ライフサイエンスコーパス: CPT-I

1 CPT I exerts significantly less control over ketogenesis

2 CPT-I converts long-chain fatty acyl-CoAs to acylcarniti

3 CPT-I has two structural genes (alpha and beta) that are

4 -B and porin proteins, but only about 27-29% CPT-I activity.

5 vity to malonyl-CoA and Km for carnitine) as CPT I in skeletal muscle and liver mitochondria, respect

6 Because CPT-I and long-chain acyl-CoA synthetase appear to be as

7 In addition, both CPT I and the inner membrane enzyme, CPT II, have proved

8 5% of the total CPT activity and 50% of both CPT-I, as well as long-chain acyl-CoA synthase activity,

9 a), migrated differently on SDS gels, as did CPT I from liver and muscle mitochondria.

10 um response factor (SRF), and GATA4 enhanced CPT-I reporter gene expression 4-36-fold in CV-1 cells.

11 ng systems the flux control coefficients for CPT I over ketogenesis specifically and over total carbo

12 the individual flux control coefficients for CPT I over ketogenesis, CO2 production and total carbon

13 lusion is that flux control coefficients for CPT I over oxidative fluxes from palmitate (or palmitoyl

14 fy a new mechanism for regulation of hepatic CPT-I by phosphorylation.

15 s encoding carnitine palmitoyltransferase I (CPT I) isoforms or beta-galactosidase (control).

16 soforms of carnitine palmitoyltransferase I (CPT I), which control mitochondrial fatty acid oxidation

17 he expression of the liver isoform of CPT-I (CPT-I alpha).

18 Carnitine palmitoyltransferase I (CPT-I) catalyzes the rate-controlling step in the pathwa

19 Carnitine palmitoyltransferase I (CPT-I) catalyzes the rate-determining step in mitochondr

20 Carnitine palmitoyltransferase I (CPT-I) catalyzes the transfer of long chain fatty acyl g

21 Carnitine palmitoyltransferase I (CPT-I) is a key enzyme involved in the regulation of fat

22 entiation [carnitine palmitoyltransferase I (CPT-I) isoforms] were measured.

23 Carnitine palmitoyltransferase-I (CPT-I) catalyzes the rate-controlling step of fatty acid

24 s with the carnitine palmitoyltransferase-I (CPT-I) inhibitor reduced the liver-to-blood ratio by 64%

25 hibitor of carnitine palmitoyltransferase-I (CPT-I), a key enzyme for mitochondrial fatty acid oxidat

26 e proteins carnitine palmitoyltransferase-I (CPT-I), long-chain acyl-CoA synthetase (LCAS), and volta

27 attenuate carnitine palmitoyltransferase-I (CPT-I)-supported bioenergetics, the rate-limiting step f

28 ne region of phosphorylation was detected in CPT-I isolated from CKII-treated mitochondria.

29 n-stimulated glucose metabolism induced by L-CPT I overexpression itself, net insulin-stimulated inco

30 Whereas the signal for L-CPT I was more abundant than that for M-CPT I in RNA iso

31 However, L-CPT I overexpression failed to decrease intracellular tr

32 ver-type carnitine palmitoyltransferase I (L-CPT I) expressed in Pichia pastoris, two contiguous disc

33 iously described cDNA for rat liver CPT I (L-CPT I) gave rise to products with the same kinetic chara

34 glycogen and [(3)H]deoxyglucose uptake in L-CPT I-transduced, palmitate-treated cells were significa

35 CPT I cDNA probes revealed the presence of L-CPT I mRNA in liver and heart and its absence from skele

36 In the context of L-CPT I overexpression, palmitate preincubation produced a

37 lt reveals that the major sensitization of L-CPT I to malonyl-CoA observed upon deletion of residues

38 Two to 3-fold overexpression of L-CPT I, the endogenous isoform in L6 cells, proportionall

39 hen labeled with [3H]etomoxir, recombinant L-CPT I and putative M-CPT I, although having approximatel

40 vitro transcription and translation of the L-CPT I and putative M-CPT I cDNAs.

41 our previously described cDNA for rat liver CPT I (L-CPT I) gave rise to products with the same kine

42 M-CPT I mRNA, which was absent from liver, was readily det

43 Northern blots using L- and M-CPT I cDNA probes revealed the presence of L-CPT I mRNA

44 lude that the BAT cDNA does in fact encode M-CPT I.

45 or L-CPT I was more abundant than that for M-CPT I in RNA isolated from whole epididymal fat pad, thi

46 f a plasmid construct containing the human M-CPT I gene promoter region fused to a luciferase gene re

47 cle-type carnitine palmitoyltransferase I (M-CPT I) was characterized in primary cardiac myocytes in

48 g muscle carnitine palmitoyltransferase I (M-CPT I), an enzyme involved in mitochondrial fatty acid u

49 g muscle carnitine palmitoyltransferase I (M-CPT I), an enzyme that catalyzes the rate-limiting step

50 the muscle isoform of mitochondrial CPT I (M-CPT I).

51 ated that the hypoxia-mediated blunting of M-CPT I gene expression occurs at the transcriptional leve

52 The expression of M-CPT I in hearts of mice null for PPARalpha was approxima

53 Oleate induced steady-state levels of M-CPT I mRNA 4.5-fold.

54 nd translation of the L-CPT I and putative M-CPT I cDNAs.

55 etomoxir, recombinant L-CPT I and putative M-CPT I, although having approximately the same predicated

56 yte transfection studies demonstrated that M-CPT I promoter activity is repressed during cardiac myoc

57 r did not induce cardiac expression of the M-CPT I gene in the PPARalpha null mice.

58 The M-CPT I gene promoter fatty acid response element (FARE-1)

59 receptor (RXR) response element within the M-CPT I gene promoter, and is PPARalpha-dependent.

60 ckling rats as our model system, we measured CPT I activity and carbon flux from palmitate to ketone

61 the unique sensitivity of the outer membrane CPT I to the simple molecule, malonyl-CoA.

62 encodes the muscle isoform of mitochondrial CPT I (M-CPT I).

63 ent in the neonatal rat heart, to the muscle CPT-I which predominates in adult rat heart, takes place

64 ividually transfected into cardiac myocytes, CPT-I/luciferase reporter gene expression was significan

65 Thus this new CPT I related protein may be specialized for the metabol

66 to impact significantly upon the activity of CPT I or CPT II.

67 erties and migration profiles on SDS gels of CPT I in brown and white adipocytes, indicate that the m

68 transferases, including the liver isoform of CPT I, which is also expressed in brain; however, it dis

69 ther their site of action is at the level of CPT I (outer membrane), CPT II (inner membrane), carniti

70 PGC-1 alpha will stimulate the expression of CPT-I alpha in primary rat hepatocytes.

71 This induction of CPT-I alpha gene expression requires the thyroid hormone

72 ill enhance the thyroid hormone induction of CPT-I alpha indicating that PGC-1 alpha is a coactivator

73 ivity and rendered malonyl-CoA inhibition of CPT-I from competitive to uncompetitive.

74 ulate the expression of the liver isoform of CPT-I (CPT-I alpha).

75 gest that a switch from the liver isoform of CPT-I, prominent in the neonatal rat heart, to the muscl

76 [gamma-32P]ATP resulted in radiolabeling of CPT-I only by CKII.

77 , immunoblotting, and altered sensitivity of CPT-I activity to malonyl-CoA in the stimulated cells.

78 C-1 alpha participates in the stimulation of CPT-I alpha gene expression by thyroid hormone and sugge

79 cing the inhibitory effect of malonyl-CoA on CPT-I.

80 ter-membrane carnitine palmitoyltransferase (CPT I) over hepatic ketogenesis because its role in cont

81 A)-sensitive carnitine palmitoyltransferase (CPT-I) is localized on the outer mitochondrial membrane

82 f the muscle carnitine palmitoyltransferase (CPT-I) isoform as measured by Northern analysis, immunob

83 llular neutral lipid consistent with reduced CPT I activity and diminished FAO capacity.

84 d by a marked decrease in the liver-specific CPT-I mRNA, thus supporting the developmental fidelity o

85 2 hr), Cyt c (12-72 hr), and muscle-specific CPT-I (48-72 hr).

86 protein immunoblotting analysis showed that CPT-I, as well as the inner CPT-II, was localized in the

87 the thyroid hormone response element in the CPT-I alpha gene promoter and the first intron of the CP

88 ha gene promoter and the first intron of the CPT-I alpha gene.

89 d at 30 min by pretreatment of rats with the CPT-I inhibitor etomoxir.

90 is fundamentally different from lipids where CPT-I substrate sensitivity and availability is impaired

91 y of hepatic FOP DV to changes of HMFAO with CPT-I inhibition and hypoxia suggests potential usefulne