Stimulation of transient versus sustained ERK1/2 phosphorylation by relative chitinase-like proteins CHI3L1 and CHI3L2 correlates with different kinase localization and biological outcome

Aim. To determine 293 and U373 cell response and ERK1/2 activation profile after CHI3L1 or CHI3L2 treatment. Methods. Specific activation and localization of ERK1/2 kinases after CHI3L1 or CHI3L2 addition to unsupplemented cell medium were evaluated by Western blots, immunofluorescence and confocal...

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Date:2011
Main Authors: Areshkov, P.O., Avdieiev, S.S., Iershov, A.V., Kavsan, V.M.
Format: Article
Language:English
Published: Інститут молекулярної біології і генетики НАН України 2011
Series:Вiopolymers and Cell
Online Access:https://nasplib.isofts.kiev.ua/handle/123456789/155649
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Journal Title:Digital Library of Periodicals of National Academy of Sciences of Ukraine
Cite this:Stimulation of transient versus sustained ERK1/2 phosphorylation by relative chitinase-like proteins CHI3L1 and CHI3L2 correlates with different kinase localization and biological outcome / P.O. Areshkov, S.S. Avdieiev, A.V. Iershov, V.M. Kavsan // Вiopolymers and Cell. — 2011. — Т. 27, № 5. — С. 343-346. — Бібліогр.: 12 назв. — англ.

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Digital Library of Periodicals of National Academy of Sciences of Ukraine
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Summary:Aim. To determine 293 and U373 cell response and ERK1/2 activation profile after CHI3L1 or CHI3L2 treatment. Methods. Specific activation and localization of ERK1/2 kinases after CHI3L1 or CHI3L2 addition to unsupplemented cell medium were evaluated by Western blots, immunofluorescence and confocal microscopy. To determine whether CHI3L1 or CHI3L2 can enhance mitogenesis, [3H]thymidine incorporation in cellular DNA was measured. Results. The obtained results show that ERK1/2 phosphorylation was stimulated in both cell types (293 and U373 cells) following addition of CHI3L2 or CHI3L1 in dose- and time-dependent manner. Unexpectedly, in opposite to CHI3L1, the dose-dependent decreasing of measured mitogenesis parameters was observed in 293 and U373 cells. In both cell types the treatment with CHI3L2 gave more sustained than CHI3L1 MAPK-pathway activation with prolonged phospho-ERK1/2 nuclear accumulation in 293 cells. Conclusions. In contrast to the activation of ERK1/2 phosphorylation by CHI3L1 cell treatment, that leads to a proliferative signal, the activation of these kinases by CHI3L2 addition inhibits cell mitogenesis and proliferation in serum starved 293 and U373 cells. Keywords: chitinase 3-like 1 protein (CHI3L1), chitinase 3-like 2 protein (CHI3L2), MAP kinase, mitogenesis.