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| 1 | Role and Mechanism of Integrin-linked Kinase in the Pathogenesis of Chronic Allograft Nephropathy显示文摘 | YuxinWang Hequn Zou Tianyu Lv Yangling Shi Ling Chen Wenying Zhou Qingqin Li | 2007 | 器官移植内科学杂志2007，2，4： | 4 |
| 2 | Deregulation of tumor suppressive ASXL1−PTEN/AKT axis in myeloid malignancies显示文摘Mutations of epigenetic regulators are pervasive in human tumors.ASXL1 is frequently mutated in myeloid malignancies.We previously found that ASXL1 forms together with BAP1 a complex that can deubiquitinylate mono-ubiquitinylated lysine 119 on histone H2A(H2AK119ub1),a Polycomb repressive mark.However,a complete mechanistic understanding of ASXL1 in transcriptional regulation and tumor suppression remains to be defined.Here,we find that depletion of Asxl1 confers murine 32D cells to IL3-independent growth at least partly due to sustained activation of PI3K/AKT signaling.Consistently,Asxl1 is critical for the transcriptional activation of Pten,a key negative regulator of AKT activity.Then we confirm that Asxl1 is specifically enriched and required for H2AK119 deubiquitylation at the Pten promoter.Interestingly,ASXL1 and PTEN expression levels are positively correlated in human blood cells and ASXL1 mutations are associated with lower expression levels of PTEN in human myeloid malignancies.Furthermore,malignant cells with ASXL1 downregulation or mutations exhibit higher sensitivity to the AKT inhibitor MK2206.Collectively,this study has linked the PTEN/AKT signaling axis to deregulated epigenetic changes in myeloid malignancies.It also provides a rationale for mechanism-based therapy for patients with ASXL1 mutations. | Lei Cao Xianyou Xia Yu Kong Fengqin Jia Bo Yuan Rui Li Qian Li YuxinWang Mingrui Cui Zhongye Dai Huimin Zheng Jesper Christensen Yuan Zhou Xudong Wu | 2020 | Journal of Molecular Cell Biology2020，12，9： | 0 |
| 3 | Influence of mycophenolate mofetil (MMF) upon thematuration and allo-stimulatory activity of cultured progenitors of dendritic cells and the effectson the tolerance induction in allograft recipients显示文摘To investigate the influence of mycophenolate mofetil (MMF) upon the maturation and the allo-stimulatory activity of cultured progenitors of dendritic cells (DCp), and to evaluate the effects of the pre-treated dentritic cells of recipients with MMF on the tolerance induction as well as its possible mechanism, GM-CSF and MMF were added to the in vitro cultured progenitor cells, and the immuno-phenotypical analysis was performed by means of flow cytometry. The secretion of IL-12 was detected by ELISA and the stimulatory activities of DCp on allogeneic T cells were observed by mixed lymphocyte reaction. Twenty-four C57BL/6 mice were divided into 3 groups (each with 8 mice), in which group A of mice accepted allografts of heart from BALB/c mice, group B of mice had received untreated DCp from donors of BALB/c mice 7 days before transplantation, and C57BL/6 mice in group C were treated by injection with MMF-treated allografts of heart from BALB/c mice 7 days before transplantation. The survival times of allografts and the changes of the cytokine levels in sera of the recipient mice were observed after transplantation. The experimental results showed that MMF could significantly inhibit the expressions of the co-stimulatory molecules CD80 and CD86 on DCs and the secretion of IL-12 and the allo-stimulatory activities of DCs were also markedly inhibited. The survival times of allografts in group B of mice were longer than those in group A, while the group C showed the longest survival times of allografts, with a marked reduction in the production of the Th1 type cytokines. It is evident that MMF has a suppressive effect on the maturation and allo-stimulatory activities of the cultured dendritic cell progenitors, thus leading to a donor specific tolerance in heart-transplanted recipients. | CONGHUIHAN YUXINWANG QINGLIANG MINGZHANG YINGWANG MINGYIN ZHILIANMING KELIZHENG | 2005 | Journal of Microbiology and Immunology2005，3，1： | 0 |
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