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1 g]isoquinolin-5-yl)isobenzo-furan-1(3H)-one (noscapine).
2 tic arrest and then apoptosis in response to noscapine.
3 bstituted aromatic halides including 9-bromo noscapine.
4 ignificantly lower than [9-Br-Nos]IBr(2) and Noscapine.
5 averine, papaverine, glaucine, rotundine and noscapine.
6 involved in the formation of papaverine and noscapine.
7 looxygenase-2 promoter was also inhibited by noscapine.
8 e antiproliferative and apoptotic effects of noscapine.
9 1 in the cellular response to treatment with noscapine.
10 fect tubulin polymerization differently from noscapine.
11 at mitosis at concentrations much lower than noscapine.
12 bserved arrest in mitosis in the presence of noscapine.
13 rt herein that two brominated derivatives of noscapine, 5-bromonoscapine (5-Br-nosc) and reduced 5-br
14 hat the cytotoxic agent 7A-O-demethoxy-amino-noscapine (7A-aminonoscapine) binds to the colchicine si
15 Here, we present one such analog, 9-nitro-noscapine (9-nitro-nos), which binds tubulin and induces
16 ike the other existing drugs in this regime; noscapine (a non-opioid alkaloid) is testified to be an
17 our workflow to the biosynthetic pathway of noscapine, a benzylisoquinoline alkaloid (BIA) with a lo
22 ndantly expressed in opium poppy stems where noscapine accumulation is highest among plant organs.
25 n vivo, and we describe a novel mechanism of noscapine action through EP2 prostaglandin E2 receptor-m
30 is study, we found that apoptosis induced by noscapine, an anti-microtubule drug previously shown to
31 Here we demonstrate that a tubulin-binding noscapine analog, (R)-9-bromo-5-((S)-4,5-dimethoxy-1,3-d
34 ), have higher tubulin binding activity than noscapine and affect tubulin polymerization differently
35 lytic activity toward oxidation of morphine, noscapine and heroin at reduced overpotentials in wide p
36 ulse voltammetric determination of morphine, noscapine and heroin yields calibration curves with the
39 these compounds bound to tubulin shows that noscapine and its 7-aniline derivative do not compete fo
41 of three major narcotic components, heroin, noscapine and morphine at micromolar concentration witho
44 ive discusses the advancing understanding of noscapine and related analogues in the fight against mal
46 isiae to achieve the microbial production of noscapine and related pathway intermediates, complementi
48 ylisoquinoline alkaloids including morphine, noscapine, and papaverine, in the specialized cytoplasm
49 ther propose that the anticancer activity of noscapine arises from a bioactive metabolite that binds
52 ave previously discovered the opium alkaloid noscapine as a microtubule interacting agent that binds
53 ave previously identified the opium alkaloid noscapine as a microtubule interacting agent that binds
54 the naturally occurring antitussive alkaloid noscapine as a tubulin-binding agent that attenuates mic
56 eviously that an antitussive plant alkaloid, noscapine, binds tubulin, displays anticancer activity,
62 ies reveal that even at high concentrations, noscapine does not alter the tubulin polymer/monomer rat
64 t, unlike many other microtubule inhibitors, noscapine does not significantly promote or inhibit micr
65 s denatonium, quinine, dextromethorphan, and noscapine, dose-dependently relaxed the pre-contracted g
66 required for subsequent apoptosis induced by noscapine, establishing a link between the two events.
67 cence staining of microtubules after 24 h of noscapine exposure at 20 muM elucidated chromosomal abno
68 constitute a 14-step biosynthetic pathway of noscapine from the simple alkaloid norlaudanosoline by e
72 ing enzymes responsible for the synthesis of noscapine have been recently discovered to be clustered
74 vation of PKA and the antifibrotic effect of noscapine in HLFs were blocked by the EP2 prostaglandin
75 ), which mediated the antifibrotic effect of noscapine in HLFs, as assessed with the PKA inhibitor, P
76 c and Rd 5-Br-nosc are also more active than noscapine in inhibiting the proliferation of various hum
79 ioavailable and is 250-fold more potent than noscapine in reducing cell proliferation in rapidly divi
81 findings thus indicate a great potential for noscapine in the treatment of paclitaxel-resistant human
82 or the first time the antifibrotic effect of noscapine in vitro and in vivo, and we describe a novel
83 posed pathway leading from (S)-reticuline to noscapine includes (S)-scoulerine, (S)-canadine, and (S)
87 valuated novel 9'-substituted suzuki-coupled noscapine ionic liquid(s) as effectual anticancer drug(s
97 angiogenesis in tumors, we hypothesized that noscapine mediates its effects by modulating the NF-kapp
98 sed a significant reduction in the levels of noscapine, narcotoline, and a putative downstream secobe
99 investigated the chemo-sensitizing effect of Noscapine (Nos) at low concentrations in conjunction wit
101 pium alkaloids (morphine, codeine, thebaine, noscapine, papaverine and narceine) in poppy seeds and b
103 We suggest that the 7A-methoxy group of noscapine prevents binding to tubulin due to a steric cl
106 ntifibrotic effects of the antitussive drug, noscapine, recently found to bind microtubules and affec
109 r results demonstrate that p.o.-administered noscapine significantly inhibits the progression of mela
112 ates, allowing gene function to be linked to noscapine synthesis and a novel biosynthetic pathway to
114 y, cell cycle distribution, and apoptosis on noscapine treatment in four cell lines derived from the
117 c murine model of established s.c. melanoma, noscapine treatment resulted in an 85% inhibition of tum
118 ly, these cells undergo apoptotic death upon noscapine treatment, accompanied by activation of the c-
123 higher affinity than the founding compound, noscapine, without changing total microtubule polymer ma