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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.
20              First, incubation of GAPDH with palmitoyl-CoA (0.5-5 microM) resulted in the dramatic co
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
30 g acyl donor palmitate and a nonhydrolyzable palmitoyl-CoA analog.
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
33                           In the presence of palmitoyl-CoA and CRALBP, Muller cell membranes synthesi
34 2 (At3g19260)-encoded ceramide synthase uses palmitoyl-CoA and dihydroxy LCB substrates.
35 toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapentaenoyl-CoA) than toward shor
36 ibit ceramide formation from sphingosine and palmitoyl-CoA and from sphingosine and palmitate.
37  binding as indicated by the K(m) values for palmitoyl-CoA and glycerol 3-phosphate.
38                             Values of Km for palmitoyl-CoA and H-Ras are 4.3 +/- 1.2 and 0.8 +/- 0.3
39 ough purified FATP4 exhibited high levels of palmitoyl-CoA and lignoceroyl-CoA synthetase activity, e
40                                     Although palmitoyl-CoA and octanoyl-CoA provided reducing equival
41 -/-) mice had a reduction in activity toward palmitoyl-CoA and oleoyl-CoA (58 and 64% of wild-type, r
42                           We also found that palmitoyl-CoA and oleoyl-CoA inhibited K+ flux through r
43 8-unsaturated acyl-CoA and low activity with palmitoyl-CoA and ricinoleoyl (12-hydroxyoctadec-9-enoyl
44                                         Both palmitoyl-CoA and S-hexadecyl-CoA increased the associat
45                       Although the saturated palmitoyl-CoA and stearoyl-CoA showed a lower apparent K
46 the known negative effectors of GK activity, palmitoyl-CoA, and GK regulatory protein.
47 sis of saturated long-chain fatty acyl-CoAs (palmitoyl-CoA approximately myristoyl-CoA >> stearoyl-Co
48 inetics; however, the enzyme did not utilize palmitoyl-CoA as substrate.
49 ion, and substrate affinity studies revealed palmitoyl-CoA as the most likely ligand for these LTPs,
50                                   The Kd for palmitoyl-CoA binding was about 5-fold higher despite th
51 acid residue region constitutes the putative palmitoyl-CoA-binding site in L-CPTI.
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,
57                                              Palmitoyl-CoA competes with Atg30 for Atg37 binding.
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
61  pathway with specificity for myristoyl- and palmitoyl-CoA esters and/or their derivatives.
62      Second, incubation of GAPDH with [(14)C]palmitoyl-CoA followed by SDS-PAGE and autoradiography i
63 ion of a glycosylated lysosomal protein with palmitoyl-CoA hydrolase activity comparable with palmito
64 rvamicin IIB resulted in 2-fold increases in palmitoyl-CoA hydrolysis by thioesterase.
65 yl-CoA, which serves as the acceptor for M+4 palmitoyl-CoA in chain elongation.
66                         To study the role of palmitoyl-CoA in the pancreatic acinar cell, rat pancrea
67 ivity and stimulating the oxidation of liver palmitoyl-CoA in the PPARalpha null mice.
68                          An altered k(m) for palmitoyl-CoA in the presence of fatty acid or anionic p
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
74                                 Furthermore, palmitoyl-CoA levels were maintained, whereas the levels
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
78                   Importantly, APT1 reversed palmitoyl-CoA-mediated inhibition of PFK-1 activity.
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
81 ctivity demonstrates a modest preference for palmitoyl-CoA over other fatty acyl-CoA substrates.
82         Lauroyl-CoA oxidase activity but not palmitoyl-CoA oxidase activity was increased several-fol
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
87  kDa with a stoichiometry of one molecule of palmitoyl-CoA per GAPDH tetramer.
88                                      Second, palmitoyl-CoA prevented the quenching of bSULT1A1 fluore
89 sis is initiated by condensation of Ser with palmitoyl-CoA producing 3-ketodihydrosphinganine (3-KDS)
90       Here we report the identification of a palmitoyl-CoA:protein S-palmitoyltransferase activity th
91                Fourth, formation of the [14C]palmitoyl CoA-radiolabeled PKC adduct could be prevented
92                Third, incubation of the [14C]palmitoyl CoA-radiolabeled PKC moiety with neutral hydro
93                                              Palmitoyl-CoA released Ca2+ from internal stores (EC50 =
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
96                            In the absence of palmitoyl-CoA, retinyl ester synthesis was not observed.
97 a suggest the presence of an IP3-insensitive palmitoyl-CoA-sensitive Ca2+ store in pancreatic acinar
98                                          The palmitoyl-CoA-sensitive pool was distinct from, and over
99                       The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxici
100                                              Palmitoyl-CoA serves as the palmitate donor.
101                     Triacsin-C, which blocks palmitoyl-CoA synthesis, and L-cycloserine, which blocks
102 gnoceroyl-CoA synthetase activity (C24:0) to palmitoyl-CoA synthetase activity (C16:0), characteristi
103        While TgACAT1 preferentially utilizes palmitoyl-CoA, TgACAT2 has broader fatty acid specificit
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
108 ysoPI, lysoPS, lysoPE, or lysoPG and prefers palmitoyl-CoA to oleoyl-CoA as the acyl donor.
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
111                   Increased accessibility of palmitoyl-CoA to the mitochondrial matrix with the pore-
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
117 ecylglycidic acid, an inhibitor of carnitine-palmitoyl-CoA transferase I.
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
121         Second, multiple extractions of [14C]palmitoyl CoA-treated PKC with butanol did not remove th
122 ase arises from condensation of alanine with palmitoyl-CoA via serine palmitoyltransferase (SPT), as
123                                         When palmitoyl-CoA was added to the sucrose gradient fraction
124  of protein fluorescence, and the binding of palmitoyl-CoA was highly cooperative (Hill constant of 1
125                            The dependence on palmitoyl-CoA was highly cooperative with a Hill constan
126          A previous study had suggested that palmitoyl-CoA was the preferred substrate of PPT2.
127  mtGPAT knockout mitochondria did not prefer palmitoyl-CoA, was sensitive to inactivation by NEM, was
128 ximal doses of IP3 or cyclic ADP-ribose plus palmitoyl-CoA were additive.
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
133                  Simultaneous interaction of palmitoyl-CoA with both the nucleotide and phenol bindin
134 oylated because the specific activity of [3H]palmitoyl-CoA within cells is indeterminate.

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