Longfei Xia
Jiangsu University
13 Papers
3 Citations
Longfei Xia is an academic researcher from Jiangsu University. The author has contributed to research in topics: Beta 2-Glycoprotein I & Signal transduction. The author has an hindex of 7, co-authored 13 publications.
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Papers
TF/FVIIa/PAR2 promotes cell proliferation and migration via PKCα and ERK-dependent c-Jun/AP-1 pathway in colon cancer cell line SW620
TL;DR: It is suggested that c-Jun/AP-1 activation is required for TF/FVIIa/PAR2-induced SW620 cell proliferation and migration and pharmacological inhibition of this pathway might be a novel strategy for colon cancer therapy.
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Anti-β(2)GPI/β(2)GPI induced TF and TNF-α expression in monocytes involving both TLR4/MyD88 and TLR4/TRIF signaling pathways
TL;DR: The results show that treatment of monocytes or THP-1 cells with anti-β(2)GPI/β( 2)G PI complex could increase TF, MyD88, TRIF as well as TNF-α (tumor necrosis factor alpha) expression and TLR4 and its adaptors might be molecular targets for therapy of antiphospholipid syndrome.
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Both NF-κB and c-Jun/AP-1 involved in anti-β2GPI/β2GPI-induced tissue factor expression in monocytes
Longfei Xia,Hong Zhou,Lichao Hu,Hongxiang Xie,Ting Wang,Xu Ya,Jingjing Liu,Xiaolei Zhang,Jinchuan Yan +8 more
TL;DR: The results indicate that both NF-κB and c-Jun/AP-1 can be activated and play important roles in the process of anti-β2GPI/β2 GPI-induced TF expression in monocytes, thereby contributing to the pathological processes of antiphospholipid syndrome.
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Activation of MAPKs in the anti-β2GPI/β2GPI-induced tissue factor expression through TLR4/IRAKs pathway in THP-1 cells
TL;DR: It is demonstrated that MAPKs were the crucial downstream targets of the anti-β(2)GPI/β( 2)G PI-triggered TLR4 signaling pathways in THP-1 cells, which may also promote better understanding of the pathogenesis of antiphospholipid syndrome.
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The Effects of NF-κB and c-Jun/AP-1 on the Expression of Prothrombotic and Proinflammatory Molecules Induced by Anti-β2GPI in Mouse
TL;DR: Results indicate that both NF-κB and c-Jun/AP-1 are involved in regulating anti-β2GPI-induced expression of prothrombotic and proinflammatory molecules in vivo and may be beneficial for the prevention and treatment of thrombosis and inflammation in patients with APS.