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Wei Dong
Researcher at Peking Union Medical College
Publications - 23
Citations - 466
Wei Dong is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 11, co-authored 13 publications receiving 353 citations. Previous affiliations of Wei Dong include Chinese Ministry of Health.
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Journal ArticleDOI
Transgenic expression of IL-33 activates CD8 + T cells and NK cells and inhibits tumor growth and metastasis in mice
Kun Gao,Xiaoying Li,Li Zhang,Lin Bai,Wei Dong,Kai Gao,Guiying Shi,Xianzhu Xia,Lingying Wu,Lianfeng Zhang +9 more
TL;DR: The results suggest that IL-33 stimulated NF-κB signaling and promoted the proliferation, activation and infiltration of CD8(+) T cells and NK cells, which resulted in the inhibition of pulmonary metastasis in B16 melanoma and LLC mice models.
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Knockdown of cytochrome P450 2E1 inhibits oxidative stress and apoptosis in the cTnT(R141W) dilated cardiomyopathy transgenic mice.
TL;DR: Knockdown of CYP2E1 significantly ameliorated the dilated left ventricle, thin wall, and dysfunctional contraction in the cTnTR141W and adriamycin-induced DCM mouse models and might be induced by hypoxemia in cardiomyopathy.
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Increasing the efficiency of CRISPR/Cas9-mediated precise genome editing in rats by inhibiting NHEJ and using Cas9 protein
TL;DR: It is shown that both Scr7 and Cas9 protein can increase the precise modification, relatively lower compared with nonhomologous end-joining (NHEJ) pathway and extremely expected to be improved.
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Heparin-Binding EGF-Like Growth Factor Induces Heart Interstitial Fibrosis via an Akt/mTor/p70s6k Pathway
TL;DR: Results suggest that HB-EGF induced heart fibrosis and proliferation of cardiac fibroblasts occurs through activation of the Akt/mTor/p70s6k pathway.
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Dkk3 prevents familial dilated cardiomyopathy development through Wnt pathway.
TL;DR: Dkk3 could prevent FDCM development in mice, especially in the compensatory stage, and probably through activation of the canonical and inhibition of the noncanonical Wnt pathway, which suggested that DKK3 could serve as a therapeutic target for the treatment of cardiomyopathy and heart failure.