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Research paper | 31-July-2017

Upregulation of CCL3/MIP‑1alpha regulated by MAPKs and NF‑kappaB mediates microglial inflammatory response in LPS‑induced brain injury

and phosphorylation of MAPKs in the brains of rats 6, 24, and 72 h after LPS administration. Additionally, LPS‑treated rats were administered an anti‑MIP‑1alpha neutralizing antibody, and the microglial reaction and the expression of both cyclooxygenase‑2 and inducible nitric oxide synthase (iNOS) were analyzed. We finally evaluated the effect of an inhibitor of P38 MAPK, an inhibitor of ERK1/2, or an inhibitor of NF‑kappaB, on the levels of CCL3/MIP‑1alpha protein and numbers of microglia in the

Xiaobo Zhu, Dee Wei, Ou Chen, Zhaohua Zhang, Jiang Xue, Shanying Huang, Weiwei Zhu, Yibiao Wang

Acta Neurobiologiae Experimentalis, Volume 76 , ISSUE 4, 304–317

research-article | 18-March-2020

Transcriptomic analysis of Bursaphelenchus xylophilus treated by a potential phytonematicide, punicalagin

modification, protein turnover and chaperones might be the main nematotoxic targets of punicalagin. The KEGG annotation aligned the DEGs to 279 pathways. The top 10 pathways that were related to life activities of B. xylophilus included oxidative phosphorylation (38 DEGs), endocytosis (35 DEGs), spliceosome (31 DEGs), ribosome (29 DEGs), RNA transport (28 DEGs), carbon metabolism (27 DEGs), ubiquitin mediated proteolysis (24 DEGs), MAPK signaling pathway (24 DEGs), peroxisome (24 DEGs) and biosynthesis of

Qun-Qun Guo, Gui-Cai Du, Ting-Ting Zhang, Mei-Juan Wang, Chao Wang, Hong-Tao Qi, Rong-Gui Li

Journal of Nematology, Volume 52 , 1–14

Mini Review | 15-March-2016

The Functions of Effector Proteins in Yersinia Virulence

Yersinia species are bacterial pathogens that can cause plague and intestinal diseases after invading into human cells through the Three Secre­tion System (TTSS). The effect of pathogenesis is mediated by Yersinia outer proteins (Yop) and manifested as down-regulation of the cytokine genes expression by inhibiting nuclear factor-κ-gene binding (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. In addition, its pathogenesis can also manipulate the disorder of host

Linglin Zhang, Meng Mei, Chan Yu, Wenwen Shen, Lixin Ma, Jiewang He, Li Yi

Polish Journal of Microbiology, Volume 65 , ISSUE 1, 5–12

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