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1 synthesis of a triene-containing C17-benzene ansamycin.
2 of structural derivatives (6-9) of phenolic ansamycins.
3 e the preparation of potent non-benzoquinone ansamycins.
4 compared with the corresponding benzoquinone ansamycins.
5 synthetic precursor of rifamycin and related ansamycins, a series of target-directed mutations and he
6 have suggested that the in vitro potency of ansamycins against Hsp90 may be enhanced in the presence
7 hydroxybenzoic acid (AHBA), precursor of the ansamycin and mitomycin antibiotics, proceeds by the ami
8 ibition of Akt activation is achievable with ansamycins and may be useful for the treatment of HER2 d
10 cins are metabolized by NQO1 to hydroquinone ansamycins and that Hsp90-mediated trans-cis isomerizati
13 sent studies demonstrate that treatment with ansamycin antibiotic geldanamycin (GA), or its less toxi
16 ino)-17-demethoxygeldanamycin (17-AAG) is an ansamycin antibiotic that binds to a conserved pocket in
18 eatment of MCF-7 cells with geldanamycin, an ansamycin antibiotic that inhibits Hsp90 function, MLK3
20 methoxygeldanamycin (17-AAG), a benzoquinoid ansamycin antibiotic, which binds to heat shock protein
22 maturation of Hsp90 target proteins and that ansamycin antibiotics abrogate the activity of such prot
25 -dependent processes to ansamycin treatment, ansamycin antibiotics disrupt signaling through some mec
26 complexes in cell lysates, and Hsp90-binding ansamycin antibiotics disrupt the activity of Hsp90-depe
30 ological intercession of Hsp90 activity with ansamycin antibiotics or depletion of BAG3 by small inte
32 amino)-17-demethoxygeldanamycin (17-AAG) are ansamycin antibiotics that bind to a highly conserved po
33 cking Sba1 displays increased sensitivity to ansamycin antibiotics, and this phenotype is rescued by
41 that some of the effects of 17-AAG and other ansamycins are due to their effects on VDAC and that thi
42 rather than cis-amide forms of benzoquinone ansamycins are metabolized by NQO1 to hydroquinone ansam
44 uch attention is focused on the benzoquinone ansamycins as anticancer agents, with several derivative
46 redicted to be involved in the production of ansamycin, benzoisochromanequinone, streptogramin using
50 DDP-induced signaling pathways revealed that ansamycins block the activation of mitogen-activated pro
51 neurodegenerative diseases, and benzoquinone ansamycin (BQA) Hsp90 inhibitors such as geldanamycin (G
53 the reduction of this series of benzoquinone ansamycins by NQO1 generates the corresponding hydroquin
58 bition after treatment with the benzoquinone ansamycins compared with the MDA468 cells; this increase
62 ot the cis-amide isomers of the benzoquinone ansamycins could be accommodated by the NQO1 active site
63 spite structural studies on the complexes of ansamycin derivatives with the ATPase domain of Hsp90, c
65 s- and cis-amide isomers of the hydroquinone ansamycins exhibited increased binding affinity for Hsp9
73 bes the influential role of the benzoquinone ansamycin geldanamycin and the resorcylic acid macrolact
75 r PC-3 and LNCaP cells with the benzoquinone ansamycin geldanamycin, an Hsp90-specific inhibitor, ind
79 eatment of tumor cells with the benzoquinone ansamycin, geldanamycin, leading to a marked reduction i
80 breast carcinoma cells with the benzoquinoid ansamycin, geldanamycin, rapidly depletes p185c-erbB-2 p
82 0 ATPase activity including the benzoquinone ansamycins, geldanamycin and 17-allylamino-17-demethoxyg
83 trans-cis isomerization of the benzoquinone ansamycins in Hsp90 inhibition has been disputed in rece
84 mulation of the high-affinity dihydroquinone ansamycins in tumor cells contributes to the antitumor a
85 tive effects of geldanamycin, a benzoquinone ansamycin, in HT22 cells were associated with a down-reg
96 ks chemical and structural similarity to the ansamycin rifampicin (Rif), an RNAP inhibitor widely use
101 Treatment of SKBr3 cells with benzoquinone ansamycins, such as geldanamycin (GA), depletes p185erbB
103 Sf9 cells with geldanamycin, a benzoquinone ansamycin that binds to hsp90 and disrupts its function,
104 of L cells with geldanamycin, a benzoquinone ansamycin that binds to hsp90 and disrupts its function,
106 when this function is interfered with by an ansamycin, there is a further shift to proteolytic degra
107 sensitivity of Hsp90-dependent processes to ansamycin treatment, ansamycin antibiotics disrupt signa
109 g a fundamentally new route to shikimate and ansamycin-type compounds, this result enables further ge
110 fied human Hsp90 by a series of benzoquinone ansamycins was examined in the presence and absence of N
111 human NQO1 to the corresponding hydroquinone ansamycins was monitored by high-performance liquid chro
112 , and HPLC analysis showed that hydroquinone ansamycins were formed by the MDA468/NQ16 cells, which c
113 bitor of NQO1, showing that the hydroquinone ansamycins were more potent Hsp90 inhibitors than their
114 C inhibitor, or geldanamycin, a benzoquinone ansamycin, which destabilizes and depletes Raf-1, marked
115 QO1 generates the corresponding hydroquinone ansamycins, which exhibit enhanced Hsp90 inhibition.
116 xtensive study with a series of benzoquinone ansamycins, which includes gel-danamycin, 17-(amino)-17-
117 cts between yeast Hsp90 and the hydroquinone ansamycins, which translated to greater interaction ener