ライフサイエンスコーパス: palmitoyl-CoA

1 ytic complex of human DHHC20 in complex with palmitoyl CoA.

2 ly formed by the conjugation of l-serine and palmitoyl-CoA.

3 the ninth and tenth carbons of stearoyl- or palmitoyl-CoA.

4 ] sensitized the Ca2+ pool to the actions of palmitoyl-CoA.

5 ntially to the enzyme-substrate complex PPT1-palmitoyl-CoA.

6 while minimally altering the apparent Km for palmitoyl-CoA.

7 eliminated some of the lag in activation by palmitoyl-CoA.

8 (CoA) in addition to its canonical substrate palmitoyl-CoA.

9 reduced with stearoyl-CoA when compared with palmitoyl-CoA.

10 biosynthesis: the condensation of serine and palmitoyl-CoA.

11 rd substrates butyryl-CoA, octanoyl-CoA, and palmitoyl-CoA.

12 m inappropriate condensation of alanine with palmitoyl-CoA.

13 PlsY was noncompetitively inhibited by palmitoyl-CoA.

14 ual preference for myristoyl-CoA rather than palmitoyl-CoA.

15 d shows the best activity in the presence of palmitoyl-CoA.

16 y stimulating the oxidation of mitochondrial palmitoyl-CoA.

17 r system to detect formation of luminal [14C]palmitoyl-CoA.

18 and was inhibited by, but did not hydrolyze, palmitoyl-CoA.

19 o effect on the K(m) values for carnitine or palmitoyl-CoA.

20 hen the purified proteins are incubated with palmitoyl-CoA.

21 the values obtained in the presence of free palmitoyl-CoA.

22 First, incubation of GAPDH with palmitoyl-CoA (0.5-5 microM) resulted in the dramatic co

23 d lipids, primarily oleoyl-CoA (18:1n-9) and palmitoyl-CoA (16:1n-7), the major monounsaturated fatty

24 ation of purified rabbit brain PKC with [14C]palmitoyl CoA (5 microM) resulted in the radiolabeling o

25 ically in the Arc and increases the level of palmitoyl-CoA (a major product of fatty acid biosynthesi

26 ion was immediately terminated with 2 microM palmitoyl-CoA, a blocker of the GTP-activated Ca2+-trans

27 eased by the addition of its lipid substrate palmitoyl-CoA, a treatment that results in autoacylation

28 omputational and experimental analyses, that palmitoyl CoA acts as a bivalent ligand where the intera

29 , alleviates negative regulation of L-serine:palmitoyl-CoA acyltransferase, upregulating production o

30 icrosomal acylation of glycerophosphate with palmitoyl-CoA-agarose was 80-100% of the values obtained

31 rol 3-phosphate and an immobilized substrate palmitoyl-CoA-agarose, synthesized both lyso-PA and PA.

32 ibited by S-hexadecyl-CoA, a nonhydrolyzable palmitoyl-CoA analog, demonstrating that covalent acylat

33 g acyl donor palmitate and a nonhydrolyzable palmitoyl-CoA analog.

34 deletion derivative, FadRDelta1-167, with a palmitoyl-CoA analogue, 9-p-azidophenoxy[9-3H]nonanoic a

35 results demonstrate the acylation of PKC by palmitoyl CoA and identify a novel mechanism which may f

36 In the presence of palmitoyl-CoA and CRALBP, Muller cell membranes synthesi

37 2 (At3g19260)-encoded ceramide synthase uses palmitoyl-CoA and dihydroxy LCB substrates.

38 toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapentaenoyl-CoA) than toward shor

39 ibit ceramide formation from sphingosine and palmitoyl-CoA and from sphingosine and palmitate.

40 binding as indicated by the K(m) values for palmitoyl-CoA and glycerol 3-phosphate.

41 Values of Km for palmitoyl-CoA and H-Ras are 4.3 +/- 1.2 and 0.8 +/- 0.3

42 ough purified FATP4 exhibited high levels of palmitoyl-CoA and lignoceroyl-CoA synthetase activity, e

43 Although palmitoyl-CoA and octanoyl-CoA provided reducing equival

44 -/-) mice had a reduction in activity toward palmitoyl-CoA and oleoyl-CoA (58 and 64% of wild-type, r

45 We also found that palmitoyl-CoA and oleoyl-CoA inhibited K+ flux through r

46 8-unsaturated acyl-CoA and low activity with palmitoyl-CoA and ricinoleoyl (12-hydroxyoctadec-9-enoyl

47 Both palmitoyl-CoA and S-hexadecyl-CoA increased the associat

48 Although the saturated palmitoyl-CoA and stearoyl-CoA showed a lower apparent K

49 the known negative effectors of GK activity, palmitoyl-CoA, and GK regulatory protein.

50 sis of saturated long-chain fatty acyl-CoAs (palmitoyl-CoA approximately myristoyl-CoA >> stearoyl-Co

51 conditions, DHHC enzymes can efficiently use palmitoyl CoA as a substrate for autoacylation.

52 inetics; however, the enzyme did not utilize palmitoyl-CoA as substrate.

53 ion, and substrate affinity studies revealed palmitoyl-CoA as the most likely ligand for these LTPs,

54 idylglycerol and preferred stearoyl-CoA over palmitoyl-CoA as the substrate.

55 The Kd for palmitoyl-CoA binding was about 5-fold higher despite th

56 acid residue region constitutes the putative palmitoyl-CoA-binding site in L-CPTI.

57 Another physiological modulator (inhibitor), palmitoyl-CoA, binds to GK with similar characteristics,

58 to hydrolyze an unbranched structure such as palmitoyl-CoA but not palmitoylcysteine or palmitoylated

59 n apparent k(m) value of about 54 microM for palmitoyl-CoA but with progressively decreasing Vmax val

60 begins with the condensation of L-serine and palmitoyl-CoA catalyzed by the PLP-dependent enzyme seri

61 s of bSULT1A1-pentachlorophenol complex with palmitoyl-CoA caused the return of protein fluorescence,

62 Palmitoyl-CoA competes with Atg30 for Atg37 binding.

63 metric analyses of intact GAPDH treated with palmitoyl-CoA demonstrated the covalent addition of palm

64 palmitoyltransferase 1b and 2) catalyze the palmitoyl-CoA-dependent incorporation of (14)C from [2-(

65 T I over oxidative fluxes from palmitate (or palmitoyl-CoA) differ markedly according to (a) the meta

66 pathway with specificity for myristoyl- and palmitoyl-CoA esters and/or their derivatives.

67 Second, incubation of GAPDH with [(14)C]palmitoyl-CoA followed by SDS-PAGE and autoradiography i

68 ion of a glycosylated lysosomal protein with palmitoyl-CoA hydrolase activity comparable with palmito

69 This poorly characterized palmitoyl-CoA hydrolase is inhibited by 24 HDAC inhibito

70 rvamicin IIB resulted in 2-fold increases in palmitoyl-CoA hydrolysis by thioesterase.

71 yl-CoA, which serves as the acceptor for M+4 palmitoyl-CoA in chain elongation.

72 fatty acid synthase (cgFAS I) to synthesize palmitoyl-CoA in situ from acetyl-CoA and malonyl-CoA.

73 To study the role of palmitoyl-CoA in the pancreatic acinar cell, rat pancrea

74 ivity and stimulating the oxidation of liver palmitoyl-CoA in the PPARalpha null mice.

75 An altered k(m) for palmitoyl-CoA in the presence of fatty acid or anionic p

76 tein alpha subunits react spontaneously with palmitoyl-CoA in vitro to form thioesterified proteins.

77 MgATP protected PFK-1 against inhibition by palmitoyl-CoA indicating that acyl-CoAs regulate PFK-1 a

78 nstrate that submicromolar concentrations of palmitoyl-CoA inhibit glyceraldehyde-3-phosphate dehydro

79 signaling pathway in the Arc and imply that palmitoyl-CoA, instead of malonyl-CoA, could be an effec

80 as about 5-fold higher despite the fact that palmitoyl-CoA is 50-fold more efficient in inhibiting Fa

81 Furthermore, palmitoyl-CoA levels were maintained, whereas the levels

82 and the non-hydrolyzable thioether analog of palmitoyl-CoA markedly accelerated Ca(2+)-induced mPTP o

83 in pancreatic acinar cells and suggest that palmitoyl-CoA may be needed for Ca2+-induced Ca2+ releas

84 oyltransferases (CPT-1/2) and attenuated the palmitoyl-CoA-mediated amplification of calcium-induced

85 Importantly, APT1 reversed palmitoyl-CoA-mediated inhibition of PFK-1 activity.

86 rivatives (oleoyl-CoA and, to lesser extent, palmitoyl-CoA) modulate RaaS binding to DNA and expressi

87 educed capacity to oxidize palmitate but not palmitoyl-CoA or acetyl-CoA in the absence of changes in

88 se catalyzes the condensation of serine with palmitoyl-CoA (or palmitoyl-acyl carrier protein), ceram

89 ctivity demonstrates a modest preference for palmitoyl-CoA over other fatty acyl-CoA substrates.

90 Lauroyl-CoA oxidase activity but not palmitoyl-CoA oxidase activity was increased several-fol

91 oxidation as measured by cyanide insensitive palmitoyl CoA oxidation (PCO) and caused activation of n

92 resistance, as reactive lipids (specifically palmitoyl-CoA [P-CoA]) can inhibit ADP transport and sub

93 nities and turnover rates for myristoyl-CoA, palmitoyl-CoA, palmitoleoyl-CoA, and oleoyl-CoA.

94 tion was revealed by systematic variation of palmitoyl-CoA, PAPS, and 7-hydroxycoumarin, the acceptor

95 The bioactive lipid intermediate palmitoyl CoA (PCoA) can inhibit mitochondrial ADP/ATP t

96 , we comparatively analyze beta-oxidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from

97 kDa with a stoichiometry of one molecule of palmitoyl-CoA per GAPDH tetramer.

98 Second, palmitoyl-CoA prevented the quenching of bSULT1A1 fluore

99 sis is initiated by condensation of Ser with palmitoyl-CoA producing 3-ketodihydrosphinganine (3-KDS)

100 Here we report the identification of a palmitoyl-CoA:protein S-palmitoyltransferase activity th

101 Fourth, formation of the [14C]palmitoyl CoA-radiolabeled PKC adduct could be prevented

102 Third, incubation of the [14C]palmitoyl CoA-radiolabeled PKC moiety with neutral hydro

103 Palmitoyl-CoA released Ca2+ from internal stores (EC50 =

104 rthermore, incubation of PFK-1 with [1-(14)C]palmitoyl-CoA resulted in robust acylation of the enzyme

105 r cell membranes incubated with radiolabeled palmitoyl-CoA resulted in the transfer of the labeled ac

106 In the absence of palmitoyl-CoA, retinyl ester synthesis was not observed.

107 a suggest the presence of an IP3-insensitive palmitoyl-CoA-sensitive Ca2+ store in pancreatic acinar

108 The palmitoyl-CoA-sensitive pool was distinct from, and over

109 The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxici

110 Palmitoyl-CoA serves as the palmitate donor.

111 Triacsin-C, which blocks palmitoyl-CoA synthesis, and L-cycloserine, which blocks

112 gnoceroyl-CoA synthetase activity (C24:0) to palmitoyl-CoA synthetase activity (C16:0), characteristi

113 While TgACAT1 preferentially utilizes palmitoyl-CoA, TgACAT2 has broader fatty acid specificit

114 brain PKC undergoes specific acylation with palmitoyl CoA that facilitates its interaction with memb

115 itoylation, implying that in the presence of palmitoyl-CoA, the complex is autopalmitoylated and comp

116 PT catalyses the condensation of serine with palmitoyl-CoA, the initial step in sphingolipid biogenes

117 olipid synthesis, condensation of serine and palmitoyl CoA to form the long chain base 3-ketosphingan

118 ysoPI, lysoPS, lysoPE, or lysoPG and prefers palmitoyl-CoA to oleoyl-CoA as the acyl donor.

119 mences with the condensation of L-serine and palmitoyl-CoA to produce 3-ketodihydrosphingosine (KDS).

120 Palmitoylation, the process of conjugating palmitoyl-CoA to proteins, plays an essential role in pr

121 The enzyme transfers a palmitoyl moiety from palmitoyl-CoA to the 6-position of the mannose ring link

122 Increased accessibility of palmitoyl-CoA to the mitochondrial matrix with the pore-

123 almitoylation, palmitate is transferred from palmitoyl-CoA to the PAT, creating a palmitoyl:PAT inter

124 of a fatty acyl chain, usually derived from palmitoyl-CoA, to specific cysteine residues on target p

125 hibitors of ceramide biosynthesis via serine palmitoyl-CoA transferase (L-cycloserine, myriocin or AR

126 we utilized myriocin to inhibit mouse serine palmitoyl-CoA transferase (SPT), the key enzyme for sphi

127 the endoplasmic reticulum (ER) enzyme serine palmitoyl-CoA transferase (SPT), the rate-limiting enzym

128 malonyl-CoA, a potent inhibitor of carnitine/palmitoyl-CoA transferase 1 (CPT1), releases CPT1 from i

129 NAD(P)H:Quinone Oxidoreductase 1, Carnitine Palmitoyl-CoA Transferase and mitochondrial respiratory

130 lyase (Sply) and by upregulating the serine palmitoyl-CoA transferase catalytic subunit gene lace, t

131 ecylglycidic acid, an inhibitor of carnitine-palmitoyl-CoA transferase I.

132 acyl-CoA synthetase (3-8-fold) and carnitine palmitoyl-CoA transferase IA (2-4-fold) mRNAs that were

133 ype and nasal gene expression of SPT (serine palmitoyl-CoA transferase) (i.e., the rate-limiting enzy

134 e induced (acyl-CoA oxidase, liver carnitine palmitoyl-CoA transferase, very long chain acyl-CoA synt

135 e suggests that the brain-specific carnitine:palmitoyl-CoA transferase-1 (CPT1c) may be a regulated t

136 Second, multiple extractions of [14C]palmitoyl CoA-treated PKC with butanol did not remove th

137 ase arises from condensation of alanine with palmitoyl-CoA via serine palmitoyltransferase (SPT), as

138 When palmitoyl-CoA was added to the sucrose gradient fraction

139 of protein fluorescence, and the binding of palmitoyl-CoA was highly cooperative (Hill constant of 1

140 The dependence on palmitoyl-CoA was highly cooperative with a Hill constan

141 A previous study had suggested that palmitoyl-CoA was the preferred substrate of PPT2.

142 mtGPAT knockout mitochondria did not prefer palmitoyl-CoA, was sensitive to inactivation by NEM, was

143 ximal doses of IP3 or cyclic ADP-ribose plus palmitoyl-CoA were additive.

144 were shown to be at least 95% impermeable to palmitoyl-CoA were used to demonstrate the membrane tran

145 Convex plots of apparent K(m)/V(max) versus [palmitoyl-CoA] were adequately modeled using an ordered

146 scission step and they cannot be replaced by palmitoyl CoA, which is known to promote, by itself, sci

147 eins acylate themselves upon incubation with palmitoyl-CoA, which is hypothesized to reflect a transi

148 attenuating respiration with L-carnitine and palmitoyl-CoA, while enhancing the inhibitory effect of

149 Simultaneous interaction of palmitoyl-CoA with both the nucleotide and phenol bindin

150 oylated because the specific activity of [3H]palmitoyl-CoA within cells is indeterminate.