 ctivates the mechanisms needed to switch the anaplerotic substrate from glucose to glutamine to accom

100 e as a major tri-carboxylic acid (TCA) cycle anaplerotic substrate to support proliferation.

101 armacological anaplerotic therapy when other anaplerotic substrates are impractical or contraindicate

102 that can be mitigated in part by alternative anaplerotic substrates in utero.

103 Use of anaplerotic substrates to reverse ammonia-induced mitoch

104 luble DODA in nutritional or pharmacological anaplerotic therapy when other anaplerotic substrates ar

105 Results include a rapid increase in ATP/ADP, anaplerotic tricarboxylic acid cycle flux, and increases

106 Blocking anaplerotic utilization of Q mimicked Q deprivation--cau