ライフサイエンスコーパス: myristate

1 tor G-protein coupling induced by phorbol 12-myristate.

2 sistent with Ca(2+)-induced extrusion of the myristate.

3 can be regulated by selectively sequestering myristate.

4 laureate and LpxL2 catalyzes the addition of myristate.

5 iated hydroxylation of the LpxL2-transferred myristate.

6 e., middle-chain triglycerides and isopropyl myristate.

7 Ionomycin and phorbol 12-myristate 13 acetate (PMA) are used to trigger NETosis.

8 yte macrophages (MDM) obtained by phorbol 12-myristate 13 acetate (PMA) treatment.

9 and 500 pm) and the PKC activator phorbol 12-myristate 13-acetate (1 nm) each inhibited human (h) Kv7

10 VACM-1/cul5 cDNA and treated with phorbol 12-myristate 13-acetate (10 and 100 nm) to induce PKC activ

11 inhibitor, decreased 100 nm 4beta-phorbol 12-myristate 13-acetate (4beta-PMA)-induced co-immunoprecip

12 or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment developed in s

13 nase Cepsilon (PKCepsilon), while phorbol 12-myristate 13-acetate (PMA) activation of PKCepsilon driv

14 IFN-gamma ex vivo in response to phorbol 12-myristate 13-acetate (PMA) and ionomycin stimulation.

15 ssion, PP cells were treated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, which signal v

16 protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) and PKC inhibitors.

17 ate-type tumor promoters, such as phorbol 12-myristate 13-acetate (PMA) and teleocidin, increase Rac1

18 osure to the potent PKC activator phorbol 12-myristate 13-acetate (PMA) at 10 nM concentration reduce

19 Activation of PKCs by phorbol 12-myristate 13-acetate (PMA) caused a redistribution of NK

20 LNCaP prostate cancer cells with phorbol 12-myristate 13-acetate (PMA) causes a strong and sustained

21 activated platelet supernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETosis.

22 In this model, we show that phorbol 12-myristate 13-acetate (PMA) immediately activates the exp

23 nced translocation in response to phorbol 12-myristate 13-acetate (PMA) in cells.

24 Treatment with the PKC activator phorbol 12-myristate 13-acetate (PMA) increased N-cadherin cleavage

25 Phorbol 12-myristate 13-acetate (PMA) increased receptor phosphoryl

26 protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) is known to protect a subset

27 tion of PKC via the phorbol ester phorbol 12-myristate 13-acetate (PMA) mimics CXCL12-mediated desens

28 Pep mitigated toxicity induced by phorbol 12-myristate 13-acetate (PMA) more effectively than SOPD-NA

29 e effects of PKC activation using phorbol 12-myristate 13-acetate (PMA) on hERG channels expressed in

30 t treatment with a combination of phorbol 12-myristate 13-acetate (PMA) plus ionophore A23187 (Io), w

31 Phorbol 12-myristate 13-acetate (PMA) promotes skin cancer in roden

32 at cells) were more responsive to phorbol 12-myristate 13-acetate (PMA) reactivation in the absence o

33 The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated apoE secretion, an

34 ) release following activation by phorbol 12-myristate 13-acetate (PMA) than cells isolated by conven

35 th pharmacological agonists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that prolonged stim

36 In the current work we used phorbol 12-myristate 13-acetate (PMA), a well recognized agonist of

37 stimulated with thrombopoietin or phorbol 12-myristate 13-acetate (PMA), alphaIIbbeta3 became activat

38 However, following treatment with phorbol 12-myristate 13-acetate (PMA), ASP translocates to the cyto

39 timulation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), but not by ionomycin.

40 protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), enhanced TaALMT1-mediated in

41 protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), in primary HUVECs was found

42 activator, topical Ing3A, but not phorbol 12-myristate 13-acetate (PMA), inhibited the growth of subc

43 enosine-5'-triphosphate (ATP) and phorbol 12-myristate 13-acetate (PMA), results in a cation influx v

44 ase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was dow

45 treated with the PKC/D1 activator phorbol 12-myristate 13-acetate (PMA), which acts as a DAG mimetic.

46 NF-kappaB reversed both H2O2- and phorbol 12-myristate 13-acetate (PMA)-induced decrease in TRPC6 pro

47 Here we studied the role of PK in phorbol 12-myristate 13-acetate (PMA)-induced megakaryocytic differ

48 deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced MMP13 promoter activi

49 sion blocked HCMV-induced but not phorbol 12-myristate 13-acetate (PMA)-induced monocyte motility, su

50 Both basal and phorbol 12-myristate 13-acetate (PMA)-induced NADPH oxidase activit

51 Bryostatin 1 impairs phorbol 12-myristate 13-acetate (PMA)-induced tumor promotion in mi

52 ), we detected a constitutive and phorbol 12-myristate 13-acetate (PMA)-induced ubiquitination of the

53 protease profiles under naive and phorbol 12-myristate 13-acetate (PMA)-stimulated conditions are rel

54 ells when stimulated with LPS and phorbol 12-myristate 13-acetate (PMA).

55 ventional and novel PKC isoforms, phorbol 12-myristate 13-acetate (PMA).

56 ned with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA).

57 activated Rac with activation by phorbol 12-myristate 13-acetate (PMA).

58 ells with a potent PKC activator, phorbol 12-myristate 13-acetate (PMA).

59 TAPI-1, while it was promoted by phorbol 12-myristate 13-acetate (PMA).

60 ession resulted in suppression of phorbol 12-myristate 13-acetate (PMA)/ionomycin-driven activation o

61 flammatory cytokine production of phorbol 12-myristate 13-acetate (PMA)/ionomycin-stimulated human pe

62 Phorbol ester [phorbol 12-myristate 13-acetate (PMA)] treatment of human bladder c

63 d by treatment with anisomycin or phorbol 12-myristate 13-acetate (PMA/12-O-tetradecanoylphorbol-13-a

64 ion of K-Rta or by treatment with phorbol 12-myristate 13-acetate (TPA) and/or n-butyrate.

65 dependent polyclonal stimulation (phorbol 12-myristate 13-acetate [PMA] plus ionomycin).

66 nal explants, we found that phorbol ester 12-myristate 13-acetate and insulin-like growth factor 1 (I

67 Phorbol 12-myristate 13-acetate and ionomycin stimulated ectodomain

68 t is only detected following cell phorbol 12-myristate 13-acetate and ionomycin stimulation and calci

69 duced NK- and T-cell responses to phorbol 12-myristate 13-acetate and ionomycin.

70 nd ERK following stimulation with phorbol 12-myristate 13-acetate and ionomycin.

71 -negative PBLs were stimulated by phorbol 12-myristate 13-acetate and ionomycin.

72 bypassed through stimulation with phorbol 12-myristate 13-acetate and ionomycin.

73 ol also blocked ERK downstream of phorbol 12-myristate 13-acetate and the P2X(7) and epidermal growth

74 imilar results were obtained with phorbol 12-myristate 13-acetate as well as activation of the Gq-cou

75 icroorganism membrane components, phorbol 12-myristate 13-acetate as well as by amyloid fibrils, inso

76 rowth factor or the phorbol ester phorbol 12-myristate 13-acetate caused rapid phosphorylation of bet

77 ernalized in response to stimulation with 12-myristate 13-acetate co-localized primarily with Rab7- a

78 ells with concanavalin A, but not phorbol 12-myristate 13-acetate combined with ionomycin, was inhibi

79 nt with the inflammatory stimulus phorbol 12-myristate 13-acetate downregulates meprin alpha expressi

80 rane translocation in response to phorbol 12-myristate 13-acetate in LNCaP cells.

81 Phorbol 12-myristate 13-acetate increased intracellular accumulatio

82 in treatment versus activation by phorbol 12-myristate 13-acetate indicated that 2B15 undergoes PKC p

83 In contrast, phorbol 12-myristate 13-acetate induced low amplitude calcium oscil

84 tumor virus promoter activity and phorbol 12-myristate 13-acetate induction of endogenous c-Jun prote

85 ty of ADAM17, activated by either phorbol 12-myristate 13-acetate or EGF.

86 t of BMT or HSCT neutrophils with phorbol 12-myristate 13-acetate or rapamycin resulted in reduced NE

87 ILC2s were then stimulated with phorbol 12-myristate 13-acetate plus ionomycin, IL-25 plus IL-33 (I

88 2s expressed CD154 in response to phorbol 12-myristate 13-acetate plus ionomycin, IL-25/IL-33, or a m

89 t of CD8(+) T cells refractory to phorbol 12-myristate 13-acetate plus ionomycin-induced ERK1/2 phosp

90 MDA-MB-435, upon stimulation with phorbol 12-myristate 13-acetate plus ionomycin.

91 ussis toxin but were abolished by phorbol 12-myristate 13-acetate pretreatment, suggesting Gq-involve

92 delta followed by incubation with phorbol 12-myristate 13-acetate resulted in an increase in p65 Ser-

93 that acute activation of PKC with phorbol 12-myristate 13-acetate shortened carbachol-evoked calcium

94 ctivation of the PKC pathway with phorbol 12-myristate 13-acetate significantly increased [Ca(2+)]i r

95 Phorbol 12-myristate 13-acetate stimulation of both cell types reve

96 hocytes after antigen receptor or phorbol 12-myristate 13-acetate stimulation, whereas CD40 signaling

97 horylated at Ser31 in response to phorbol 12-myristate 13-acetate stimulation.

98 s of CHRF cells in the absence of phorbol 12-myristate 13-acetate stimulation.

99 on of the NADPH oxidase activator phorbol 12-myristate 13-acetate to nitric oxide-producing macrophag

100 in lipin1 deficient myoblasts by phorbol 12-myristate 13-acetate transiently activated PKC and HDAC5

101 oma cells, either with or without phorbol 12-myristate 13-acetate treatment.

102 KCdelta to the plasma membrane by phorbol 12-myristate 13-acetate was enhanced in p23-depleted LNCaP

103 nse to angiotensin II (Ang II) or phorbol 12-myristate 13-acetate was markedly reduced in perfused lu

104 activating factor, ionomycin, or phorbol 12-myristate 13-acetate was significantly enhanced, indicat

105 ases by strain, PGE2, Wnt-3a, and phorbol 12-myristate 13-acetate were attenuated by inhibition of ME

106 ein kinase C (PKC) activator PMA (phorbol 12-myristate 13-acetate) in Xenopus oocytes.

107 ase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces ceramide formation through

108 relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced PKC activity but were defe

109 e also activated in most cells by phorbol 12-myristate 13-acetate, a classical inhibitor of agrin-ind

110 tion at Ser(430) is stimulated by phorbol 12-myristate 13-acetate, an activator of classic PKC isofor

111 ctivators of shedding (ionomycin, phorbol 12-myristate 13-acetate, and 4-aminophenylmercuric acetate)

112 ologic inhibitors chlorpromazine, phorbol 12-myristate 13-acetate, and cytochalasin D caused a reduct

113 among carbachol, PKC inhibitors, phorbol 12-myristate 13-acetate, and thapsigargin to modulate [Ca(2

114 onin showed a similar response to phorbol 12-myristate 13-acetate, implicating a potential role of de

115 ogenously added diacylglycerol or phorbol 12-myristate 13-acetate, known activators of PKC, leads to

116 kappaB activation induced by TNF, phorbol 12-myristate 13-acetate, lipopolysaccharide, and cigarette

117 l-methionyl-leucyl-phenylalanine, phorbol 12-myristate 13-acetate, or grass pollen allergen in whole

118 y lipoprotein, 7-ketocholesterol, phorbol 12-myristate 13-acetate, or macrophage colony-stimulated fa

119 and a prototypical phorbol ester (phorbol 12-myristate 13-acetate, PMA) to induce changes in gene exp

120 etic carbachol, the phorbol ester phorbol 12-myristate 13-acetate, the Ca(2+) ionophore ionomycin, an

121 reatoids with (-)-Indolactam-V or phorbol 12-myristate 13-acetate, two protein kinase C activators, l

122 ctive in preventing constitutive, phorbol 12-myristate 13-acetate-, and ionomycin-stimulated shedding

123 monocyte-derived macrophages and phorbol 12-myristate 13-acetate-activated THP1 macrophages.

124 ges, human monocytic THP-1 cells, phorbol 12-myristate 13-acetate-differentiated human macrophages, a

125 KC activity but were defective in phorbol 12-myristate 13-acetate-induced actin cytoskeletal reorgani

126 ation, and provided resistance to phorbol 12-myristate 13-acetate-induced apoptosis in LNCaP cells.

127 During phorbol-12-myristate 13-acetate-induced differentiation of U937 cel

128 hesis protected skin from topical phorbol 12-myristate 13-acetate-induced inflammatory assault.

129 inhibitors, unlike carbachol- or phorbol 12-myristate 13-acetate-initiated phosphorylations, suggest

130 FHFKSGSL, in PKCdelta-transfected phorbol 12-myristate 13-acetate-stimulated cells, caused membrane b

131 O2[Symbol: see text] generated by phorbol 12-myristate 13-acetate-stimulated neutrophils.

132 ctin tail with cell extracts from phorbol 12-myristate 13-acetate-stimulated Raw 264.7 macrophages re

133 -9 transcription was decreased in phorbol 12-myristate 13-acetate-stimulated THP-1 macrophages to an

134 eta and TNF-alpha were reduced in phorbol 12-myristate 13-acetate-treated MCs developed from RasGRP4-

135 , c-fos and egr-1, in response to phorbol 12-myristate 13-acetate.

136 ethionyl-leucyl-phenylalanine, or phorbol 12-myristate 13-acetate.

137 nstream effectors ROCK and JNK by phorbol 12-myristate 13-acetate.

138 ly application of proinflammatory phorbol 12-myristate 13-acetate.

139 ndispensable for such activity by phorbol 12-myristate 13-acetate.

140 tion of IL-6 in response to 4beta phorbol 12-myristate 13-acetate.

141 urst was preserved in response to phorbol 12-myristate 13-acetate.

142 e cultured unstimulated (U), with phorbol 12-myristate 13-acetate/ionomycin (PI) or lipopolysaccharid

143 uction upon stimulation with both phorbol 12-myristate 13-acetate/ionomycin and CMV-peptide-loaded an

144 celerated T cell activation under phorbol 12-myristate 13-acetate/ionomycin treatment conditions.

145 n through CD3/CD28 stimulation or phorbol 12-myristate 13-acetate/ionomycin treatment enhances P2 pro

146 hytohaemagglutinin/interleukin-2, phorbol 12-myristate 13-acetate/ionomycin, prostratin, panobinostat

147 n of GIMAP6 led to enhancement of phorbol 12-myristate 13-acetate/ionomycin-mediated activation signa

148 132 abrogated HIV-1 production in phorbol 12-myristate 13-acetate/ionomycin-stimulated human CD4+ T c

149 ltured overnight with and without phorbol 12-myristate 13-acetate/ionomycin.

150 sely, direct activation of PKC by phorbol 12-myristate,13-acetate potentiated GluK2/GluK5.

151 nduced by common stimuli, such as phorbol-12-myristate-13-acetate (PMA) and androgens, but show diffe

152 P-1 monocytes were activated with phorbol-12-myristate-13-acetate (PMA) and differentiated into M1 ma

153 c myelogenous leukemia cells with phorbol-12-myristate-13-acetate (PMA) induces megakaryocytic differ

154 -chip and free radical release by phorbol-12-myristate-13-acetate (PMA) stimulation was demonstrated

155 can be differentiated in vitro by phorbol-12-myristate-13-acetate (PMA) treatment to produce platelet

156 uman monocytes pre-activated with phorbol-12-myristate-13-acetate (PMA) were added back into whole bl

157 UDCA and further activated using phorbol-12-myristate-13-acetate (PMA).

158 The stimulation of tissue with phorbol-12-myristate-13-acetate and ionomycin, recapitulating CAVD

159 either anti-CD3 plus anti-CD28 or phorbol-12-myristate-13-acetate and ionomycin.

160 n, whereas activation of PKC with phorbol-12-myristate-13-acetate potentiated the Ci-VSP-induced decl

161 contrast, the phorbol ester PMA (phorbol-12-myristate-13-acetate, a pharmacological mimic of the dow

162 Calpha-activator and TJ-disruptor phorbol-12-myristate-13-acetate, similarly reduced TJ integrity, wh

163 tory processes in THP-1 cells and phorbol-12-myristate-13-acetate-differentiated macrophages in respo

164 d B-cell lines partially restored phorbol-12-myristate-13-acetate-induced cell death.

165 In addition, LeTx repressed phorbol-12-myristate-13-acetate-induced mouse mammary tumor virus p

166 Phorbol-12-myristate-13-acetate/ionomycin-induced MAPK signaling wa

167 osine antagonist, 10 micromol/L) and phorbol myristate acetate (phorbol ester, 10 micromol/L), and in

168 n improved biofuel cell operating on phorbol myristate acetate (PMA) activated THP-1 human monocytic

169 produce large amounts of CXCL8 after phorbol myristate acetate (PMA) or cytokine treatment.

170 147 to interfere with the ability of phorbol myristate acetate (PMA) to promote FLNB-mediated cytopla

171 while activation of NF-kappaB2 with phorbol myristate acetate (PMA) upregulated fermentative glycoly

172 ed within the microfluidic device to phorbol myristate acetate (PMA), a known promoter of oxidative b

173 ck neuregulin release in response to phorbol myristate acetate (PMA), suggesting that other proteinas

174 ime dependently downregulated during phorbol myristate acetate (PMA)-induced monocyte-to-macrophage d

175 ufficient for converting Nox4 into a phorbol myristate acetate (PMA)-inducible phenotype, while Nox2-

176 nd controls and then stimulated with phorbol myristate acetate (PMA).

177 Using phorbol myristate acetate (PMA)/ionomycin and anti-CD3 activatio

178 PKC activation by phorbol ester (phorbol myristate acetate [PMA]) reduced insulin-induced p-Tyr-I

179 , following stimulation ex vivo with phorbol myristate acetate and ionomycin for 5 hours.

180 However, in response to phorbol myristate acetate and ionomycin, duodenal LPLs from etha

181 kine staining after stimulation with phorbol myristate acetate and ionomycin, we examined gamma inter

182 After stimulation of MM6 cells by phorbol myristate acetate and ionophore A23187, a perinuclear ri

183 d encoding FSTL1 and stimulated with phorbol myristate acetate and lipopolysaccharide.

184 Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylation and t

185 Stimulation by phorbol myristate acetate enhanced WT channel gating, and this e

186 TLC and phorbol myristate acetate increased cytosolic pMARCKS and decrea

187 Phorbol myristate acetate induced TTF1 protein degradation in th

188 utant T29A/S97A failed to respond to phorbol myristate acetate or GF109203X.

189 eous inflammation induced by topical phorbol myristate acetate or imiquimod, reduced the inflammation

190 ta), hyaluronan oligosaccharides, or phorbol myristate acetate or were passaged and subcultured in mo

191 phil extracellular traps (NETs) with phorbol myristate acetate released high concentrations of PZP in

192 d to differentiate by treatment with phorbol myristate acetate revealed three major proteins of ~25,

193 decreased aggregation potential upon phorbol myristate acetate stimulation, decreased platelet degran

194 After antigen-receptor ligation or phorbol myristate acetate stimulation, FcmuR expression was up-r

195 g protease inhibitors, ionomycin and phorbol myristate acetate stimulation, small interfering RNA kno

196 Phorbol myristate acetate, a known stimulator of NF-kappaB, incr

197 their cognate growth factors or with phorbol myristate acetate, activation of mTORC1 required an Akt-

198 ronan oligosaccharides, IL-1beta, or phorbol myristate acetate, CD44 fragmentation was enhanced.

199 vating factor, calcium ionophore, or phorbol myristate acetate, develops within 120 minutes in a redu

200 ivation of protein kinase C (PKC) by phorbol myristate acetate, Gq/11-coupled GPCR, or epidermal grow

201 After cells were stimulated with phorbol myristate acetate, the amount of phosphorylated mitogen-

202 he 7,12-dimethyl-benzanthracene plus phorbol myristate acetate-induced skin chemical carcinogenesis m

203 After stimulation with phorbol myristate acetate-ionomycin, high gamma interferon and l

204 l benzanthracene when applied before phorbol myristate acetate.

205 ha, tumor necrosis factor-alpha, and phorbol myristate acetate.

206 than NETs induced by bacteria or by phorbol-myristate acetate.

207 sion of AP1LUC reporter induction by phorbol myristate acetate.

208 Following ex vivo stimulation with phorbol myristate acetate/ionomycin, PSC patients showed signifi

209 including anti-CD3/CD28 antibodies, phorbol myristate acetate/phytohemagglutinin, and prostratin, as

210 Phorbol-myristate-acetate-induced formation of neutrophil extrac

211 protein (MAP) kinases in response to phorbol myristate acid (PMA), H(2)O(2), UV, and anisomycin stimu

212 free plasma (PFP) or in buffer using phorbol myristate actetate or calcium ionophore.

213 rol, and monoacylglycerol with palmitate and myristate acyl chains.

214 their fatty-acylated N-termini, containing N-myristate and either a polybasic cluster (in Src) or pal

215 th this, ATFs were able to utilize exogenous myristate and form beta-oxidation intermediates, suggest

216 stimulated with lipopolysaccharide, phorbol myristate and ionomycin (agonists).

217 -the addition of fatty acid moieties such as myristate and palmitate to proteins--is essential for th

218 cted HeLa cell cultures elongated laurate to myristate and palmitate.

219 The location of the buried myristate and structure of Ca2+-free Ncs1 are quite diff

220 ur results imply dual differential roles for myristate and the amino acids at the N terminus of L1.

221 an HIV-1 Gag protein, lacking the N-terminal myristate and the C-terminal p6 (DP6-Gag), could bind to

222 We hypothesized that the myristate and the conserved residues at the N terminus o

223 ons are all dependent on both the N-terminal myristate and the presence of the PPII helix.

224 oemulsion formulations composed of isopropyl myristate and Tween 80 encapsulating a fluorescent dye w

225 ggregation pheromones methyl laurate, methyl myristate, and methyl palmitate, attracting healthy flie

226 roduced odorants methyl laurate (ML), methyl myristate, and methyl palmitate.

227 aturated fatty acids (SFAs) such as laurate, myristate, and palmitate increased cellular triglyceride

228 es three regulatory components, PI(4,5)P(2), myristate, and RNA, to ensure plasma membrane specificit

229 Functional differences between myristate- and palmitate-derived sphingolipids were obse

230 NMR resonances of myristate attached to GCAP1 are exchange-broadened, upfi

231 her wildtype PSI1 or PSI1 G2A with a mutated myristate attachment site in the psi1-1 background sugge

232 nverting the glycine at the proposed site of myristate attachment to alanine (G2A).

233 ite in the psi1-1 background suggesting that myristate attachment was not essential for PSI1 function

234 n mutated critical residues in the predicted myristate binding pocket of c-Src.

235 tructures can effectively target the Bcr-Abl myristate binding site and provides new leads for develo

236 f ligands that are capable of binding to the myristate binding site and rationalize the findings base

237 ost & Microbe, Zhu et al. (2017) report on a myristate binding site within the cellular protein heme

238 kinase but was also bound to the regulatory myristate binding site.

239 ular Bcr-Abl kinase activity that target the myristate binding site.

240 Inhibiting HO-2 expression, or blocking myristate binding with a heme analog, led to marked incr

241 ydrophobic beta sandwich to be essential for myristate binding.

242 al myristate for binding to the c-Abl kinase myristate-binding pocket and that the exposed myristoyl

243 hat of myristoylated c-Abl by binding to the myristate-binding pocket in the C-lobe of the kinase dom

244 Thus, HO-2 is a cellular myristate-binding protein that negatively regulates both

245 be achieved with inhibitors that bind to the myristate-binding site and that combining allosteric and

246 pectrometry, we show that GNF-2 binds to the myristate-binding site of Abl, leading to changes in the

247 In the c-Abl tyrosine kinase, myristate binds within a hydrophobic pocket at the base

248 Furthermore, treatment with the SFA myristate, but not palmitate, induced hypertrophy and au

249 d an external supply of certain fatty acids, myristates (C:14).

250 ty against caprylate (C8), laurate (C12) and myristate (C14).

251 cal hexa-acylated lipid A species, bearing a myristate (C14:0) and 3-hydroxylaurate (3-OH C12:0) at t

252 imurium, removal of the secondary laurate or myristate chain in lipid A results in bacterial attenuat

253 While Salmonella msbB mutants lacking the myristate chain in lipid A were investigated widely as a

254 ntaacylated lipid A lacking the secondary 3'-myristate chain, causes extensive 4'-dephosphorylation.

255 a secondary laurate chain or a laurate and a myristate chain, respectively.

256 dicted from a structural model of the UNC119-myristate complex, we identified highly conserved phenyl

257 ane binding is likely through suppression of myristate-dependent hydrophobic interaction because muta

258 )P2 interaction, rather than indirectly by a myristate-dependent mechanism.

259 he present study sought to determine whether myristate-derived d16 sphingolipids are represented amon

260 This segment not only presents the myristate during c-Abl inhibition but may also trigger p

261 tes 2' acyl chain variation, and that the MA myristate enhances membrane binding efficiency but not s

262 NMR resonances of the attached myristate exhibit Ca(2+)-dependent chemical shifts and N

263 nduces a conformational change that triggers myristate exposure, and that the CaM-binding domain of M

264 provide evidence for a PI(4,5)P2 trigger of myristate exposure.

265 that GNF-2 competes with the NH(2)-terminal myristate for binding to the c-Abl kinase myristate-bind

266 cleaves thioesters) completely removed [(3)H]myristate from hSlo1, suggesting the involvement of a hy

267 s this orientation without the presence of a myristate group, driven only by electrostatic interactio

268 Finally, the myristate group, which is mandatory for anchoring the co

269 n the MA protein, triggering exposure of the myristate group.

270 to an understanding of the potential role of myristate in AM ecology.

271 e association of Src kinases, but a role for myristate in regulating other aspects of Src biology has

272 s of Abl tyrosine kinase: one that carries a myristate in the N terminus and the other that is defici

273 s and SPTLC3 did not appear to contribute to myristate-induced autophagy, whereas only d16 sphingolip

274 affinity strongly by facilitating efficient myristate insertion and PI(4,5)P2 binding.

275 npolar solvents, n-heptane (n-Hp), isopropyl myristate (IPM), and methyl laurate (ML) were used.

276 Myristate is a novel potential substrate for sphingoid b

277 nclude that the protein environment near the myristate is not influenced by Mg(2+) or Ca(2+) binding

278 ted into mature virions, suggesting that the myristate is not required for the association of L1 with

279 The C14 end of the myristate is surrounded by residues in the protein core,

280 modification of proteins with the fatty acid myristate, is critical for membrane targeting and cell s

281 Lack of the myristate lipid tail disrupted the lysosomal translocati

282 intramolecular binding of an NH(2)-terminal myristate lipid.

283 In addition, myristate may open up several avenues from a more applie

284 de synthase 5 in cardiomyocyte autophagy and myristate-mediated hypertrophy.

285 viral fusion peptide, whereby the N-terminal myristate mediates initial, reversible peptide-membrane

286 Our findings suggest that the myristate moiety is cryptically disposed in the prefusio

287 heme oxygenase (HO-2) specifically binds the myristate moiety of Gag.

288 also triggers exposure of an amino-terminal myristate moiety, which anchors Gag to the membrane.

289 lated pentaacylated lipid A with a secondary myristate moiety.

290 might integrate three regulatory components, myristate, phosphatidylinositol-(4,5)-bisphosphate, and

291 allosteric inhibitors which bind within the myristate pocket of Abl.

292 Myocardial sphingoid base synthesis utilizes myristate; these sphingolipids are functionally non-redu

293 TT: the addition of the 14 carbon fatty acid myristate to a glycine residue exposed on a caspase-3-cl

294 h catalyses the attachment of the fatty acid myristate to protein substrates (N-myristoylation).

295 oyltransferase (NMT) attaches the fatty acid myristate to the N-terminal glycine of proteins to sort

296 hment of the 14-carbon saturated fatty acid, myristate, to the amino-terminal glycine residue of a su

297 ristate was expected since LpxO modifies the myristate transferred by LpxL2 to the lipid A.

298 A crystal structure revealed that HO-2 binds myristate via a hydrophobic channel adjacent to the heme

299 dduct, elicited by adding ca. 3 mol equiv of myristate, was comparable to that observed in clinical A

300 sisting of bovine serum albumin, Co(2+), and myristate were studied by isothermal titration calorimet