首页> 外文期刊>Cellular Signalling >Repeat exposure to polyinosinic:polycytidylic acid induces TLR3 expression via JAK-STAT signaling and synergistically potentiates NF kappa B-RelA signaling in ARPE-19 cells
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Repeat exposure to polyinosinic:polycytidylic acid induces TLR3 expression via JAK-STAT signaling and synergistically potentiates NF kappa B-RelA signaling in ARPE-19 cells

机译:重复暴露于多胞苷:聚环酰基酸诱导TLR3表达通过JAK-STAT信号传导和协同增强NF Kappa B-Rela信号传导在ARPE-19细胞中

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摘要

Dry age-related macular degeneration (AMD), accounting for approximately 90% of AMD cases, is characterized by photoreceptor death, retinal pigment epithelium (RPE) dysfunction and, ultimately, geographic atrophy - the localized death of RPE leading to loss of the center of the visual field. The pathological etiology of AMD is multifactorial, but innate immune signaling and inflammation are involved in early stages of the disease. Although numerous single-nucleotide polymorphisms in innate immune genes are associated with dry AMD, no single gene appears to cause dry AMD.
机译:干燥年龄相关的黄斑变性(AMD),占AMD病例的约90%,以感光死亡,视网膜颜料上皮(RPE)功能障碍以及最终,地理萎缩 - RPE的局部死亡导致中心失去了 视野。 AMD的病因病因是多因素,但先天免疫信号传导和炎症涉及疾病的早期阶段。 虽然在先天免疫基因中的许多单核苷酸多态性与干燥AMD有关,但没有单一基因似乎引起干燥AMD。

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