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IL-32–dependent effects of IL-1β on endothelial cell functions
Increasing evidence demonstrates that interleukin (IL)–32 is a pro-inflammatory cytokine, inducing IL-1α, IL-1β, IL-6, tumor necrosis factor (TNF)–α, and chemokines via nuclear factor (NF)–κB, p38 mitogen-activated protein kinase (MAPK), and activating protein (AP)-1 activation. Here we report that...
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| Main Authors: | , , , , , |
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| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
National Academy of Sciences
2009
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2656174/ https://ncbi.nlm.nih.gov/pubmed/19228941 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0813334106 |
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