ライフサイエンスコーパス: palmitoyl

1 pid (dioleoylphosphatidylcholine (DOPC) or 1-palmitoyl 2-oleoyl phosphatidylcholine (POPC)), and a lo

2 oleoyl-phosphatidylglycerol (POPG); and 5% 1-palmitoyl 2-oleoyl-diphosphatidylglycerol/cardiolipin (C

3 in phospholipid bilayers consisting of: 1) 1-palmitoyl 2-oleoyl-phosphatidylcholine (POPC); 2) 1-palm

4 yl 2-oleoyl-phosphatidylcholine (POPC); 2) 1-palmitoyl 2-oleoyl-phosphatidylethanolamine (POPE); and

5 (POPE); and 3) a mixture of 75% POPE, 20% 1-palmitoyl 2-oleoyl-phosphatidylglycerol (POPG); and 5% 1

6 1-(Palmitoyl)-2-(5-keto-6-octene-dioyl) phosphatidylcholine

7 tudied at both triolein/water and triolein/1-palmitoyl, 2-oleoylphosphatidylcholine/water interfaces

8 mit transmembrane oxygen permeability of a 1-palmitoyl,2-oleoylphosphatidylcholine phospholipid bilay

9 nes, and oxidized phospholipids, including 1-palmitoyl-2-(5'-oxovaleroyl)-sn-glycero-3-phosphocholine

10 ve oxidized phospholipids (OxPLs), such as 1-palmitoyl-2-(5'-oxovaleroyl)-sn-glycero-3-phosphocholine

11 EI can form as a phospholipase product of 1-palmitoyl-2-(5,6-epoxyisoprostane E2)-sn-glycero-3-phosp

12 ecule quantitated within plaque material, [1-palmitoyl-2-(5-oxo-valeroyl)-sn-glycero-3-phosphocholine

13 The truncated tail phospholipids, 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine

14 of this homo-association upon addition of 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine

15 l)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-(9'-oxononanoyl)-sn-glycero-3-phosphocholine

16 ally encoded fluorescent PS biosensor, and 1-palmitoyl-2-(dipyrrometheneboron difluoride)undecanoyl-s

17 yl-lysophosphatidylcholine (2-AA-LPC) from 1-palmitoyl-2-[(14)C]arachidonoyl-sn-glycero-3-phosphochol

18 hatidylcholine-containing OxPL, including (1-palmitoyl-2-[9-oxo-nonanoyl] PC), representing a major p

19 Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox

20 helial cell (EC) response, the products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PA

21 rted that oxidized phospholipids (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine [Ox

22 (HAECs) with inflammatory lipids (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine [Ox

23 RATIONALE: Oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine

24 n products of the unsaturated phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphocholine.

25 eased oxidized phospholipid derivatives of 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine (

26 oxidatively modified phosphatidylcholine, 1-palmitoyl-2-azelaoyl-sn-glydecero-3-phosphocholine, effi

27 phatidylcholine (PEPC-d(31)) and 1-[(2)H(31)]palmitoyl-2-docosahexaenoylphosphatidylcholine (PDPC-d(3

28 ed the molecular organization of 1-[(2)H(31)]palmitoyl-2-eicosapentaenoylphosphatidylcholine (PEPC-d(

29 l)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC)

30 yl)-sn-glycero-3-phosphocholine (POVPC) or 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine, two o

31 aleroyl)-sn-glycero-3-phosphocholine], and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine, were

32 he structure and dynamics of human tBid in 1-palmitoyl-2-hydroxy-sn-glycero-3-[phospho-RAC-(1-glycero

33 Treatment of the purified Vo sector with 1-palmitoyl-2-hydroxy-sn-glycero-3-[phospho-rac-(1-glycero

34 yl-sn-glycero-3-phosphoglycerol (POPG) and 1-palmitoyl-2-oleoyl diacylglycerol (PODAG) stimulate the

35 used to explore behavior of capsaicin in a 1-palmitoyl-2-oleoyl phosphatidylcholine bilayer and with

36 mitoyl-2-oleoylglycerol (POP) (8.6-17.7%), 1-palmitoyl-2-oleoyl-3-stearoyl-glycerol (POS) (12.6-19.6%

37 y anionic phosphoglycerides and found that 1-palmitoyl-2-oleoyl-phosphatidic acid or 1-palmitoyl-2-ol

38 ), dioleoylphosphatidylcholine (DOPC), and 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC) bilayers.

39 .Galphai1beta1gamma2 complex embedded in a 1-palmitoyl-2-oleoyl-phosphatidylcholine bilayer, using cr

40 c LUVs in which sphingomyelin (SM) or SM + 1-palmitoyl-2-oleoyl-phosphatidylcholine was exchanged int

41 able to release ATP from ATP-loaded lipid (1-palmitoyl-2-oleoyl-phosphatidylcholine) vesicles devoid

42 1-palmitoyl-2-oleoyl-phosphatidic acid or 1-palmitoyl-2-oleoyl-phosphatidylglycerol (</=15 mol %) in

43 oleoyl-phosphatidylethanolamine (DOPE) and 1-palmitoyl-2-oleoyl-phosphatidylserine (POPS) were prepar

44 By contrast, replacement with 1-palmitoyl-2-oleoyl-phosphatidylserine stimulated C1P tra

45 sence of up to 20 mol% alpha-tocopherol in 1-palmitoyl-2-oleoyl-phosphocholine inhibits leakage of ph

46 toyl-2-oleoyl-sn-glycero-3-phosphoglycerol/1-palmitoyl-2-oleoyl-sn-glycero -3-phosphatidylcholine) ve

47 itoyl-2-oleoyl-sn-glycero-3-phosphocholine/1-palmitoyl-2-oleoyl-sn-glycero- 3-phosphoglycerol bilayer

48 roduction of the negatively charged lipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidic acid acid (

49 -glycero-3-phosphatidylglycerol (DMPG) and 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POP

50 acterial membranes containing zwitterionic 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylethanolamine

51 hosphatidylethanolamine (POPE) and anionic 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylglycerol (PO

52 yl-sn-glycero-3-phosphatidylcholine (POPC)/1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylglycerol (PO

53 negatively charged membrane lipids, POPG (1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-(1'-rac-glycerol

54 sphocholine (POPC), the negatively charged 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-(1'-rac-glycerol

55 od, to study the binding of TAT to anionic 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-1'-rac-glycerol

56 oyl-sn-glycero-3-phosphocholine (POPC) and 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-L-serine (POPS)

57 -oleoyl-sn-glycero-3-phosphocholine (POPC)/1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-l-serine (POPS))

58 toyl-2-oleoyl-sn-glycero-3-phosphocholine, 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-L-serine (POPS),

59 tion constant, K(Dapp), between Cu(2+) and 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-l-serine (POPS),

60 ho-(1'-rac-glycerol) (sodium salt)), POPS (1-palmitoyl-2-oleoyl-sn-glycero-3-phospho-l-serine (sodium

61 Two synthetic PC isomers, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (PC(16:0/

62 d bilayers via the enzymatic hydrolysis of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (PC), a z

63 g amounts of the unsaturated phospholipids 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) an

64 dependent on the surface concentration of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) an

65 MR indicates that in membranes composed of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) an

66 g a physiologically relevant phospholipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) in

67 The interaction of humic acids (HAs) with 1-palmitoyl-2-oleoyl-Sn-glycero-3-phosphocholine (POPC) la

68 phospho-1'-rac-glycerol (POPG) and neutral 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) li

69 ieved that Na(+) ions specifically bind to 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) me

70 significant influence on the structure of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) me

71 , whereas for the unsaturated phospholipid 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) th

72 yl-sn-glycero-3-phosphocholine (DPPC), and 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC)),

73 eoyl-sn-glycero-3-phosphocholine (DOPC) or 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC), b

74 iscs prepared with the zwitter-ionic lipid 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC), t

75 ined data modeling, we show that the ApoA1-1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC)-ba

76 a suggest that the size and composition of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC)-co

77 and negatively charged phosphatidylserine (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC)/1-

78 ave been made using exchangeable mimics of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine and 1,2-d

79 r dynamics simulations in a fully hydrated 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine bilayer e

80 In a 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine lipid bil

81 n and bovine rhodopsins were inserted into 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine lipid nan

82 an in vitro assay based on solid-supported 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine membranes

83 Studies with membranes containing POPC (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine) yielded

84 oyl-sn-glycero-3-phosphocholine) and POPC (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine).

85 form into lipid bilayers composed of POPC, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine, 1-palmit

86 icantly stronger than its association with 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine, in bilay

87 our barrel-stave pores in a fully hydrated 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine/1-palmito

88 ers and monolayers of Ceramide/Cholesterol/1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocyholine at varyi

89 to 20 mol %) on the lipid polymorphism of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoethanolamine (POP

90 ere, we show that infection-derived lipids 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoglycerol (POPG) a

91 r ratios of 1:5 to 1:40 for protein/lipid (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoglycerol), large

92 cyl sulfate micelles and phospholipid (1:1 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoglycerol/1-palmit

93 Interestingly, the common phospholipid 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18

94 cardiolipin, bradykinin fragment 1-8, and 1-palmitoyl-2-oleoyl-sn-glycerol.

95 dipalmitoylphosphatidylcholine (DPPC) and 1-palmitoyl-2-oleoylphosphatidylcholine (POPC) are examine

96 Abeta(1-42) monomer with the zwitterionic 1-palmitoyl-2-oleoylphosphatidylcholine (POPC) bilayer con

97 chol), N-palmitoylsphingomyelin (PSM), and 1-palmitoyl-2-oleoylphosphatidylcholine (POPC), electron p

98 ed and tested for Cl(-)/NO3(-) exchange in 1-palmitoyl-2-oleoylphosphatidylcholine/cholesterol large

99 boadenylic acid and synthetic phospholipid 1-palmitoyl-2-oleoylphosphatidylglycerol is competent to i

100 hosphatidylcholine (PC; dipalmitoyl PC and 1-palmitoyl-2-stearoyl PC (DPPC and PSPC, respectively)) s

101 n by lipoteichoic acid (TLR2/6 activator) or palmitoyl (3)-Cys-Ser-Lys(4)-OH (TLR2/1 activator) but n

102 demonstrate that pretreatment of LSECs with palmitoyl-3-cysteine-serine-lysine-4 (P3C; TLR1/2 ligand

103 one or in combination with a TLR-2 stimulus (palmitoyl-3-cysteine-serine-lysine-4 [Pam3CSK4]) or a TL

104 AD family members possess both stearoyl- and palmitoyl-ACP Delta(9) desaturase activity, including th

105 The identification of two Delta9 palmitoyl-ACP desaturases responsible for omega-7 FA bio

106 athway proceeds via Delta(9) desaturation of palmitoyl-ACP followed by elongation of the product.

107 Knockdown of the palmitoyl acyl transferase DHHC21 eliminates activation

108 13(skc4) mice with a deficiency in DHHC13, a palmitoyl-acyl transferase encoded by Zdhhc13.

109 lso called Hip14l), one of 24 genes encoding palmitoyl acyltransferase (PAT) enzymes in the mouse.

110 own as DHHC17), a single member of the broad palmitoyl acyltransferase (PAT) family, produces marked

111 4 palmitoylation, we set out to identify the palmitoyl acyltransferase (PAT) involved.

112 Our results also suggest that zDHHC3, a palmitoyl acyltransferase (PAT), catalyzes the palmitoyl

113 report that the recycling endosome-resident palmitoyl acyltransferase DHHC2 interacts with and palmi

114 The cell surface palmitoyl acyltransferase DHHC5 regulates a growing numb

115 post-translational modification mediated by palmitoyl acyltransferase enzymes, a group of Zn(2+)-fin

116 We identified DHHC-12 as the principal palmitoyl acyltransferase that palmitoylates gephyrin.

117 or flagellar targeting, including a specific palmitoyl acyltransferase, are conserved in this organis

118 Here, we identified the palmitoyl acyltransferases (Asp-His-His-Cys (DHHC) PATs)

119 e report a novel function of DHHC-containing palmitoyl acyltransferases (PATs) in mediating endotheli

120 enzymes are evolutionarily conserved protein palmitoyl acyltransferases (PATs).

121 otein targeting, is catalyzed by DHHC-family palmitoyl acyltransferases (PATs).

122 takes place at membranes and is mediated by palmitoyl acyltransferases (PATs).

123 Thus, both palmitoyl acyltransferases and acyl thioesterases displa

124 Overexpression of selected DHHC palmitoyl acyltransferases increased palmitoylation of A

125 le N-myristoyltransferase (NMT) and multiple palmitoyl acyltransferases, and these enzymes and their

126 the Asp-His-His-Cys (DHHC) motif-containing palmitoyl acyltransferases.

127 ere identified on over half of the family of palmitoyl-acyltransferases (PATs) that mediate protein p

128 ort on a novel permeation enhancer, Dimethyl palmitoyl ammonio propanesulfonate (PPS), with excellent

129 Lipid anchors composed of palmitoyl and farnesyl moieties in H-, N-, and K-Ras are

130 xtensive molecular dynamics simulations on N-palmitoyl and N-stearoyl sphingomyelin.

131 ve examined how saturated sphingomyelin (SM; palmitoyl and stearoyl SM (PSM and SSM, respectively)) a

132 Driven by the opposite preference of tH palmitoyls and farnesyl for ordered and disordered membr

133 n complex with 1-lauroylglycerol, myristoyl, palmitoyl, and stearoyl substrate analogs enable identif

134 Herein, palmitoyl ascorbate (PA) as a prooxidant for hydrogen pe

135 rocarbon lengths ranging from formyl (C1) to palmitoyl (C16) as well as negatively charged dicarboxyl

136 )-CoA inhibited synthesis of 11cROL, whereas palmitoyl (C16:0)-CoA promoted synthesis of 11cROL.

137 levels of the fatty acid transport molecule palmitoyl carnitine.

138 , and 1 long-chain acylcarnitine metabolite (palmitoyl carnitine; median change, 7.83 [-5.64 to 26.99

139 timulated IS, showing that beta-oxidation of palmitoyl-carnitine is not required for its stimulation

140 This is associated with increased palmitoyl-carnitine oxidation and increased reactive oxy

141 A nonhydrolyzable ether analog of palmitoyl-carnitine stimulated IS, showing that beta-oxi

142 ressed KO hearts, OXPHOS gene expression and palmitoyl-carnitine-supported mitochondrial function wer

143 ility of ordered domains formed by SM analog/palmitoyl ceramide (PCer) interactions.

144 ior of N-palmitoyl sphingomyelin (PSM) and N-palmitoyl ceramide (PCer) mixtures in excess water has b

145 bilayers also influenced the segregation of palmitoyl ceramide and dipalmitoylglycerol into an order

146 of saturated phospholipids, cholesterol, and palmitoyl ceramide mixtures.

147 The ordered, palmitoyl ceramide-rich phase started to form above 2 mo

148 sttranslational modification with N-terminal palmitoyl chains also seems to be quite important.

149 at Cys322 and Cys323 as well as between the palmitoyl chains and the neighboring lipids.

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

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

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

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

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

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

156 2 (At3g19260)-encoded ceramide synthase uses palmitoyl-CoA and dihydroxy LCB substrates.

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

158 8-unsaturated acyl-CoA and low activity with palmitoyl-CoA and ricinoleoyl (12-hydroxyoctadec-9-enoyl

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

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

161 Palmitoyl-CoA competes with Atg30 for Atg37 binding.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Orm proteins bind to and inhibit serine:palmitoyl-coenzyme A transferase, the first enzyme in sp

184 for both the peptide N-myristoylated-GCG and palmitoyl-coenzyme A.

185 is required for the stable formation of the palmitoyl-Erf2 intermediate, the first step of palmitoyl

186 eoyl glycerol, docosahexaenoyl ethanolamide, palmitoyl ethanolamide, and oleoyl ethanolamide.

187 is study, we conjugated GALA with lauryl and palmitoyl fatty acid tails as model hydrophobic moieties

188 olesterol depletion test, demonstrating that palmitoyl-gB limits outward cholesterol diffusion.

189 veal that one of the major species produced, palmitoyl-glycerophosphocholine, is generated by iPLA2be

190 membrane-binding fluorophore-cysteine-lysine-palmitoyl group (mCLING), which labels the plasma membra

191 (2-aminothiazol-4-yl-LIGRL-NH(2)) bound to a palmitoyl group (Pam) via polyethylene glycol (PEG) link

192 Notably the palmitoyl group at Cys322 shows considerably greater con

193 a posttranslational modification in which a palmitoyl group is added to a protein via a thioester li

194 -charged amino acids, which could facilitate palmitoyl group transfer to substrate cysteine.

195 In contrast, the palmitoyl group was mostly preserved during electron tra

196 ally stable bioisosteres of the ester-linked palmitoyl group.

197 he first step, autopalmitoylation, an enzyme-palmitoyl intermediate is formed.

198 tion, including active site thioester-linked palmitoyl intermediates.

199 observation that even in the absence of the palmitoyl, K-Ras4A can be active at the plasma membrane.

200 lated mitochondrial respiration supported by palmitoyl-l-carnitine was significantly lower in POAF pa

201 ization of individual peaks, we identified N-palmitoyl-l-leucine as a new splicing inhibitor that blo

202 olamide (4) stearoyl-L-valinolamide (5), and palmitoyl-L-valinolamide (6) were investigated in mice a

203 t PRCD is post-translationally modified by a palmitoyl lipid group at the cysteine residue linked wit

204 challenging task because of the tendency of palmitoyl loss during sample preparation and tandem MS a

205 ion-induced dissociation often led to facile palmitoyl loss, and electron capture dissociation freque

206 carbonate buffer could result in significant palmitoyl losses.

207 e modifications, such as succinyl lysine and palmitoyl lysine.

208 e was a causal link between the absence of a palmitoyl moiety and restricted collision coupling by in

209 tradecylcarbamyl chain to mimic the native N-palmitoyl moiety and various small amino acids residues

210 the sequence c16-xyL3K3-CO2H where c16 is a palmitoyl moiety and xy represents the heme binding regi

211 The enzyme transfers a palmitoyl moiety from palmitoyl-CoA to the 6-position of

212 diffusion limits imposed by the absence of a palmitoyl moiety in the C terminus of the A(2A) receptor

213 The palmitoyl moiety is then transferred to a protein substr

214 During the second step, the palmitoyl moiety is transferred to a protein substrate,

215 s known, and this gene encodes the plastidic palmitoyl-monogalactosyldiacylglycerol Delta7 desaturase

216 A conserved palmitoyl-motif is necessary and sufficient to target LI

217 in (TPLENK) were coated with the polymer - N-palmitoyl-N-monomethyl-N,N-dimethyl-N,N,N-trimethyl-6-O-

218 o N-Ras in a farnesyl-dependent, but neither palmitoyl- nor guanosine triphosphate (GTP)-dependent, f

219 sphingomyelin (PSM), cholesterol, and either palmitoyl oleoyl phosphatidyl choline or dioleoyl phosph

220 itol 4,5-bisphosphate (PIP2)) PLs containing palmitoyl-oleoyl and dimyristoyl fatty acid chains.

221 phatidylcholine/dioleoyl-phosphatidylcholine/palmitoyl-oleoyl-phos phatidylcholine/cholesterol (DSPC/

222 ng one to six peptides that were embedded in palmitoyl-oleoyl-phosphatidylcholine (POPC) lipid bilaye

223 hingomyelinase activity on lipid mixtures of palmitoyl-oleoyl-phosphatidylcholine, sphingomyelin, cer

224 llapse of dipalmitoylphosphatidylcholine and palmitoyl-oleoyl-phosphatidylglycerol monolayers.

225 was identified which confers specificity for palmitoyl- or stearoyl-CoA, respectively, in both yeast

226 from lymphocyte cell kinase (LCK: myristoyl, palmitoyl, palmitoyl), RhoA (geranylgeranyl), and K-Ras

227 the palmitoylation reaction occurs through a palmitoyl-PAT covalent intermediate that involves the co

228 ed from palmitoyl-CoA to the PAT, creating a palmitoyl:PAT intermediate and releasing reduced CoA.

229 making it the ideal fragmentation method for palmitoyl peptide analysis.

230 rge difference in hydrophobicity between the palmitoyl peptides and their unmodified counterparts cou

231 wing them to be simultaneously analyzed with palmitoyl peptides for relative quantification of palmit

232 stability of palmitoylation in several model palmitoyl peptides under different incubation and fragme

233 Triacylated palmitoyl-PG species were diminished in strains deleted

234 l (OOL), 1,2,3-trioleyl (OOO), 1,2-dioleyl-3-palmitoyl (POO), 1,2-dilinoleoyl-3-oleyl (OLL) and 1-ole

235 Using complementary palmitoyl protein purification approaches and quantitati

236 tative enzyme activity measurements of human palmitoyl protein thioesterase (PPT1) and tripeptidyl pe

237 used by a deficiency of the lysosomal enzyme palmitoyl protein thioesterase 1 (PPT1).

238 to a deficiency in the lysosomal hydrolase, palmitoyl protein thioesterase 1 (PPT1).

239 odegenerative disorder caused by the loss of palmitoyl protein thioesterase-1 (PPT1) activity.

240 rage disease (LSD) caused by a deficiency in palmitoyl protein thioesterase-1 (PPT1).

241 al storage disease caused by a deficiency in palmitoyl protein thioesterase-1 (PPT1).

242 otential role as a lipid anchor, whereas the palmitoyl-protein interaction observed for Cys322 sugges

243 CLN1 encodes a lysosomal enzyme, palmitoyl-protein thioesterase 1 (PPT1).

244 tivating mutations in the CLN1 gene encoding palmitoyl-protein thioesterase-1 (PPT1) cause INCL, thos

245 erative lysosomal storage disorder caused by palmitoyl-protein thioesterase-1 (PPT1) deficiency.

246 t is caused by inactivating mutations in the palmitoyl-protein thioesterase-1 (PPT1) gene.

247 Despite our knowledge that palmitoyl-protein thioesterase-1 (PPT1)-deficiency cause

248 utations in the gene (CLN1 or PPT1) encoding palmitoyl-protein thioesterase-1 (PPT1).

249 enerative disorder caused by a deficiency of palmitoyl-protein thioesterase-1 (PPT1).

250 amically palmitoylated proteins regulated by palmitoyl-protein thioesterases.

251 More than 150 putative palmitoyl proteins were identified in ECs using acyl-bio

252 ble variation between the sets of identified palmitoyl-proteins and so there remains some uncertainty

253 rce to help researchers prioritise candidate palmitoyl-proteins for investigation.

254 The palmitoyl-proteins identified from each method by mass s

255 t least some of the variability in published palmitoyl proteomes is due to methodological differences

256 , S-(2,3-bis(palmitoyloxy)-(2R,2S)-propyl)-N-palmitoyl-(R)-Cys-Ser-Lys(4)-OH; however, a higher pepti

257 domain (TMD) as well as via covalently bound palmitoyl residues.

258 cyte cell kinase (LCK: myristoyl, palmitoyl, palmitoyl), RhoA (geranylgeranyl), and K-Ras (farnesyl)

259 , cholesterol association with fluid dihydro-palmitoyl SM bilayers was stronger than seen with palmit

260 toyl SM bilayers was stronger than seen with palmitoyl SM under similar conditions.

261 We have compared the properties of oleoyl or palmitoyl SM with comparable dihydro-SMs, because the hy

262 SXXS-containing CD3delta segment in LPPG (1-palmitoyl-sn-glycero-3-phospho-(1'-rac-glycerol) (sodium

263 1,2-dioleoyl-sn-glycero-3-phosphocholine/1,2-palmitoyl-sn-glycero-3-phosphocholin e/cholesterol.

264 hosphocholine (PC(16:0/18:1)) and 1-oleoyl-2-palmitoyl-sn-glycero-3-phosphocholine (PC(18:1/16:0)), w

265 and 1-(4-hydroxy-3,5-dimethoxy) cinnamoyl-2-palmitoyl-sn-glycero-3-phosphocholine exhibited good ant

266 Compound 1-(4-hydroxy-3-methoxy) cinnamoyl-2-palmitoyl-sn-glycero-3-phosphocholine exhibited good ant

267 Thermal behavior of N-palmitoyl sphingomyelin (PSM) and N-palmitoyl ceramide (

268 gated in a model membrane system composed of palmitoyl sphingomyelin (PSM), cholesterol, and an unsat

269 n data are presented for ternary mixtures of palmitoyl sphingomyelin (PSM), cholesterol, and either p

270 e spontaneous radius of curvature for pure N-palmitoyl sphingomyelin bilayers is estimated to be 43-1

271 l-ceramide interaction can exist either with palmitoyl sphingomyelin or with dipalmitoyl phosphatidyl

272 lar, saturated, long-chain C16:0 ceramide (N-palmitoyl sphingosine) and nonsaturated, very long chain

273 Significant decreases in serum palmitoyl-, stearoyl-, and oleoyl-lysophosphatidylcholin

274 sis indicated significant decreases in serum palmitoyl-, stearoyl-, oleoyl-, and linoleoyl-LPC levels

275 4, the rate of hydrolysis of the active site palmitoyl thioester intermediate is increased, resulting

276 ermediate is increased, resulting in reduced palmitoyl transfer to a Ras2 substrate.

277 lmitoyl-Erf2 intermediate, the first step of palmitoyl transfer to protein substrates.

278 drial biogenesis and expression of carnitine palmitoyl transferase (CPT1a), a metabolic enzyme that c

279 due to inhibition of the activity of serine-palmitoyl transferase (SPT) and the expression of its SP

280 rst time that Chlamydomonas expresses serine palmitoyl transferase (SPT), the first enzyme in (phyto)

281 yslipidemia, we pursued inhibitors of serine palmitoyl transferase (SPT).

282 e, up-regulated gene expression of carnitine palmitoyl transferase 1, and down-regulated sterol regul

283 tty acid mitochondrial transporter carnitine palmitoyl transferase 1.

284 Because the carnitine palmitoyl transferase 1a (CPT1a) is a protein that catal

285 Levels of carbamyl-palmitoyl transferase 1a and ATP synthase subunit ATP5G1

286 sion of the fatty-acid transporter carnitine palmitoyl transferase 1c, which was recently linked to r

287 d hearts coincides with a shift of carnitine palmitoyl transferase I from muscle to increased liver i

288 Acutely increased carnitine palmitoyl transferase I in normal rodent hearts has been

289 of de novo ceramide synthesis, using the Ser palmitoyl transferase inhibitor myriocin, and heterozygo

290 la bronchiseptica PagP (PagPBB) is a lipid A palmitoyl transferase that is required for resistance to

291 of fatty acid oxidation, including carnitine palmitoyl transferase-1, and the integral transcriptiona

292 xidation due to down-regulation of carnitine palmitoyl transferase-II (CPT-II), decreased antioxidant

293 hway by one of these genes, PFA4, encoding a palmitoyl transferase.

294 te acyltransferase and an increase in serine palmitoyl transferase.

295 utation in the neuronal isoform of carnitine palmitoyl-transferase (CPT1C) gene.

296 hondrial acylcarnitine carrier and carnitine-palmitoyl-transferase 1 gene expression, two key compone

297 HSAN1 is due to dominant mutations in serine palmitoyl-transferase subunit 1 (SPT1).

298 oved by either pharmacological inhibition of palmitoyl transferases or site-directed mutagenesis.

299 itoylation is mediated by the Golgi-resident palmitoyl transferases zDHHC9/14/18 and is followed by d

300 els is controlled by two of the 23 mammalian palmitoyl-transferases, zDHHC22 and zDHHC23.

301 n by lowering the steady state amount of the palmitoyl-zDHHC9 intermediate.