Protein kinase C and toll-like receptor signaling.

Protein kinase C and toll-like receptor signaling.
复制标题

DOI:
10.4061/2011/537821
复制
发表时间:
2011
期刊:
影响因子:
--
通讯作者:
Lennartz MR
Lennartz MR
中科院分区:
其他
文献类型:
--
作者:
Loegering DJ;Lennartz MR

文献摘要

被引文献

相似文献

蛋白激酶C(PKC)是一个激酶家族,与多种疾病有关,包括癌症和心血管疾病。PKC亚型在这些疾病状态中可能具有不同的,有时是相反的作用。Toll样受体(TLR)是结合病原体并刺激细胞因子分泌的模式识别受体家族。长期以来,人们已经知道PKC抑制剂减少巨噬细胞的LPS刺激的细胞因子分泌,将PKC活化与TLR信号传导联系起来。最近的研究表明,PKC-α、-δ、-ε和-β直接参与TLR通路的多个步骤。它们与TLR或受体复合物的近端组分结合。这些亚型还参与MAPK、RhoA、TAK 1和NF-κB的下游活化。因此,PKC活化密切参与TLR信号传导和先天免疫应答。
Protein kinase C (PKC) is a family of kinases that are implicated in a plethora of diseases, including cancer and cardiovascular disease. PKC isoforms can have different, and sometimes opposing, effects in these disease states. Toll-like receptors (TLRs) are a family of pattern recognition receptors that bind pathogens and stimulate the secretion of cytokines. It has long been known that PKC inhibitors reduce LPS-stimulated cytokine secretion by macrophages, linking PKC activation to TLR signaling. Recent studies have shown that PKC-α, -δ, -ε, and -ζ are directly involved in multiple steps in TLR pathways. They associate with the TLR or proximal components of the receptor complex. These isoforms are also involved in the downstream activation of MAPK, RhoA, TAK1, and NF-κB. Thus, PKC activation is intimately involved in TLR signaling and the innate immune response.