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  1. Artikel ; Online: Observation of inserted oxocarbonyl species in the tantalum cation-mediated activation of carbon dioxide dictated by two-state reactivity.

    Han, Jia / Liu, Pengcheng / Qiu, Binglin / Wang, Guanjun / Liu, Shilin / Zhou, Xiaoguo

    Dalton transactions (Cambridge, England : 2003)

    2023  Band 53, Heft 1, Seite(n) 171–179

    Abstract: Reductive activation of carbon dioxide ( ... ...

    Abstract Reductive activation of carbon dioxide (CO
    Sprache Englisch
    Erscheinungsdatum 2023-12-19
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1472887-4
    ISSN 1477-9234 ; 1364-5447 ; 0300-9246 ; 1477-9226
    ISSN (online) 1477-9234 ; 1364-5447
    ISSN 0300-9246 ; 1477-9226
    DOI 10.1039/d3dt03593j
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Infrared photodissociation spectroscopy of mass-selected [TaO

    Han, Jia / Yang, Yang / Qiu, Binglin / Liu, Pengcheng / Wu, Xiangkun / Wang, Guanjun / Liu, Shilin / Zhou, Xiaoguo

    Physical chemistry chemical physics : PCCP

    2023  Band 25, Heft 18, Seite(n) 13198–13208

    Abstract: We report a joint experimental and theoretical study on the structures of gas-phase [ ... ...

    Abstract We report a joint experimental and theoretical study on the structures of gas-phase [TaO
    Sprache Englisch
    Erscheinungsdatum 2023-05-10
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1476244-4
    ISSN 1463-9084 ; 1463-9076
    ISSN (online) 1463-9084
    ISSN 1463-9076
    DOI 10.1039/d3cp01384g
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Inhibition of 32Dp210 cells harboring T315I mutation by a novel derivative of emodin correlates with down-regulation of BCR-ABL and its downstream signaling pathways.

    Li, Jing / Chen, Yingyu / Chen, Buyuan / Chen, Cai / Qiu, Binglin / Zheng, Zhihong / Zheng, Jing / Liu, Tingbo / Wang, Wenfeng / Hu, Jianda

    Journal of cancer research and clinical oncology

    2014  Band 141, Heft 2, Seite(n) 283–293

    Abstract: Purpose: The clinical outcome of chronic myeloid leukemia (CML) patients has been changed dramatically due to the development of imatinib (IM). However, the emergence of IM resistance, commonly associated with point mutations within the BCR-ABL kinase ... ...

    Abstract Purpose: The clinical outcome of chronic myeloid leukemia (CML) patients has been changed dramatically due to the development of imatinib (IM). However, the emergence of IM resistance, commonly associated with point mutations within the BCR-ABL kinase domain, remains a major clinical problem. Here, we investigated the effects of E35, a novel derivative of emodin, on the IM-resistant 32Dp210-T315I cells.
    Methods: Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide and colony formation assay. Induction of apoptosis was confirmed by DNA fragmentation assay and annexin V/PI staining assay. Real-time quantitative PCR was used to access the BCR-ABL gene expression. Changes of related signaling molecules were detected through Western blot.
    Results: E35 was found to potently inhibit proliferation of 32Dp210-T315I cells with an average IC50 of 2.4 µM at 48 h. Colony formation was almost fully suppressed in 1.0 μM E35 group. DNA fragmentation and annexin V/PI staining assay exhibited the typical DNA fragmentation and the increased proportion of early apoptotic cells, respectively. The induction of apoptosis was associated with increase of Bax to Bcl-2 expression ratio and activation of caspase cascades involving decrease of pro-caspase 9 and pro-caspase 3 and increase of PARP cleavage. The protein expression of P210(BCR-ABL) and p-P210(BCR-ABL) was down-regulated in the presence of E35, although the mRNA levels remained almost unchanged. Moreover, the activation of the P210(BCR-ABL) downstream signaling pathways including CrkL, Akt/mTOR and MEK/ERK was fully suppressed by E35.
    Conclusion: Our study indicated that E35 might be a potential antileukemia agent against IM resistance in CML.
    Mesh-Begriff(e) Apoptosis/drug effects ; Benzamides/pharmacology ; Blotting, Western ; Cell Proliferation/drug effects ; Colony-Forming Units Assay ; Down-Regulation ; Drug Resistance, Neoplasm/drug effects ; Emodin/chemistry ; Emodin/pharmacology ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Mutation/genetics ; Piperazines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Pyrimidines/pharmacology ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Tumor Cells, Cultured
    Chemische Substanzen Benzamides ; Piperazines ; Protein Kinase Inhibitors ; Pyrimidines ; RNA, Messenger ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Emodin (KA46RNI6HN)
    Sprache Englisch
    Erscheinungsdatum 2014-09-14
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 134792-5
    ISSN 1432-1335 ; 0171-5216 ; 0084-5353 ; 0943-9382
    ISSN (online) 1432-1335
    ISSN 0171-5216 ; 0084-5353 ; 0943-9382
    DOI 10.1007/s00432-014-1820-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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