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dc.contributor.author | Makeeva A. | |
dc.contributor.author | Rodriguez-Montesinos J. | |
dc.contributor.author | Zelenikhin P. | |
dc.contributor.author | Nesmelov A. | |
dc.contributor.author | Preissner K. | |
dc.contributor.author | Cabrera-Fuentes H. | |
dc.contributor.author | Ilinskaya O. | |
dc.date.accessioned | 2018-04-05T07:09:27Z | |
dc.date.available | 2018-04-05T07:09:27Z | |
dc.date.issued | 2017 | |
dc.identifier.issn | 0962-9351 | |
dc.identifier.uri | http://dspace.kpfu.ru/xmlui/handle/net/129750 | |
dc.description.abstract | © Copyright 2017 Anna Makeeva et al. Extracellular bacterial ribonucleases such as binase from Bacillus pumilus possess cytotoxic activity against tumor cells with a potential for clinical application. Moreover, they may induce activation of tumor-derived macrophages either into the M1-phenotype with well-documented functions in the regulation of the antitumor immune response or into M2-macrophages that may stimulate tumor growth, metastasis, and angiogenesis. In this study, binase or endogenous RNase1 (but not RNA or short oligonucleotides) stimulated the expression of activated NF-κB p65 subunit in macrophages. Since no changes in MyD88 and TRIF adaptor protein expression were observed, toll-like receptors may not be involved in RNase-related NF-κB pathway activation. In addition, short exposure (0.5 hr) to binase induced the release of cytokines such as IL-6, MCP-1, or TNF-α (but not IL-4 and IL-10), indicative for the polarization into antitumor M1-macrophages. Thus, we revealed increased expression of activated NF-κB p65 subunit in macrophages upon stimulation by binase and RNase1, but not RNA or short oligonucleotides. | |
dc.relation.ispartofseries | Mediators of Inflammation | |
dc.title | Antitumor macrophage response to bacillus pumilus ribonuclease (Binase) | |
dc.type | Article | |
dc.relation.ispartofseries-volume | 2017 | |
dc.collection | Публикации сотрудников КФУ | |
dc.source.id | SCOPUS09629351-2017-2017-SID85036662282 |