JBIR-52, a new antimycin-like compound, from Streptomyces sp. ML55

@article{Kozone2009JBIR52AN,
  title={JBIR-52, a new antimycin-like compound, from Streptomyces sp. ML55},
  author={Ikuko Kozone and Jun-ya Ueda and Motoki Takagi and Kazuo Shin‐ya},
  journal={The Journal of Antibiotics},
  year={2009},
  volume={62},
  pages={593-595}
}
GRP78/Bip is a molecular chaperone in the endoplasmic reticulum (ER) induced by ER stress that promotes protein folding and has an important role as a survival factor in solid tumors by providing resistance to both chemotherapy and hypoglycemic stress.1 Thus, specific downregulators of GRP78 expression can reasonably be expected to become promising drugs in cancer chemotherapy.2 In the course of our screening program for downregulators of GRP78 expression, we have isolated versipelostatin A-F,3… 
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TLDR
JBIR-04 and -05 inhibited the expression of GRP78 induced by 2-deoxyglucose in human fibrosarcoma HT1080 cells, but their activities were highly reduced compared with those of 3 and SW-163A.
A Novel Antimycin-like Compound, JBIR-06, from Streptomyces sp. ML55
A novel compound of antimycin family, JBIR-06 (1), was isolated from Streptomyces sp. ML55. The structure of 1 was established as a twelve-membered macrocyclic skeleton with a
Prunustatin A, a Novel GRP78 Molecular Chaperone Down-regulator Isolated from Streptomyces violaceoniger
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Punustatin A inhibited the expression of GRP78 induced by 2-deoxyglucose in human fibrosarcoma HT1080 cells accompanied by global cell death without showing cytotoxicity under normal nutrient condition.
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Results suggest that the alpha-L-oleandropyranosyl (1-->4)-beta-D-digitoxopyranosol residue in the sugar moiety may play an important role in down-regulating GRP78 expression induced by 2-deoxyglucose.
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[structure: see text] Versipelostatin is the first compound which specifically inhibits the expression of GRP78 and the resultant robust cell death under stress conditions, in contrast to the weak
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Findings are consistent with the notion that induction of ER molecular chaperones leads to the acquisition of cy toprotection in the face of ATP depletion, but inhibition of protein translation by cycloheximide was found to only partially attenuate the observed cytoprotective effect, raising the possibility that other, as yet to be identified, nonprotein synthesis-dependent mechanisms may also play a role in the observed Cytoprotection.
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The findings show that disrupting the UPR during glucose deprivation could be an attractive approach for selective cancer cell killing and could provide a chemical genomic basis for developing UPR-targeting drugs against solid tumors.
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