ライフサイエンスコーパス: C10

1 C10 binding with mutant forms of Rho that are altered in

2 C10 mutant MyBP-C failed to incorporate into myofilament

3 C10 peptide binding blocks access to OASS catalytic resi

4 C10-AMS can be used to study fatty acid recycling in oth

5 ysis rate constants of the studied FA (C8:0, C10:0>>C18:1 n-9>>C12:0>C14:0>C16:0 approximately C16:1

6 ctiveness of C18:1/C10-EPC relative to C18:0/C10-EPC (and to many other cationic lipoids) was suggest

7 The saturated C18:0/C10-EPC remained lamellar in mixtures with biomembrane-m

8 royldecanoyl-ethylphosphatidylcholine (C18:0/C10-EPC).

9 eral times more extensive than that of C18:0/C10-EPC.

10 xture of CAI-1 moieties, including C8-CAI-1, C10-CAI-1, Ea-C8-CAI-1 and Ea-C10-CAI-1.

11 (wt/wt)]; in contrast, the unsaturated C18:1/C10-EPC exhibited a lamellar-nonlamellar phase transitio

12 Indeed, FRET experiments showed that C18:1/C10-EPC exhibits lipid mixing with negatively charged me

13 Thus, C18:1/C10-EPC lipoplexes are likely to easily fuse with membra

14 ason for the superior effectiveness of C18:1/C10-EPC relative to C18:0/C10-EPC (and to many other cat

15 eoyldecanoyl-ethylphosphatidylcholine (C18:1/C10-EPC) and stearoyldecanoyl-ethylphosphatidylcholine (

16 volve the successive oxidation of carbon 10 (C10) to a carboxylic group by TcCHH, a cytochrome P450 o

17 13)C ENDOR then reveals the locations of (13)C10 and reactive (13)C11 of linoleic acid relative to th

18 +) as a cofactor, whereas it yields only 18% C10 GDP but 82% C15 FDP in the presence of Mg(2+).

19 ins at the 3 and 3' positions, which are 3OH-C10 and 3OH-C14 chains, respectively.

20 ed in new symmetric lipid A species with 3OH-C10 or 3OH-C14 chains at both the 3 and 3' positions, as

21 l diphosphate synthase 1 (PcIDS1) yields 96% C10-geranyl diphosphate (GDP) and only 4% C15-farnesyl d

22 in, including a truncated macrolactone and a C10 E-alkene, which were 400- and 50-fold less active th

23 s to the C-terminal serine residue of both a C10 model peptide and full-length MccE492.

24 They also describe a C10/CCL6 target gene cascade in which C10/CCL6 induction

25 ze increasing from 3.8 nm for decanoic acid (C10) to 4.4 nm for C18.

26 noic acid (C9), nonadecafluorodecanoic acid (C10), heneicosafluoroundecanoic acid (C11) and pentacosa

27 is able to convert medium-chain fatty acids (C10-C14) into their corresponding terminal olefins using

28 KD = 0.3 microm, and five to six additional C10 molecules with KD = 7 microm.

29 Additionally, C10-AMS stopped the ability of Vibrio cholerae to recycl

30 r ILs constructed from the very low affinity C10 scFv.

31 antiproteases comparable to those seen after C10/CCL6 neutralization.

32 em to versatile medium chain fatty alcohols (C10 &C12).

33 378-3415 cm(-1)), C8 (3339-3369 cm(-1)), and C10 (3381-3390 cm(-1)) H-bonded rings.

34 with the E-isomers during the C5 --> C10 and C10 --> C15 reactions.

35 iphosphate analogues with fluorine at C2 and C10 acted as inhibitors of DCS, but intriguingly, after

36 as a functional assay, we found that C2 and C10 are partially functionally redundant, and some but n

37 ogenic variants clustered in the C3, C6, and C10 domains (18 of 22, 82%, P<0.001 versus Genome Aggreg

38 MyBP-C with variants in the C3, C6, and C10 domains was expressed in rat ventricular myocytes.

39 that are highly enriched in saturated C8 and C10 fatty acids.

40 parately exposed to a mixture of C6, C8, and C10 monoalkylated PFPAs and a mixture of C6/C6, C6/C8, a

41 The sorption of C6, C8, and C10 monoalkylated PFPAs and C6/C6, C6/C8, and C8/C8 dial

42 ve perfluoroalkyl sulfonates (C4, C6-C8, and C10).

43 s introduce a cis-double bond between C9 and C10 of saturated fatty acyl chains.

44 oduction of a cis double bond between C9 and C10 of stearoyl-ACP.

45 ctive asymmetric aldol to install the C9 and C10 relative and absolute stereochemistry (for natural a

46 form the B-ring and the accompanying C9 and C10 stereocenters.

47 onvergent approach that unites the C1-C9 and C10-C22 fragments using Sonogashira coupling and Boland

48 tions of the stereogenic centers C8, C9, and C10 have been determined to be the same as for migrastat

49 f the cucurbitacins, epimeric at C8, C9, and C10, 51, was synthesized via a highly regio- and stereos

50 ith systematic variations at C7, C8, C9, and C10.

51 ersible thioether linkage between Cys499 and C10 of the chromophore, providing the basis for the blue

52 f rapamycin, C10 regulator of kinase II, and C10 regulator of kinase-like, suggesting that PDGFRalpha

53 increased serum concentrations of lysine and C10:2 carnitine.

54 octanoylcarnitine, C9-nonanoylcarnitine, and C10-decanoylcarnitine, lipid species known to be associa

55 Treatment with anti-C10/CCL6 decreased the levels of mRNA encoding matrix me

56 At pH6.5, antibody C10 locks all virus surface E proteins, and at pH5.0, it

57 growth factor receptor (EGFR) scFv antibody C10 was increased using molecular evolution and yeast di

58 ross-neutralization activity showed antibody C10 as one of the most potent.

59 This suggests antibody C10 could be a good therapeutic candidate.

60 ed rings (C6a/C6a), conformers 1A and 2B are C10 single H-bonded rings, conformers 1C and 2D are doub

61 itoring important biomarker classes, such as C10 demethylated terpanes, alphaalphaalpha-steranes, and

62 promised, but the cutoff appeared earlier at C10.

63 Finally, the carboxyl group at C10 is methylated by TcCCMT, a member of the SABATH meth

64 provide evidence that hydrogen(s) present at C10 of AA play a critical role in the catalysis of prost

65 ic and electronic effects of substituents at C10 of the anthracene core.

66 c interactions drive formation of the AtOASS.C10 peptide complex.

67 (AtOASS) and the C-terminal ligand of AtSAT (C10 peptide) as a function of temperature and salt conce

68 tients with cirrhosis (Child-Pugh classes B7-C10) with demonstrated patent portal veins and without h

69 First, receptor-positive B78H1-C10 cells expressing gH/gL fused with receptor-negative

70 in-coated poly(bisphenol A decane ether) (BA-C10) films prepared with chloroform and tetrahydrofuran

71 ing microscopy of the molecular rotor BODIPY C10 in the membranes of live Escherichia coli bacteria t

72 uterated bis-allylic carbons to include both C10 and C13 leads to a massive increase in the PKIE for

73 sm for cristae abnormalities because of both C10 mutation and C2/C10 loss.

74 xpression of antA was influenced the most by C10-HSL and to a lesser extent by other acyl-HSLs, inclu

75 and three fibronectin-like domains termed C0-C10.

76 analyzed for methane, carbon dioxide, and C1-C10 volatile organic compounds (VOCs).

77 -C11 pi system that would be required for C1-C10 bond formation in the first step of catalysis.

78 n of a variety of perfluoro alkyl groups (C1-C10) and a CF2COOEt moiety.

79 Thus, the C1-C14 and C15-C10 bonds are formed on the opposite faces of the 14,15

80 ids with systematic modifications at the C2, C10, and C3'N positions were synthesized and their struc

81 and selectivities of C-C bond cleavage in C2-C10 n-alkanes on metal catalysts and provide a general d

82 cess to analogues in the Northern region (C2-C10).

83 nol enhanced IFN-gamma production whereas C2-C10 alcohols reduced the release of this cytokine.

84 malities because of both C10 mutation and C2/C10 loss.

85 Finally, C2/C10 DKO mice partially phenocopied mutant C10 KI mice wi

86 Using the first C2/C10 double knockout (DKO) mice, we report that C10 patho

87 0 pathogenesis and the normal function of C2/C10 are intimately linked.

88 atients with C10 mutations, we found that C2/C10 DKO mice have disrupted mitochondrial cristae, becau

89 tissues, tying mutant C10 pathogenesis to C2/C10 function.

90 interval: 1.24, 6.67) for shorter chain (C4-C10) fatty acid intakes demonstrated increased risk for

91 rencing 3570 possible compounds including C4-C10 perfluoro- and polyfluoroalkyl, polyfluorochloroalky

92 Here a new global emission inventory of C4-C10 perfluoroalkanesulfonic acids (PFSAs) from the life

93 ree site-selective allylic oxidations at C5, C10, and C13, which led to the two-phase synthesis of ta

94 olated C-terminal half of cardiac MyBP-C (C5-C10) had effects similar to those of the full-length pro

95 Nine ionic PFASs including C6-C10 perfluoroalkyl carboxylic acids (PFCAs), C4 and C6-C

96 noble metal catalysts to yield branched C7 -C10 hydrocarbons in the gasoline volatility range.

97 required oxygen substituents at C1, C2, C7, C10, and C13.

98 up was selectively introduced to the C6, C7, C10 and the central C21 position of diazafenestrane syst

99 chain alcohols to micromolar amounts for C7-C10 alcohols.

100 ction of long-chain aliphatic diazides (C8 , C10 , and C12 ).

101 The probes are labeled on C5, C8, C10, C12, and C16 of stearic acid.

102 e analyzed for a suite of PFSAs (C4, C6, C8, C10) and selected PFOS precursors (MeFOSAA, EtFOSAA, FOS

103 fluoroalkane sulfonic acids (PFSAs; C4,C6,C8,C10) and perfluorooctane sulfonamide (FOSA).

104 gment and an insoluble C'-terminal SpyTag-C8-C10 fragment that remains associated with thick filament

105 ification of nontargeted DADMAC C8:C8 and C8:C10, two widely used biocides previously unreported in e

106 idative cleavage reactions at C9,C10 and C9',C10'.

107 hich allowed for the installation of the C9'-C10' (Z)-olefin.

108 Samples fortified with C8, C9, C10, and C11 were shown to be stable after remaining at

109 wer limit of quantitation (LLOQ) for C8, C9, C10, C11, and C13 was determined to be 25 ng/L in water.

110 endial by oxidative cleavage reactions at C9,C10 and C9',C10'.

111 tially removed the 9-cis-ring site at the C9,C10 double bond from this substrate, providing an all-tr

112 ns (J-K), for the formation of the C5-C6, C9-C10, and C17-C18 double bonds, a Suzuki-Molander C21-C22

113 -Wadsworth-Emmons olefination to form the C9-C10 bond, and Evans methylation to install the C-8 cente

114 vity and that, in fact, engagement of the C9-C10 diol as an acetonide actually leads to notably enhan

115 tion to form the b ring and the attendant C9/C10 configuration of the natural product.

116 tively exclude rotation around either the C9=C10, C11=C12, or C13=C14 bond show that formation of the

117 MC) fatty acids, caprylic (C8:0) and capric (C10:0) were incorporated into palm olein by 1,3-specific

118 Indeed, four such chemokines, CCL6/C10/MIP-related protein-1, CCL9/MIP-1gamma/MIP-related p

119 activation in murine lung epithelial cells (C10 line).

120 in murine alveolar epithelial type II cells (C10) and primary lung fibroblasts confirmed that asbesto

121 es, but was only accessible to longer chain (C10-C16) MTS compounds in the open state.

122 ans-enoyl-ACPs) and unexpected medium-chain (C10:1, C14:1) and polyunsaturated long-chain (C16:3) acy

123 howed diminished affinity for shorter chain (C10-C16) fatty acids and weak substrate-induced high spi

124 led-helix (CHCHD) domain 2 (C2) and CHCHD10 (C10) were recently identified as causing Parkinson's dis

125 taken to define the role(s) of the chemokine C10/CCL6 in the pathogenesis of IL-13-induced alteration

126 PAs containing C10 to C18 saturated acyl chains were not effective acti

127 hile this route does not provide the correct C10 stereochemistry, it showcases an efficient method to

128 tive survival compared with CP B7 to 9 or CP C10 to 15, in which surgery is contraindicated.

129 9, 11, 13 species and the presence of cyclic C10.

130 ) to Cys243 (C9), and Cys161 (C7) to Cys266 (C10).

131 ese hamster DC3F cells, the TOP1 mutant DC3F/C10 cells demonstrated cross-resistance to the cytotoxic

132 singly lipophilic octanoate (C8), decanoate (C10) and dodecanoate (C12) derivatives were evaluated in

133 rmination of delta-lactones (delta-C8, delta-C10) and gamma-lactones (gamma-C6, gamma-C8, gamma-C10).

134 iganin and its unnatural diastereoisomer (+)-C10-epi-giganin has been completed in a total of 13 line

135 proceeds through either geranyl diphosphate (C10) or trans-farnesyl diphosphate (C15), to yield monot

136 n some particular fatty acids distributions: C10:0, C12:0 and C22:0) concerning the physicochemical p

137 ding C8-CAI-1, C10-CAI-1, Ea-C8-CAI-1 and Ea-C10-CAI-1.

138 enesis of the btaI2 (luxI) allele eliminated C10-HSL accumulation and reduced lipase production.

139 a-1 and c-jun expression in asbestos-exposed C10 cells.

140 In contrast, prior exposure of gB-expressing C10 cells to soluble gD did not promote subsequent fusio

141 higher level was achieved when gB-expressing C10 cells were exposed to a combination of soluble gH/gL

142 econd, fusion occurred when gH/gL-expressing C10 cells preexposed to soluble gD were subsequently coc

143 th ELO1 converting C4 to C10, ELO2 extending C10 to C14, and ELO3 elongating C14 to C18.

144 The caterpillar-shaped (catSP) Fab C10:ZIKV complex shows Fabs locking the E protein raft s

145 The helical tail structure of Fab C10:DENV3 clubSP showed although the Fab locked an E pro

146 Complex formation of DENV and ZIKV with Fab C10 stabilize the viruses allowing cryoEM structural det

147 Five fatty acid methyl esters (FAMEs), C10-C20 n-alkanes, and four monoaromatic compounds were

148 t was hypothesized that fl-C2, fl-C4, and fl-C10 adopted primarily extended molecular conformations o

149 cally with chain length for fl-C2 through fl-C10; however, fl-C15 did not follow this trend but inste

150 trates that these residues are important for C10 peptide binding and that changes at these positions

151 d for oven-baked products, in particular for C10-C12 SCCPs, thus indicating that thermal decompositio

152 Despite the clear preference for C10 beta-turn structures in the basic unit, however, the

153 sphate and dimethylallyl diphosphate to form C10 prenyl diphosphates that can be elongated by the add

154 thway with unlabeled AA but abstraction from C10 predominating when the methylene group at position 1

155 pg/injection) for standard fatty acids from C10 to C24 and spanned approximately 2 orders of magnitu

156 FSD-C10, a Fasudil derivative, was shown to reduce severity

157 FSD-C10-treated mice showed a longer, thicker and more inten

158 FSD-C10-treated microglia significantly inhibited Th1/Th17 c

159 T cells, and the conditioned medium from FSD-C10-treated microglia promoted OPC survival and oligoden

160 Addition of FSD-C10 directly promoted remyelination in a chemical-induce

161 study, we further analyzed the effect of FSD-C10 on neuroprotection and remyelination.

162 Importantly, the CNS of FSD-C10-treated mice showed a shift of activated macrophages

163 ogether, these findings demonstrate that FSD-C10 promotes neural repair through mechanisms that invol

164 However, whether FSD-C10 can promote neuroregeneration remains unknown.

165 nd gamma-lactones (gamma-C6, gamma-C8, gamma-C10).

166 te (DMAPP, C5) and geranyl diphosphate (GPP, C10) to give (E,E)-FPP (C15).

167 en and the protruding angular methyl groups (C10, C13 methyls) in the beta face calls for adequate re

168 d along with the E-isomers during the C5 --> C10 and C10 --> C15 reactions.

169 er of incorporation of fatty acids was C22:0>C10:0>C8:0, to the extent of 53%, 42.5%, 35.8%, respecti

170 s of autoxidation products (octane, hexanal, C10 hydrocarbons) and other compounds that could origina

171 Forced expression of TGFalpha in C10 tumor cells led to the generation of autocrine and p

172 The inhibitor C10-AMS [5'-O-(N-decanylsulfamoyl)adenosine], which mimi

173 ases with clade I enzymes catalyzing initial C10-C1 or C11-C1 ring closures and clade II enzymes cata

174 the beetle larvae suggests flux control into C10 vs. C15 isoprenoids could be accomplished by these i

175 Virus entry into C10 cells was energy dependent, and intracellular envelo

176 During entry into C10 cells, virion envelope glycoproteins rapidly became

177 In this paper, we studied HSV entry into C10 murine melanoma cells and identified a third entry p

178 e oxides) allowed assignment at the isomeric C10 epoxy-ene carbon as Z in the new isomer and the E co

179 (C8-HSL), and N-decanoyl-homoserine lactone (C10-HSL).

180 ignant murine alveolar epithelial cell line, C10.

181 the sugar ring, thus forming a 10-membered, C10 turn.

182 nzymatic activity, whereas poorly metastatic C10, C19, and C23 tumor cells express much lower levels.

183 at kill Mtb, we identified a small molecule, C10, that blocks tolerance to oxidative stress, acid str

184 ated similarly in affected tissues of mutant C10 knock-in (KI) mice, demonstrating that L-OPA1 cleava

185 C2/C10 DKO mice partially phenocopied mutant C10 KI mice with the development of cardiomyopathy and a

186 s response in affected tissues, tying mutant C10 pathogenesis to C2/C10 function.

187 SOA precursors were n-decane (n-C10), n-pentadecane (n-C15), n-heptadecane (n-C17), tric

188 For a subset of alkane precursors (n-C10, n-C15, and JP-10), maximum SOA yields were estimate

189 mation of even the simplest PAH-naphthalene (C10 H8 )-via the hydrogen-abstraction/acetylene-addition

190 H6 ) intermediate together with naphthalene (C10 H8 ) under combustion-like conditions by photo-ioniz

191 l clones expressing high (C9) or negligible (C10) levels of TGFalpha were implanted into the cecal wa

192 The Cambodian clone NF135.C10 consistently produced gametocytes and generated subs

193 challenged by mosquitoes infected with NF135.C10 and 4 of 5 challenged with NF54 developed parasitemi

194 The tumor microenvironment of C9, but not C10, contained cells enriched in vascular endothelial gr

195 C9, but not C10, tumor cells metastasized to regional lymph nodes in

196 inct locations on Rho for the two classes of C10-binding sites.

197 rthermore, we discovered that deuteration of C10 promotes the formation of the resolving lipid mediat

198 ble gH/gL triggered a low level of fusion of C10 cells expressing gD and gB; a much higher level was

199 of C10/CCL6 and highlight the importance of C10/CCL6 and signaling via CCR1 in the pathogenesis of t

200 s confirmed that C10(mut) causes the loss of C10 domain interaction with myosin LMM.

201 med from the reaction of OH with a series of C10 (cyclo)alkanes, with 0-3 rings, in order to better u

202 For a series of C10 aliphatic ketones differing in shape but not size, D

203 nstrate that IL-13 is a potent stimulator of C10/CCL6 and highlight the importance of C10/CCL6 and si

204 aled that virions attached to the surface of C10 cells were localized to membrane invaginations, wher

205 While the developed asymmetric synthesis of C10 substituted anthrones is anticipated to find wider a

206 C9 tumors was threefold higher than that of C10 tumors.

207 includes the removal of the 3 position 3-OH C10 fatty acid.

208 ], and retention of 3-hydroxydecanoate [3-OH C10 fatty acid]) were determined for Pseudomonas aerugin

209 at P. aeruginosa PagL recognizes either 3-OH C10 or 3-OH C14.

210 th free (R)-3-hydroxydecanoic acid [(R)-3-OH-C10:0] representing the strongest immune elicitor.

211 figs as 5,6-dihydro-6-pentyl-2H-pyran-2-one (C10 massoia lactone).

212 zes and detects (S)-3-hydroxytridecan-4-one (C10-CAI-1), whereas Vibrio harveyi produces and detects

213 ing functional group variations at C9 and/or C10 and C11 of ring C has been accomplished.

214 In solution, bolaforms with C8 or C10 chains between glucal headgroups form nanoscale vesi

215 atty acid and to its cognate substrate 3-oxo-C10 AHL (Acyl-Homoserine Lactone).

216 te plant growth, treatments with C6-HSL, oxo-C10-HSL, or oxo-C14-HSL resulted in different transcript

217 ution of a serine-ligated P450 variant, P411-C10, yielded a lineage of engineered P411 enzymes that t

218 Par-C10 cells were used to functionally isolate the apical a

219 ion was increased by Ca(2+) ionophore in Par-C10 and HSY salivary cell lines.

220 acinar cells and apical PMCA activity in Par-C10 cells.

221 immortalized/cancer salivary cell lines (Par-C10, HSY, HSG), indicating significant differences betwe

222 In vitro studies using Par-C10 acinar cells demonstrated that when compared with L(

223 er affinity compared to that of the parental C10 scFv.

224 ells with a luminescent complex, Tb/DTPA-PDA-C10, we observed DEFRET between the Tb3+ complex and ext

225 hesis with 2, we found that neryl phosphate (C10 phosphate) can be recognized by MraY/MurX to generat

226 the retinal polyene chain between positions C10 and C15 as well as the Schiff base nitrogen in the g

227 arbonyl cations 1d-4d support a degree of Pt-C10 multiple bonding, increasing in the order 3 < 4 < 2

228 a targeted null mutation of CCR1, a putative C10/CCL6 receptor, also decreased IL-13-induced inflamma

229 letons vary widely from neryl pyrophosphate (C10) to natural rubber (C>10,000).

230 We show that (R)-C10 massoia lactone is reduced to (R)-delta-decalactone

231 g chiral GC-GC-MS, we show that only the (R)-C10 massoia lactone is found in musts and wines.

232 to alicyclic hydrocarbons in the size range C10 to C17.

233 ion kinase, mechanistic target of rapamycin, C10 regulator of kinase II, and C10 regulator of kinase-

234 ated substitution reaction of the bay-region C10 acetoxy group in four stereoisomeric 7,8,9,10-tetraa

235 trisubstituted tetrahydrofuran representing C10-C18 of the toxin was prepared via a highly stereosel

236 the Cys(155) -Cys(185) disulphide bond of S(C10) -Rnase, resulting in a significant increase of its

237 e C-terminal 10 residues of Arabidopsis SAT (C10 peptide) at 2.9-A resolution.

238 of short-chain chlorinated paraffins (SCCPs, C10-13) and an additional characterization of medium-cha

239 xindole carboxylation (dr 5.2:1.0) that sets C10 configuration in a potential diazonamide precursor.

240 hat wild type Rho binds between five and six C10 oligomers per hexamer with KD = 0.3 microm, and five

241 a C-C bond within the geometrically stressed C10 framework.

242 factors identifies nuclear factor Y subunit C10 (NF-YC10) as a GAPC-binding protein.

243 the GAF domain of Cph1 predicts a C5-Z,syn, C10-Z,syn, C15-Z,anti configuration for the chromophore

244 protein cross-linking assays confirmed that C10(mut) causes the loss of C10 domain interaction with

245 ough mechanistic studies, we discovered that C10 inhibits Mtb respiration, revealing a link between r

246 In addition, we found that C10 prevents the selection for INH-resistant mutants and

247 0 double knockout (DKO) mice, we report that C10 pathogenesis and the normal function of C2/C10 are i

248 The C10 peptide binds to the AtOASS homodimer in a 2:1 compl

249 The C10-C11, C16-C17, C9-O, and C18-O bonds have been create

250 The C10-C21 n-alkanes of petrodiesel were metabolized at sig

251 Interaction between AtOASS and the C10 peptide is tight (Kd = 5-100 nM) over a range of tem

252 , Tx-67, with a succinate group added at the C10 position of Taxol, was synthesized and identified as

253 Addition of a methyl group at the C10 position of the steroid has a significant impact on

254 640 ng/g wet weight) closely followed by the C10 and C11 homologues.

255 the cytochrome P450 enzyme that cleaves the C10-C19 carbon-carbon bond of androgens to form estrogen

256 mL oxidase reveal a likely mechanism for the C10 oxidation of TirE.

257 w insights into the structural basis for the C10/C12 and C12/C14 hydroxylation patterns for the 12-(Y

258 losing metathesis (RCM) strategy to form the C10-C11 olefinic bond failed.

259 species, which abstracts an H atom from the C10 site of the substrate.

260 Although this mutation causes changes in the C10 domain of cMyBP-C (cMyBP-C(C10mut)), which binds to

261 lation and epoxidation routes to install the C10 axial alcohol.

262 idues (Thr-74, Ser-75, and Gln-147) lock the C10 peptide in the binding site.

263 ndividual short-chain IDSs (scIDSs) make the C10, C15, and C20 isoprenyl diphosphates separately.

264 Selective hydrolysis of the C10 amide of lead compound 2 and subsequent derivatizati

265 Analysis of the C10 and C15 products from incubations with avian FPP syn

266 AtOASS binding of the C10 peptide displays negative cooperativity at higher te

267 o demonstrate that the C-terminal Ile of the C10 peptide is required for molecular recognition by At-

268 is work, which defines the importance of the C10 stereochemistry for this class of inhibitors of GAR

269 An unexpected, overriding impact of the C10 stereochemistry in stereoselectivity and reaction ra

270 The pronounced impact of the C10 stereochemistry on the successful construction of a

271 addition to the natural product, each of the C10-C11 diastereomers of cytostatin was divergently prep

272 es catalyze significant hydroxylation of the C10-C12 atoms of palmitate.

273 Stepwise cleavage of the C10-C19 and O-O bonds of the peroxohemiacetal extrudes f

274 e of the presence and stereochemistry of the C10-methyl and C11-hydroxy groups for potent PP2A inhibi

275 , we determined the cryoEM structures of the C10-ZIKV complex at pH levels mimicking the extracellula

276 n dynamically transition via breakage of the C10/Cys-494 thioether bond, opposite rotations of the A

277 e of a 3'-C1 and/or 4'-C1 substituent on the C10 phenyl ring increased cytotoxicity in the MCF-7 cell

278 series possessed a 3'-C1 substituent on the C10 phenyl ring.

279 city and the m-Cl substituent present on the C10 side chain did not induce any large change in activi

280 ramolecular Mannich cyclization based on the C10 stereochemistry was discovered.

281 eaction with an N-acyliminium ion to set the C10 quaternary stereocenter, a mild dissolving-metal cle

282 om their corresponding CoA thioesters to the C10 hydroxyl of 10-deacetylbaccatin III.

283 alignment of the C-S bond with regard to the C10-C11 pi system that would be required for C1-C10 bond

284 These C10/CCL6 and CCR1 manipulations did not alter the produc

285 cids or acylcarnitines (ranging from C2:0 to C10:0) fail to achieve a stable conformation with oxy-Mb

286 hesis is modular, with ELO1 converting C4 to C10, ELO2 extending C10 to C14, and ELO3 elongating C14

287 s, we synthesized 12 peroxy acids with C8 to C10 carbon backbones and mono- or diperoxy acid function

288 EGFR-expressing A431 tumor cells compared to C10 scFv (KD=264 nM).

289 The better compound (TPP(+)C10) contained 10 carbon atoms within the linker chain a

290 Moreover, TPP(+)C10 significantly inhibited the growth of TA3/Ha tumors

291 antineoplastic activity and safety of TPP(+)C10 warrant further comprehensive evaluation.

292 al, synthetic array of natural and unnatural C10, C20, C30, and C40 polyisoprenol sugar pyrophosphate

293 ion in MM was not influenced by the FA used (C10 or C18).

294 Therefore, by using C10 to dissect Mtb persistence, we discovered that INH r

295 at sn-2 position in modified products were: C10:0, 4%; C16:0, 13%; C18:1, 66%; and C18:2, 15.4%.

296 tocrine and paracrine EGFR networks, whereas C10 tumors were unable to signal through EGFR.

297 ribe a C10/CCL6 target gene cascade in which C10/CCL6 induction is required for optimal IL-13 stimula

298 smaller amounts of lipid IV(A) modified with C10 or C12 acyl groups, Y. pseudotuberculosis contained

299 Similar to patients with C10 mutations, we found that C2/C10 DKO mice have disrup

300 s that small amounts of neryl diphosphate (Z-C10) and (Z,E)-FPP are formed along with the E-isomers d