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941.
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Lan Yu Zeng-Fu Shang Salim Abdisalaam Kyung-Jong Lee Arun Gupta Jer-Tsong Hsieh Aroumougame Asaithamby Benjamin P.C. Chen Debabrata Saha 《Nucleic acids research》2016,44(18):8842-8854
Defects in kinetochore-microtubule (KT-MT) attachment and the spindle assembly checkpoint (SAC) during cell division are strongly associated with chromosomal instability (CIN). CIN has been linked to carcinogenesis, metastasis, poor prognosis and resistance to cancer therapy. We previously reported that the DAB2IP is a tumor suppressor, and that loss of DAB2IP is often detected in advanced prostate cancer (PCa) and is indicative of poor prognosis. Here, we report that the loss of DAB2IP results in impaired KT-MT attachment, compromised SAC and aberrant chromosomal segregation. We discovered that DAB2IP directly interacts with Plk1 and its loss inhibits Plk1 kinase activity, thereby impairing Plk1-mediated BubR1 phosphorylation. Loss of DAB2IP decreases the localization of BubR1 at the kinetochore during mitosis progression. In addition, the reconstitution of DAB2IP enhances the sensitivity of PCa cells to microtubule stabilizing drugs (paclitaxel, docetaxel) and Plk1 inhibitor (BI2536). Our findings demonstrate a novel function of DAB2IP in the maintenance of KT-MT structure and SAC regulation during mitosis which is essential for chromosomal stability. 相似文献
943.
CHARACTERIZATION AND EXPRESSION PROFILES OF FIVE POSSIBLE CYTOCHROME P450 GENES FROM Liposcelis entomophila (ENDERLEIN) (PSOCOPTERA: LIPOSCELIDIDAE)
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944.
The antagonistic regulation of abscisic acid‐inhibited root growth by brassinosteroids is partially mediated via direct suppression of ABSCISIC ACID INSENSITIVE 5 expression by BRASSINAZOLE RESISTANT 1
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Xiaorui Yang Yang Bai Jianxiu Shang Ruijiao Xin Wenqiang Tang 《Plant, cell & environment》2016,39(9):1994-2003
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Peng Li Yongyun Li Liqi Zhu Zhi Yang Jie He Lihua Wang Qingfeng Shang Hui Pan Huixue Wang Xiong Ma Bin Li Xianqun Fan Shengfang Ge Renbing Jia He Zhang 《生物化学与生物物理学报:疾病的分子基础》2018,1864(3):709-720
Liver fibrosis is overly exuberant wound healing that leads to portal hypertension or liver cirrhosis. Recent studies have demonstrated the functions of bone morphogenetic protein 9 (BMP9) in liver fibrosis, and thus, targeting liver-specific BMP9 abnormalities will become an attractive approach for developing therapeutics to treat liver fibrosis. Here, we reveal that BMP9 serves as a valuable serum diagnostic indicator and efficient therapeutic target to attenuate liver fibrogenesis. Our analysis of biopsies from liver fibrotic patients revealed that higher BMP9 levels accompanied advanced stages of liver fibrosis. In mouse models, recombinant Bmp9 overexpression accelerated liver fibrosis, and adenovirus-mediated Bmp9 knockdown attenuated liver fibrogenesis. Intriguingly, BMP9 directly stimulated hepatic stellate cell activation via the SMAD signaling pathway to enhance hepatic fibrosis. Moreover, an inhibitory monoclonal antibody targeting Bmp9 was efficacious in treatment of mice with liver fibrosis. These observations delineate a novel model in which BMP9 directly drives SMAD/ID1 signaling in hepatic stellate cells, which modulates liver fibrogenesis development. Moreover, the findings unveil a promising surrogate biomarker for the diagnosis of hepatic fibrosis, thereby representing an efficient “BMP9 neutralization” approach in alleviating hepatic fibrosis. 相似文献
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Junjie Zhang Yimin Shang Entao Wang Wenfeng Chen Philippe de Lajudie Benyin Li Chen Guo Xu Yang Jianqiang Zheng Chunzeng Liu 《Plant and Soil》2018,425(1-2):201-215