ライフサイエンスコーパス: myristate

1 laureate and LpxL2 catalyzes the addition of myristate.

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

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

4 iated hydroxylation of the LpxL2-transferred myristate.

5 omer disruption was reversible by removal of myristate.

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

7 can be regulated by selectively sequestering myristate.

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 Using phorbol 12-myristate 13-acetate (PMA) as a tool to dissect PKC resp

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

20 Although phorbol 12-myristate 13-acetate (PMA) caused limited translocation

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

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

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

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

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

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

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

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

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

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

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

32 , in combination with IL-1beta or phorbol 12-myristate 13-acetate (PMA) treatment, results in a marke

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

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

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

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

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

38 responses to the tumor promoter, phorbol-12-myristate 13-acetate (PMA), in cells with varying TSPO l

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

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

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

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

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

44 -type PKD3 in LNCaP cells blocked phorbol 12-myristate 13-acetate (PMA)-induced apoptosis in associat

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

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

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

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

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

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

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

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

53 phosphorylation in H(2)O(2)- and phorbol 12-myristate 13-acetate (PMA)-treated cardiomyocytes.

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 tigated cis elements regulated by phorbol 12-myristate 13-acetate (PMA).

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

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

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

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

72 duced NK- and T-cell responses to 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 (wild-type PKCdelta stimulated by phorbol 12-myristate 13-acetate or constitutively active PKCdelta)

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

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

88 ifferentiation of thymocytes with phorbol 12-myristate 13-acetate plus ionomycin results in transcrip

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

90 2s expressed CD154 in response to phorbol 12-myristate 13-acetate plus ionomycin, IL-25/IL-33, or a m

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

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

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

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

95 PKD activation by treatment with phorbol 12-myristate 13-acetate results in phosphorylation of two s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 cytosis by the phorbol ester PMA (phorbol 12-myristate 13-acetate).

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

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

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

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

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

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

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

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

119 ch as cigarette smoke condensate, phorbol 12-myristate 13-acetate, okadaic acid, hydrogen peroxide, l

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

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

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

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

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

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

126 KD1-Ser744 phosphorylation in the phorbol 12-myristate 13-acetate-dependent mechanism that increases

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

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

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

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

131 yed apoptosis and cell death upon phorbol 12-myristate 13-acetate-induced Mk differentiation.

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

133 32, Go6983, and Rottlerin, by the phorbol 12-myristate 13-acetate-mediated and time-dependent loss of

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

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

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

137 -9 transcription was decreased in phorbol 12-myristate 13-acetate-stimulated THP-1 macrophages to an

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

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

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

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

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

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

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

145 f toxic contact eczema induced by phorbol 12-myristate 13-acetate.

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

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

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

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

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

151 132 abrogated HIV-1 production in phorbol 12-myristate 13-acetate/ionomycin-stimulated human CD4+ T c

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

153 muscarinic M1 receptor agonist or phorbol-12-myristate, 13-acetate (PMA).

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

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

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

157 t of cells with the PKC activator phorbol-12-myristate-13-acetate (PMA) potently stimulated phosphory

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

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

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

161 In contrast, phorbol 12-myristate-13-acetate (TPA) -induced cleavage of HB-EGF,

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

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

164 ure of cells to 3 or 100 nM 4beta-phorbol 12-myristate-13-acetate induced co-immunoprecipitation of d

165 impaired response was evident after phorbol myristate-13-acetate stimulation.

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

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

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

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

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

171 However, TbHK1 is inhibited by myristate, a critical fatty acid in T. brucei biology.

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

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

174 Topical application of phorbol myristate acetate (PMA) elicits intense local inflammati

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

176 147 to interfere with the ability of phorbol myristate acetate (PMA) to promote FLNB-mediated cytopla

177 st assays following stimulation with phorbol myristate acetate (PMA) was detected in neutrophils isol

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

179 In contrast, treatment with phorbol myristate acetate (PMA), a protein kinase C activator, d

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

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

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

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

184 NADPH oxidase activators, including phorbol myristate acetate (PMA).

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

186 (IgE-activated mast cell supernates, phorbol myristate acetate [PMA; to activate TACE], TNFalpha, and

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

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

189 ulation, despite normal responses to phorbol myristate acetate and ionomycin, and possessed decreased

190 activated by CD3 cross-linking or by phorbol-myristate acetate and ionomycin, or by phytohemagglutini

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

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

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

194 nd Abeta(1-42) to be as effective as phorbol myristate acetate at differentiating THP-1 monocytes bas

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

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

197 TLC and phorbol myristate acetate increased cytosolic pMARCKS and decrea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 sion of AP1LUC reporter induction by phorbol myristate acetate.

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

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

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

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

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

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

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

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

222 sphate (PIP2) and MA induces the exposure of myristate and promotes membrane binding.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 ydrophobic beta sandwich to be essential for myristate binding.

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

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

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

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

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

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

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

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

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

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

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

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

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

258 de of glucosamine with secondary laurate and myristate chains on the distal unit.

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

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

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

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

263 Myristate dissociated these assemblies when incubated wi

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

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

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

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

268 -range structural changes but do not trigger myristate exposure.

269 xtended lipid conformation and of triggering myristate exposure.

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

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

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

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

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

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

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

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

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

279 Myristate is a novel potential substrate for sphingoid b

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

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

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

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

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 However, the myristate of HIV-2 MA is more tightly sequestered than t

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

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

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

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

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

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