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1 biosynthesis: the condensation of serine and palmitoyl-CoA.
2 ] sensitized the Ca2+ pool to the actions of palmitoyl-CoA.
3 ntially to the enzyme-substrate complex PPT1-palmitoyl-CoA.
4 while minimally altering the apparent Km for palmitoyl-CoA.
5 eliminated some of the lag in activation by palmitoyl-CoA.
6 (CoA) in addition to its canonical substrate palmitoyl-CoA.
7 reduced with stearoyl-CoA when compared with palmitoyl-CoA.
8 rd substrates butyryl-CoA, octanoyl-CoA, and palmitoyl-CoA.
9 m inappropriate condensation of alanine with palmitoyl-CoA.
10 PlsY was noncompetitively inhibited by palmitoyl-CoA.
11 ual preference for myristoyl-CoA rather than palmitoyl-CoA.
12 d shows the best activity in the presence of palmitoyl-CoA.
13 y stimulating the oxidation of mitochondrial palmitoyl-CoA.
14 r system to detect formation of luminal [14C]palmitoyl-CoA.
15 and was inhibited by, but did not hydrolyze, palmitoyl-CoA.
16 the ninth and tenth carbons of stearoyl- or palmitoyl-CoA.
17 o effect on the K(m) values for carnitine or palmitoyl-CoA.
18 hen the purified proteins are incubated with palmitoyl-CoA.
19 the values obtained in the presence of free palmitoyl-CoA.
21 d lipids, primarily oleoyl-CoA (18:1n-9) and palmitoyl-CoA (16:1n-7), the major monounsaturated fatty
22 ation of purified rabbit brain PKC with [14C]palmitoyl CoA (5 microM) resulted in the radiolabeling o
23 ically in the Arc and increases the level of palmitoyl-CoA (a major product of fatty acid biosynthesi
24 ion was immediately terminated with 2 microM palmitoyl-CoA, a blocker of the GTP-activated Ca2+-trans
25 eased by the addition of its lipid substrate palmitoyl-CoA, a treatment that results in autoacylation
26 , alleviates negative regulation of L-serine:palmitoyl-CoA acyltransferase, upregulating production o
27 icrosomal acylation of glycerophosphate with palmitoyl-CoA-agarose was 80-100% of the values obtained
28 rol 3-phosphate and an immobilized substrate palmitoyl-CoA-agarose, synthesized both lyso-PA and PA.
29 ibited by S-hexadecyl-CoA, a nonhydrolyzable palmitoyl-CoA analog, demonstrating that covalent acylat
31 deletion derivative, FadRDelta1-167, with a palmitoyl-CoA analogue, 9-p-azidophenoxy[9-3H]nonanoic a
32 results demonstrate the acylation of PKC by palmitoyl CoA and identify a novel mechanism which may f
35 toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapentaenoyl-CoA) than toward shor
39 ough purified FATP4 exhibited high levels of palmitoyl-CoA and lignoceroyl-CoA synthetase activity, e
41 -/-) mice had a reduction in activity toward palmitoyl-CoA and oleoyl-CoA (58 and 64% of wild-type, r
43 8-unsaturated acyl-CoA and low activity with palmitoyl-CoA and ricinoleoyl (12-hydroxyoctadec-9-enoyl
47 sis of saturated long-chain fatty acyl-CoAs (palmitoyl-CoA approximately myristoyl-CoA >> stearoyl-Co
49 ion, and substrate affinity studies revealed palmitoyl-CoA as the most likely ligand for these LTPs,
52 Another physiological modulator (inhibitor), palmitoyl-CoA, binds to GK with similar characteristics,
53 to hydrolyze an unbranched structure such as palmitoyl-CoA but not palmitoylcysteine or palmitoylated
54 n apparent k(m) value of about 54 microM for palmitoyl-CoA but with progressively decreasing Vmax val
55 begins with the condensation of L-serine and palmitoyl-CoA catalyzed by the PLP-dependent enzyme seri
56 s of bSULT1A1-pentachlorophenol complex with palmitoyl-CoA caused the return of protein fluorescence,
58 metric analyses of intact GAPDH treated with palmitoyl-CoA demonstrated the covalent addition of palm
59 palmitoyltransferase 1b and 2) catalyze the palmitoyl-CoA-dependent incorporation of (14)C from [2-(
60 T I over oxidative fluxes from palmitate (or palmitoyl-CoA) differ markedly according to (a) the meta
63 ion of a glycosylated lysosomal protein with palmitoyl-CoA hydrolase activity comparable with palmito
69 tein alpha subunits react spontaneously with palmitoyl-CoA in vitro to form thioesterified proteins.
70 MgATP protected PFK-1 against inhibition by palmitoyl-CoA indicating that acyl-CoAs regulate PFK-1 a
71 nstrate that submicromolar concentrations of palmitoyl-CoA inhibit glyceraldehyde-3-phosphate dehydro
72 signaling pathway in the Arc and imply that palmitoyl-CoA, instead of malonyl-CoA, could be an effec
73 as about 5-fold higher despite the fact that palmitoyl-CoA is 50-fold more efficient in inhibiting Fa
75 and the non-hydrolyzable thioether analog of palmitoyl-CoA markedly accelerated Ca(2+)-induced mPTP o
76 in pancreatic acinar cells and suggest that palmitoyl-CoA may be needed for Ca2+-induced Ca2+ releas
77 oyltransferases (CPT-1/2) and attenuated the palmitoyl-CoA-mediated amplification of calcium-induced
79 rivatives (oleoyl-CoA and, to lesser extent, palmitoyl-CoA) modulate RaaS binding to DNA and expressi
80 educed capacity to oxidize palmitate but not palmitoyl-CoA or acetyl-CoA in the absence of changes in
83 oxidation as measured by cyanide insensitive palmitoyl CoA oxidation (PCO) and caused activation of n
84 resistance, as reactive lipids (specifically palmitoyl-CoA [P-CoA]) can inhibit ADP transport and sub
85 tion was revealed by systematic variation of palmitoyl-CoA, PAPS, and 7-hydroxycoumarin, the acceptor
86 , we comparatively analyze beta-oxidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from
89 sis is initiated by condensation of Ser with palmitoyl-CoA producing 3-ketodihydrosphinganine (3-KDS)
94 rthermore, incubation of PFK-1 with [1-(14)C]palmitoyl-CoA resulted in robust acylation of the enzyme
95 r cell membranes incubated with radiolabeled palmitoyl-CoA resulted in the transfer of the labeled ac
97 a suggest the presence of an IP3-insensitive palmitoyl-CoA-sensitive Ca2+ store in pancreatic acinar
102 gnoceroyl-CoA synthetase activity (C24:0) to palmitoyl-CoA synthetase activity (C16:0), characteristi
104 brain PKC undergoes specific acylation with palmitoyl CoA that facilitates its interaction with memb
105 itoylation, implying that in the presence of palmitoyl-CoA, the complex is autopalmitoylated and comp
106 PT catalyses the condensation of serine with palmitoyl-CoA, the initial step in sphingolipid biogenes
107 olipid synthesis, condensation of serine and palmitoyl CoA to form the long chain base 3-ketosphingan
109 mences with the condensation of L-serine and palmitoyl-CoA to produce 3-ketodihydrosphingosine (KDS).
110 The enzyme transfers a palmitoyl moiety from palmitoyl-CoA to the 6-position of the mannose ring link
112 almitoylation, palmitate is transferred from palmitoyl-CoA to the PAT, creating a palmitoyl:PAT inter
113 we utilized myriocin to inhibit mouse serine palmitoyl-CoA transferase (SPT), the key enzyme for sphi
114 the endoplasmic reticulum (ER) enzyme serine palmitoyl-CoA transferase (SPT), the rate-limiting enzym
115 malonyl-CoA, a potent inhibitor of carnitine/palmitoyl-CoA transferase 1 (CPT1), releases CPT1 from i
116 lyase (Sply) and by upregulating the serine palmitoyl-CoA transferase catalytic subunit gene lace, t
118 acyl-CoA synthetase (3-8-fold) and carnitine palmitoyl-CoA transferase IA (2-4-fold) mRNAs that were
119 e induced (acyl-CoA oxidase, liver carnitine palmitoyl-CoA transferase, very long chain acyl-CoA synt
120 e suggests that the brain-specific carnitine:palmitoyl-CoA transferase-1 (CPT1c) may be a regulated t
122 ase arises from condensation of alanine with palmitoyl-CoA via serine palmitoyltransferase (SPT), as
124 of protein fluorescence, and the binding of palmitoyl-CoA was highly cooperative (Hill constant of 1
127 mtGPAT knockout mitochondria did not prefer palmitoyl-CoA, was sensitive to inactivation by NEM, was
129 were shown to be at least 95% impermeable to palmitoyl-CoA were used to demonstrate the membrane tran
130 Convex plots of apparent K(m)/V(max) versus [palmitoyl-CoA] were adequately modeled using an ordered
131 scission step and they cannot be replaced by palmitoyl CoA, which is known to promote, by itself, sci
132 eins acylate themselves upon incubation with palmitoyl-CoA, which is hypothesized to reflect a transi
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