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NF-κB signaling pathway as target for antiplatelet activity
| dc.contributor.author | Rojas, Armando | |
| dc.contributor.author | Fuentes, Eduardo | |
| dc.contributor.author | Palomo, Iván | |
| dc.date.accessioned | 2017-10-05T17:37:46Z | |
| dc.date.available | 2017-10-05T17:37:46Z | |
| dc.date.issued | 2016 | |
| dc.identifier.uri | http://repositorio.ucm.cl/handle/ucm/356 | |
| dc.description.abstract | In different nucleated cells, NF-κB has long been considered a prototypical proinflammatory signaling pathway with the expression of proinflammatory genes. Although platelets lack a nucleus, a number of functional transcription factors are involved in activated platelets, such as NF-κB. In platelet activation NF-κB regulation events include IKKβ phosphorylation, IκBα degradation, and p65 phosphorylation. Multiple pathways contribute to platelet activation and NF-κB is a common pathway in this activation. Therefore, in platelet activation the modulation of NF-κB pathway could be a potential new target in the treatment of inflammation-related vascular disease therapy (antiplatelet and antithrombotic activities). | es_CL |
| dc.language.iso | en | es_CL |
| dc.rights | Atribución-NoComercial-SinDerivadas 3.0 Chile | * |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | * |
| dc.source | Blood Reviews, 30(4), 309-315 | es_CL |
| dc.subject | Platelet activation | es_CL |
| dc.subject | NF-κB | es_CL |
| dc.subject | Thrombin | es_CL |
| dc.subject | sCD40L/CD40L | es_CL |
| dc.subject | Toll-like receptors | es_CL |
| dc.subject | RAGE | es_CL |
| dc.subject | PPARs | es_CL |
| dc.title | NF-κB signaling pathway as target for antiplatelet activity | es_CL |
| dc.type | Article | es_CL |
| dc.ucm.facultad | Facultad de Medicina | es_CL |
| dc.ucm.indexacion | Scopus | es_CL |
| dc.ucm.indexacion | Isi | es_CL |
| dc.ucm.uri | sibib2.ucm.cl:2066/science/article/pii/S0268960X16000138 | es_CL |
| dc.ucm.doi | doi.org/10.1016/j.blre.2016.03.002 | es_CL |
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Excepto si se señala otra cosa, la licencia de la publicación se describe como Atribución-NoComercial-SinDerivadas 3.0 Chile