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2 mma-quinide, and 1,3,4-O-tris[3,4-(dimethoxy)cinnamoyl]-1,5-gamma-quinide), finding dissociation cons
3 feoyl-1,5-gamma-quinide, 3-O-[3,4-(dimethoxy)cinnamoyl]-1,5-gamma-quinide, 3,4-O-bis[3,4-(dimethoxy)c
4 -1,5-gamma-quinide, 3,4-O-bis[3,4-(dimethoxy)cinnamoyl]-1,5-gamma-quinide, and 1,3,4-O-tris[3,4-(dime
7 atives, compound 1-(4-hydroxy-3,5-dimethoxy) cinnamoyl-2-acyl-sn-glycero-3-phosphocholine exhibited e
9 osphocholine and 1-(4-hydroxy-3,5-dimethoxy) cinnamoyl-2-palmitoyl-sn-glycero-3-phosphocholine exhibi
11 ests that the extinction coefficient for the cinnamoyl acyl-enzyme is larger than previously measured
14 rization of polarized alkenes, employing the cinnamoyl chromophore as a retinal surrogate under UV-ir
15 BZO1 is to synthesize the benzoate precursor cinnamoyl CoA rather than to generate benzoyl CoA from b
18 xpression of the lignin monomer biosynthetic cinnamoyl CoA reductase and cinnamyl alcohol dehydrogena
20 ication in intact plants, a microRNA against cinnamoyl CoA-reductase1 driven by the promoter from cel
21 BA beta-oxidative pathway (cinnamic acid --> cinnamoyl-CoA --> 3-hydroxy-3-phenylpropanoyl-CoA --> 3-
22 sgenic lines accumulated the PhCHD substrate cinnamoyl-CoA and the upstream pathway intermediate cinn
24 e crystal structure of (N,N-dimethyl-p-amino)cinnamoyl-CoA bound at the enzyme active site, the shiel
25 benzenoid network and provide evidence that cinnamoyl-CoA formation by Ph-CNL in the peroxisomes is
26 first step in the beta-oxidative pathway is cinnamoyl-CoA formation, likely catalyzed by a member of
29 , we have identified a petunia gene encoding cinnamoyl-CoA hydratase-dehydrogenase (PhCHD), a bifunct
31 dicated that the irx4 mutation occurred in a cinnamoyl-CoA reductase (CCR) gene within a highly conse
34 s tremula x Populus alba) down-regulated for cinnamoyl-CoA reductase (CCR), the enzyme catalyzing the
35 lcohol dehydrogenase (CAD; EC 1.1.1.195) and cinnamoyl-CoA reductase (CCR; EC 1.2.1.44) activities in
36 suppression of the petunia (Petunia hybrida) cinnamoyl-CoA reductase 1 (PhCCR1), which catalyzes the
37 e, chalcone isomerase, isoflavone reductase, cinnamoyl-CoA reductase and caffeic acid O-methyltransfe
38 oA ligase, caffeoyl-CoA O-methyltransferase, cinnamoyl-CoA reductase and cinnamyl alcohol dehydrogena
39 to ) with a region on chromosome 9 harboring cinnamoyl-CoA reductase, a key enzyme in monolignol synt
40 oA ligase, caffeoyl-CoA O-methyltransferase, cinnamoyl-CoA reductase, and cinnamyl alcohol dehydrogen
41 affeoyl-CoA O-methyltransferase1 [CCoAOMT1], cinnamoyl-CoA reductase1 [CCR1], ferulate 5-hydroxylase
42 lytic mechanism and substrate specificity of cinnamoyl-CoA reductases from sorghum (Sorghum bicolor),
43 rate specificity for feruloyl-CoA over other cinnamoyl-CoA thioesters, and the T154Y mutation in SbCC
44 PhCHD revealed it most efficiently converts cinnamoyl-CoA to 3-oxo-3-phenylpropanoyl-CoA, thus formi
45 ith the bound substrate 4-(N,N-dimethylamino)cinnamoyl-CoA using X-ray diffraction data to a resoluti
46 -carbons of the substrates, hexadienoyl-CoA, cinnamoyl-CoA, and (N,N-dimethyl-p-amino)cinnamoyl-CoA h
47 al tropane alkaloids of E. coca, cocaine and cinnamoyl cocaine, were present in highest concentration
48 Purified enzymes were used to synthesize cinnamoyl-coenzyme A (CoA), p-coumaroyl-CoA, feruloyl-Co
50 late 5-hydroxylase) and ccr1g (deficient for cinnamoyl-coenzyme A reductase) lines, albeit to a lower
53 philic block copolymers were prepared from a cinnamoyl-containing hydrophobic norbornene monomer and
54 ptor (MOR) antagonism, but the unsubstituted cinnamoyl derivative (6a) had partial MOR agonist activi
57 lic acid esterase B, FAEB) was shown to be a cinnamoyl esterase (CE), efficiently releasing hydroxyci
59 on these substrates, but it is not known if cinnamoyl esterases can break these cross-links by cleav
65 -rhamnosides, flavonol-3-O-(dihydrophaseoyl, cinnamoyl)glycoside-7-O-rhamnosides and flavonol-3-O-(ma
66 other flavonol-glycosides, and flavonol-3-O-(cinnamoyl)glycoside-7-O-rhamnosides, flavonol-3-O-(dihyd
67 of the 14beta-cinnamoyl series and that the cinnamoyl group itself may in fact be the dominant bindi
68 es of ligands has been synthesized where the cinnamoyl group of the 14-cinnamoylamino morphinones has
72 rain responds to picomolar concentrations of cinnamoyl-HSL and thus, produces cinnamoyl-HSL in excess
73 trations of cinnamoyl-HSL and thus, produces cinnamoyl-HSL in excess of the levels required for a sig
74 w that this signal is cinnamoyl-HSL and that cinnamoyl-HSL is produced by the LuxI homolog BraI and d
76 of Bradyrhizobium to produce and respond to cinnamoyl-HSL shows that aryl-HSL production is not uniq
78 integrated to propose a binding mode for the cinnamoyl inhibitors at the active site of HIV-1 IN.
80 nt metabolite, followed by N-[4'-hydroxy-(E)-cinnamoyl]-l-aspartic acid and N-[3',4'-dihydroxy-(E)-ci
83 ay a major role in the binding of the 14beta-cinnamoyl series and that the cinnamoyl group itself may
87 aximum at 498 nm resembling the natural 4-OH-cinnamoyl-thioester chromophore of the photoactive yello
88 parallel arrangement of covalently attached cinnamoyl units suitable for stereoselective photodimeri
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