Institution
Dalian Medical University
Education•Dalian, China•
About: Dalian Medical University is a education organization based out in Dalian, China. It is known for research contribution in the topics: Cancer & Apoptosis. The organization has 15623 authors who have published 9993 publications receiving 164145 citations.
Topics: Cancer, Apoptosis, Cell growth, Metastasis, PI3K/AKT/mTOR pathway
Papers published on a yearly basis
Papers
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TL;DR: CKIP-1 inhibits macrophage proliferation specifically at the late stage after M-CSF stimulation by inhibiting TRAF6-mediated Akt activation, and results in increased proliferation and decreased apoptosis of macrophages in vitro and CK IP-1−/− mice spontaneously develop a macrophagous splenomegaly and myeloproliferation.
Abstract: Macrophages play pivotal roles in development, homeostasis, tissue repair and immunity. Macrophage proliferation is promoted by macrophage colony-stimulating factor (M-CSF)-induced Akt signaling; yet, how this process is terminated remains unclear. Here, we identify casein kinase 2-interacting protein-1 (CKIP-1) as a novel inhibitor of macrophage proliferation. In resting macrophages, CKIP-1 was phosphorylated at Serine 342 by constitutively active GSK3β, the downstream target of Akt. This phosphorylation triggers the polyubiquitination and proteasomal degradation of CKIP-1. Upon M-CSF stimulation, Akt is activated by CSF-1R-PI3K and then inactivates GSK3β, leading to the stabilization of CKIP-1 and β-catenin proteins. β-catenin promotes the expression of proliferation genes including cyclin D and c-Myc. CKIP-1 interacts with TRAF6, a ubiquitin ligase required for K63-linked ubiquitination and plasma membrane recruitment of Akt, and terminates TRAF6-mediated Akt activation. By this means, CKIP-1 inhibits macrophage proliferation specifically at the late stage after M-CSF stimulation. Furthermore, CKIP-1 deficiency results in increased proliferation and decreased apoptosis of macrophages in vitro and CKIP-1−/− mice spontaneously develop a macrophage-dominated splenomegaly and myeloproliferation. Together, these data demonstrate that CKIP-1 plays a critical role in the regulation of macrophage homeostasis by inhibiting TRAF6-mediated Akt activation.
58 citations
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TL;DR: There are several summaries which are related to the current research progress and application of metabolomics on biomarkers of liver diseases that have broad prospects to explore the specific and sensitive biomarkersof liver diseases with metabolomics.
Abstract: Metabolomics as the new omics technique develops after genomics, transcriptomics, and proteomics and has rapid development at present. Liver diseases are worldwide public health problems. In China, chronic hepatitis B and its secondary diseases are the common liver diseases. They can be diagnosed by the combination of history, virology, liver function, and medical imaging. However, some patients seldom have relevant physical examination, so the diagnosis may be delayed. Many other liver diseases, such as drug-induced liver injury (DILI), alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), and autoimmune liver diseases, still do not have definite diagnostic markers; the diagnosis consists of history, medical imaging, and the relevant score. As a result, the clinical work becomes very complex. So it has broad prospects to explore the specific and sensitive biomarkers of liver diseases with metabolomics. In this paper, there are several summaries which are related to the current research progress and application of metabolomics on biomarkers of liver diseases.
58 citations
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TL;DR: The hospitalization rates of VTE increased steadily, and the mortality declined, and higher mortality rates were found in patients with cancer and Charlson Comorbidity Index scores > 2.
58 citations
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TL;DR: The results suggest that PB exerts oxidative stress and genotoxic effects in HepG2 cells, possibly through the mechanisms of lysosomal damage, an earlier event preceding the oxidative DNA damage.
58 citations
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TL;DR: Evidence is provided that neratinib-induced down regulation of ErbB2 occurs through ubiquitin-mediated endocytic sorting and lysosomal degradation, which provides novel insights into the mechanism of ErBB2 inhibition by Neratinib.
58 citations
Authors
Showing all 15657 results
Name | H-index | Papers | Citations |
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Jing Wang | 184 | 4046 | 202769 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Melitta Schachner | 135 | 861 | 67304 |
Yan Zhang | 107 | 2410 | 57758 |
Jau-Shyong Hong | 93 | 474 | 37172 |
Li Zhang | 92 | 918 | 35648 |
Charles G. Eberhart | 84 | 444 | 29920 |
Ying Lu | 83 | 343 | 24913 |
You-Lin Qiao | 78 | 595 | 23919 |
Wei Wei | 75 | 1068 | 29415 |
Weidong Le | 74 | 287 | 22551 |
Jin-Tai Yu | 66 | 439 | 20020 |
Wei Jiang | 65 | 660 | 18932 |
Lan Tan | 62 | 387 | 13828 |
Hua Li | 62 | 849 | 17933 |