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结节蛋白作为一种免疫蛋白,通过与p38丝裂原活化蛋白激酶相互作用增强感染诱导的细胞增殖。

Noduler an immune protein augments infection-induced cell proliferation through cross-talking with p38 MAPK.

作者信息

Satyavathi Valluri V, Narra Deepa, Nagaraju Javaregowda

机构信息

Centre of Excellence for Genetics and Genomics of Silkmoths, Centre for DNA Fingerprinting and Diagnostics, Hyderabad 500 001, India.

Centre of Excellence for Genetics and Genomics of Silkmoths, Centre for DNA Fingerprinting and Diagnostics, Hyderabad 500 001, India.

出版信息

Immunobiology. 2016 Feb;221(2):387-97. doi: 10.1016/j.imbio.2015.09.018. Epub 2015 Sep 12.

DOI:10.1016/j.imbio.2015.09.018
PMID:26433868
Abstract

Noduler, an immune protein that mediates nodule formation by binding to specific bacteria and hemocytes was previously reported in the wild tasar silkworm, Antheraea mylitta. However, the molecular mechanism underlying nodulation in lepidopterans remains unclear. The present study is performed to investigate the functional connection between Noduler with various signalling pathways. It was observed that Noduler is an upstream factor in the phenoloxidase cascade and its knockdown has no direct effect on Toll/Imd pathway inducible genes. Additionally, Noduler was shown to stimulate cell proliferation via activation of p38 mitogen-activated protein kinase (MAPK). Inhibition of p38 in the infected hemocytes cultured in vitro resulted in reduced cell proliferation and melanization. These results suggest that Noduler mediates nodulation via p38/MAPK signalling. This is the first report implicating the p38 MAPK signalling pathway in the nodulation response of insects.

摘要

结瘤蛋白是一种免疫蛋白,它通过与特定细菌和血细胞结合来介导结节形成,此前在野生柞蚕(Antheraea mylitta)中已有报道。然而,鳞翅目昆虫结节形成的分子机制仍不清楚。本研究旨在探讨结瘤蛋白与各种信号通路之间的功能联系。研究发现,结瘤蛋白是酚氧化酶级联反应中的上游因子,其敲低对Toll/Imd通路诱导基因没有直接影响。此外,结瘤蛋白通过激活p38丝裂原活化蛋白激酶(MAPK)来刺激细胞增殖。在体外培养的受感染血细胞中抑制p38会导致细胞增殖和黑化减少。这些结果表明,结瘤蛋白通过p38/MAPK信号通路介导结节形成。这是首次报道p38 MAPK信号通路与昆虫结节形成反应有关。

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