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N-formyl-Met-Leu-Phe-induced oxidative burst in DMSO-differentiated HL-60 cells requires active Hsp90, but not intact microtubules
J. Vrba, M. Modrianský
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2001
Free Medical Journals
od 1998
ROAD: Directory of Open Access Scholarly Resources
od 2001
PubMed
15744362
DOI
10.5507/bp.2004.025
Knihovny.cz E-zdroje
- MeSH
- buněčná diferenciace MeSH
- dimethylsulfoxid farmakologie MeSH
- HL-60 buňky MeSH
- kolchicin farmakologie MeSH
- lidé MeSH
- mikrotubuly účinky léků fyziologie MeSH
- N-formylmethionin-leucyl-fenylalanin farmakologie MeSH
- neutrofily metabolismus MeSH
- nokodazol farmakologie MeSH
- paclitaxel farmakologie MeSH
- proteiny tepelného šoku HSP90 metabolismus MeSH
- respirační vzplanutí účinky léků MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
In this study we examined whether microtubules and heat shock protein 90 (Hsp90) are involved in phorbol myristate acetate (PMA) and N-formyl-Met-Leu-Phe (fMLP)-induced oxidative burst in DMSO-differentiated HL-60 cells. Our results showed that microtubule interfering agents, paclitaxel (1-5 microM), colchicine (1-100 microM), nocodazole (1-20 microM), and vincristine (1-50 microM), did not affect either PMA or fMLP-induced oxidative burst. In contrast, radicicol, an inhibitor of Hsp90, inhibited fMLP-induced oxidative burst in time and concentration-dependent manner where IC50 value for 30 min pre-incubation was 16.5 +/- 3.5 microM radicicol. We conclude that both PMA and fMLP-induced oxidative burst in DMSO-differentiated HL-60 cells is microtubule-independent while the latter requires Hsp90 activity.
Citace poskytuje Crossref.org
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