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1 lignin biosynthesis in response to exogenous brassinolide.
2 surface pocket for binding the plant hormone brassinolide.
3 ids, including typhasterol, castasterone and brassinolide.
4 auxin and not with other hormones, including brassinolide.
5 h were also found to contain high amounts of brassinolide.
6 rtinol and auxin, but not to gibberellins or brassinolide.
7 ts in responses to auxins, abscisic acid and brassinolide.
8 ype can be rescued with exogenously supplied brassinolide.
9 ould be rescued by the addition of exogenous brassinolide.
10 icient in campesterol, an early precursor of brassinolide.
11 eliorated by application of a plant steroid, brassinolide.
12 ology and reduced sensitivity to the hormone brassinolide.
14 smonate, auxin and gibberellic acid, but not brassinolide and abscisic acid, and that SGT1b and its h
15 Decreased response to exogenously applied brassinolide and altered BR marker gene expression demon
17 that CYP734A1 binds active brassinosteroids, brassinolide and castasterone, as well as their upstream
18 Binding studies using BPCS, (3)H-labelled brassinolide and recombinant BRI1 fragments show that th
20 s reviewed in this article, oligosaccharins, brassinolides, and JA, can exert major effects on plant
21 rylated on threonine residues in response to brassinolide application, but not in response to systemi
23 ation of the defence hormones abscisic acid, brassinolides (applied as epibrassinolide), ethylene (ap
26 nalysis indicated that genes associated with brassinolide biosynthesis, secondary cell wall biosynthe
33 benzyladenine (BA), abscisic acid (ABA), and brassinolide (BL) did not affect the degradation rate of
34 ites from Arabidopsis seedlings treated with brassinolide (BL) for six different lengths of time.
35 rk1serk3 double mutant are almost completely brassinolide (BL) insensitive, while the double mutant h
36 ht, were attenuated by treatment with either brassinolide (BL) or the BR biosynthesis inhibitor brass
37 that signals systemic plant defense, and the brassinolide (BL) receptor, BRI1, that regulates develop
38 ed slowly with time following application of brassinolide (BL) to Arabidopsis seedlings, whereas phos
39 (AtRALF23) is significantly downregulated by brassinolide (BL) treatment of Arabidopsis seedlings or
40 including glucosylation of the bioactive BR brassinolide (BL), which is catalyzed by the UDP-glycosy
41 ted by ES1 and treated seedlings displayed a brassinolide (BL)-insensitive phenotype similar to a bri
43 otypes can be rescued by exogenously applied brassinolide but cannot be recovered by auxins, gibberel
46 al role in leaf morphogenesis, and implicate brassinolide in the margin as a key mediator in the cont
47 a major site of autophosphorylation that is brassinolide-induced in vivo and requires a kinase-activ
48 ver, treatment of Arabidopsis seedlings with brassinolide induces autophosphorylation of BRI1, which,
53 transporter activity by a WNK kinase, and a brassinolide receptor kinase by trafficking-related prot
55 that constitutive BR signaling in bes1-D and brassinolide-resistant 1-1D (bzr1-1D) mutants conferred
56 rfism could be rescued by the application of brassinolide, suggesting that DWF4 plays a role in brass
57 d responsiveness to high levels of exogenous brassinolide supporting our observations that CYP72C1 ac
58 ranscript encoding an enzyme involved in epi-brassinolide synthesis, but not those treated with CK.
59 asterone (BPCS), a biosynthetic precursor of brassinolide (the most active of the brassinosteroids).
60 L2, encode functional BR receptors that bind brassinolide, the most active BR, with high affinity.
62 rant genotype by pretreatment with exogenous brassinolide, which results in restricted shoot elongati