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  • Oxford University Press (OUP)  (36)
  • Wang, Chao  (36)
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  • Oxford University Press (OUP)  (36)
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  • 1
    Online Resource
    Online Resource
    Operando surface science methodology reveals surface effect in charge storage electrodes
    Oxford University Press (OUP) ; 2021
    In:  National Science Review Vol. 8, No. 3 ( 2021-03-19)
    Details
    In: National Science Review, Oxford University Press (OUP), Vol. 8, No. 3 ( 2021-03-19)
    Abstract: Surface and interface play critical roles in energy storage devices, calling for operando characterization techniques to probe the electrified surfaces/interfaces. In this work, surface science methodology, including electron spectroscopy and scanning probe microscopy, has been successfully applied to visualize electrochemical processes at operating electrode surfaces in an Al/graphite model battery. Intercalation of anions together with cations is directly observed in the surface region of a graphite electrode with tens of nanometers thickness, the concentration of which is one order higher than that in bulk. An intercalation pseudocapacitance mechanism and a double specific capacity in the electrode surface region are expected based on the super-dense intercalants and anion/cation co-intercalation, which are in sharp contrast to the battery-like mechanism in the electrode bulk. The distinct electrochemical mechanism at the electrode surface is verified by performance tests of real battery devices, showing that a surface-dominant, nanometer-thick graphite cathode outperforms a bulk-dominant, micrometer-thick graphite cathode. Our findings highlight the important surface effect of working electrodes in charge storage systems.
    Type of Medium: Online Resource
    ISSN: 2095-5138 , 2053-714X
    URL: Article
    DOI: 10.1093/nsr/nwaa289
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2745465-4
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  • 2
    Online Resource
    Online Resource
    A novel approach for monitoring TGF-β signaling in vivo in colon cancer
    Oxford University Press (OUP) ; 2021
    In:  Carcinogenesis Vol. 42, No. 4 ( 2021-04-30), p. 631-639
    Details
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 42, No. 4 ( 2021-04-30), p. 631-639
    Abstract: The TGF-β receptor kinase inhibitors (TRKI) have been reported to inhibit tumorigenicity in colon cancer. However, there is no direct evidence showing that these inhibitors function through inhibiting the TGF-β- mediated tumor-promoting effects in vivo. We established a TGF-β inducible reporter system by inserting a luciferase reporter gene to the vector downstream of TGF-β-inducible promoter elements, and transfected it into colon cancer cell lines. TRKIs SB431542 and LY2109761 were used to treat TGF-β inducible cells in vitro and in vivo. The luciferase activity was induced 5.24-fold by TGF-β in CT26 inducible cells, while it was marginally changed in MC38 inducible cells lacking Smad4 expression. Temporary treatment of mice with SB431542 inhibited the TGF-β pathway and TGF-β induced bioluminescence activity in vivo. Long-term treatment with LY2109761 inhibited tumorigenicity and liver metastasis in vivo in concomitant with reduced luciferase activity in the tumor. In this study, we established a model to monitor the TGF-β pathway in vivo and to compare the antitumor effects of TRKIs. Based on this novel experimental tool, we provided direct evidences that LY2109761 inhibits tumorigenicity and liver metastasis by blocking the pro-oncogenic functions of TGF-β in vivo.
    Type of Medium: Online Resource
    ISSN: 0143-3334 , 1460-2180
    URL: Article
    DOI: 10.1093/carcin/bgaa142
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1474206-8
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  • 3
    Online Resource
    Online Resource
    Elevated expression of the membrane-anchored serine protease TMPRSS11E in NSCLC progression
    Oxford University Press (OUP) ; 2022
    In:  Carcinogenesis Vol. 43, No. 11 ( 2022-12-25), p. 1092-1102
    Details
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 43, No. 11 ( 2022-12-25), p. 1092-1102
    Abstract: TMPRSS11E was found to be upregulated in human nonsmall cell lung cancer samples (NSCLC) and cell lines, and high expression was associated with poor survival of NSCLC patients. The results of in vitro and in vivo experiments showed that overexpressing TMPRSS11E resulted in A549 cell proliferation and migration promotion, while the TMPRSS11E S372A mutant with the mutated catalytic domain lost the promoting function. In addition, in mouse xenograft models, silencing TMPRSS11E expression inhibited the growth of 95D cell-derived tumors. To explore the mechanism of marked upregulation of TMPRSS11E in NSCLC cells, promoter analysis, EMSA, and ChIP assays were performed. STAT3 was identified as the transcription factor responsible for TMPRSS11E transcription. Moreover, the purified recombinant TMPRSS11E catalytic domain exhibited enzymatic activity for the proteolytic cleavage of PAR2. Recombinant TMPRSS11E catalytic domain incubation further activated the PAR2-EGFR-STAT3 pathway. These findings established a mechanism of TMPRSS11E-PAR2-EGFR-STAT3 positive feedback, and the oncogenic role of TMPRSS11E as a PAR2 modulator in NSCLC was revealed.
    Type of Medium: Online Resource
    ISSN: 0143-3334 , 1460-2180
    URL: Article
    DOI: 10.1093/carcin/bgac069
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1474206-8
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  • 4
    Online Resource
    Online Resource
    SLX4IP acts with SLX4 and XPF–ERCC1 to promote interstrand crosslink repair
    Oxford University Press (OUP) ; 2019
    In:  Nucleic Acids Research Vol. 47, No. 19 ( 2019-11-04), p. 10181-10201
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 47, No. 19 ( 2019-11-04), p. 10181-10201
    Abstract: Interstrand crosslinks (ICLs) are highly toxic DNA lesions that are repaired via a complex process requiring the coordination of several DNA repair pathways. Defects in ICL repair result in Fanconi anemia, which is characterized by bone marrow failure, developmental abnormalities, and a high incidence of malignancies. SLX4, also known as FANCP, acts as a scaffold protein and coordinates multiple endonucleases that unhook ICLs, resolve homologous recombination intermediates, and perhaps remove unhooked ICLs. In this study, we explored the role of SLX4IP, a constitutive factor in the SLX4 complex, in ICL repair. We found that SLX4IP is a novel regulatory factor; its depletion sensitized cells to treatment with ICL-inducing agents and led to accumulation of cells in the G2/M phase. We further discovered that SLX4IP binds to SLX4 and XPF–ERCC1 simultaneously and that disruption of one interaction also disrupts the other. The binding of SLX4IP to both SLX4 and XPF–ERCC1 not only is vital for maintaining the stability of SLX4IP protein, but also promotes the interaction between SLX4 and XPF–ERCC1, especially after DNA damage. Collectively, these results demonstrate a new regulatory role for SLX4IP in maintaining an efficient SLX4–XPF–ERCC1 complex in ICL repair.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkz769
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Genetic vulnerabilities upon inhibition of DNA damage response
    Oxford University Press (OUP) ; 2021
    In:  Nucleic Acids Research Vol. 49, No. 14 ( 2021-08-20), p. 8214-8231
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 49, No. 14 ( 2021-08-20), p. 8214-8231
    Abstract: Because of essential roles of DNA damage response (DDR) in the maintenance of genomic integrity, cellular homeostasis, and tumor suppression, targeting DDR has become a promising therapeutic strategy for cancer treatment. However, the benefits of cancer therapy targeting DDR are limited mainly due to the lack of predictive biomarkers. To address this challenge, we performed CRISPR screens to search for genetic vulnerabilities that affect cells’ response to DDR inhibition. By undertaking CRISPR screens with inhibitors targeting key DDR mediators, i.e. ATR, ATM, DNAPK and CHK1, we obtained a global and unbiased view of genetic interactions with DDR inhibition. Specifically, we identified YWHAE loss as a key determinant of sensitivity to CHK1 inhibition. We showed that KLHL15 loss protects cells from DNA damage induced by ATM inhibition. Moreover, we validated that APEX1 loss sensitizes cells to DNAPK inhibition. Additionally, we compared the synergistic effects of combining different DDR inhibitors and found that an ATM inhibitor plus a PARP inhibitor induced dramatic levels of cell death, probably through promoting apoptosis. Our results enhance the understanding of DDR pathways and will facilitate the use of DDR-targeting agents in cancer therapy.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkab643
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Variation of nitric oxide emission potential in plants: a possible link to leaf N content and net photosynthetic activity
    Oxford University Press (OUP) ; 2015
    In:  Journal of Plant Ecology Vol. 8, No. 3 ( 2015-6), p. 313-320
    Details
    In: Journal of Plant Ecology, Oxford University Press (OUP), Vol. 8, No. 3 ( 2015-6), p. 313-320
    Type of Medium: Online Resource
    ISSN: 1752-993X , 1752-9921
    URL: Article
    DOI: 10.1093/jpe/rtu015
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
    detail.hit.zdb_id: 2381013-0
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Cell-to-cell natural transformation in Bacillus subtilis facilitates large scale of genomic exchanges and the transfer of long continuous DNA regions
    Oxford University Press (OUP) ; 2023
    In:  Nucleic Acids Research Vol. 51, No. 8 ( 2023-05-08), p. 3820-3835
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 51, No. 8 ( 2023-05-08), p. 3820-3835
    Abstract: Natural transformation is one of the major mechanisms of horizontal gene transfer. Although it is usually studied using purified DNA in the laboratory, recent studies showed that many naturally competent bacteria acquired exogenous DNA from neighboring donor cells. Our previous work indicates that cell-to-cell natural transformation (CTCNT) using two different Bacillus subtilis strains is a highly efficient process; however, the mechanism is unclear. In this study, we further characterized CTCNT and mapped the transferred DNA in the recombinants using whole genome sequencing. We found that a recombinant strain generated by CTCNT received up to 66 transferred DNA segments; the average length of acquired continuous DNA stretches was approximately 27 kb with a maximum length of 347 kb. Moreover, up to 1.54 Mb genomic DNA (37% of the chromosome) was transferred from the donors into one recipient cell. These results suggest that B. subtilis CTCNT facilitates horizontal gene transfer by increasing the transfer of DNA segments and fostering the exchange of large continuous genomic regions. This indicates that the potency of bacterial natural transformation is underestimated using traditional approaches and reveals that DNA donor cells may play an important role in the transformation process in natural environments.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkad138
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Genome-wide CRISPR screens reveal cyclin C as synthetic survival target of BRCA2
    Oxford University Press (OUP) ; 2021
    In:  Nucleic Acids Research Vol. 49, No. 13 ( 2021-07-21), p. 7476-7491
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 49, No. 13 ( 2021-07-21), p. 7476-7491
    Abstract: Poly (ADP-ribose) polymerase inhibitor (PARPi)-based therapies initially reduce tumor burden but eventually lead to acquired resistance in cancer patients with BRCA1 or BRCA2 mutation. To understand the potential PARPi resistance mechanisms, we performed whole-genome CRISPR screens to discover genetic alterations that change the gene essentiality in cells with inducible depletion of BRCA2. We identified that several RNA Polymerase II transcription Mediator complex components, especially Cyclin C (CCNC) as synthetic survival targets upon BRCA2 loss. Total mRNA sequencing demonstrated that loss of CCNC could activate the transforming growth factor (TGF)-beta signaling pathway and extracellular matrix (ECM)-receptor interaction pathway, however the inhibition of these pathways could not reverse cell survival in BRCA2 depleted CCNC-knockout cells, indicating that the activation of these pathways is not required for the resistance. Moreover, we showed that the improved survival is not due to restoration of homologous recombination repair although decreased DNA damage signaling was observed. Interestingly, loss of CCNC could restore replication fork stability in BRCA2 deficient cells, which may contribute to PARPi resistance. Taken together, our data reveal CCNC as a critical genetic determinant upon BRCA2 loss of function, which may help the development of novel therapeutic strategies that overcome PARPi resistance.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkab540
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Plant-on-chip: Core morphogenesis processes in the tiny plant Wolffia australiana
    Oxford University Press (OUP) ; 2023
    In:  PNAS Nexus Vol. 2, No. 5 ( 2023-05-02)
    Details
    In: PNAS Nexus, Oxford University Press (OUP), Vol. 2, No. 5 ( 2023-05-02)
    Abstract: A plant can be thought of as a colony comprising numerous growth buds, each developing to its own rhythm. Such lack of synchrony impedes efforts to describe core principles of plant morphogenesis, dissect the underlying mechanisms, and identify regulators. Here, we use the minimalist known angiosperm to overcome this challenge and provide a model system for plant morphogenesis. We present a detailed morphological description of the monocot Wolffia australiana, as well as high-quality genome information. Further, we developed the plant-on-chip culture system and demonstrate the application of advanced technologies such as single-nucleus RNA-sequencing, protein structure prediction, and gene editing. We provide proof-of-concept examples that illustrate how W. australiana can decipher the core regulatory mechanisms of plant morphogenesis.
    Type of Medium: Online Resource
    ISSN: 2752-6542
    URL: Article
    DOI: 10.1093/pnasnexus/pgad141
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 3120703-0
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  • 10
    Online Resource
    Online Resource
    Integrity of zinc finger motifs in PML protein is necessary for inducing its degradation by antimony
    Oxford University Press (OUP) ; 2019
    In:  Metallomics Vol. 11, No. 8 ( 2019-08-01), p. 1419-1429
    Details
    In: Metallomics, Oxford University Press (OUP), Vol. 11, No. 8 ( 2019-08-01), p. 1419-1429
    Abstract: Antimony (Sb) belongs to the same group as arsenic (As) in the periodic table, and both share similar characteristics. However, Sb2O3 (SbIII) has no methylation capacity, unlike arsenic trioxide (As2O3). In the present study, we determined the effect of SbIII on NB4 cells and found that antimony could induce PML-RARα fusion protein degradation, reorganization of PML-NBs, and NB4 cell differentiation with low cytotoxicity. On the other hand, zinc finger motifs in PML protein are considered to be a key target binding site for arsenic-induced PML-RARα protein degradation. Interestingly, antimony and arsenic lost their ability to degrade PML-RARα fusion protein in NB4 cells following pretreatment with phenanthroline (i.e., chelator of zinc ions), indicating that the integrity of zinc finger motifs in PML-RARα fusion protein is a fundamental condition for inducing the protein's degradation by antimony and arsenic. Moreover, we found that SbIII could not induce mutant PML (e.g., A126V and L218P) solubility change and degradation, similar to As2O3. In contrast, we found that the organic antimony compound phenylstibine oxide (PSO) could induce mutant PML protein degradation. In conclusion, our results indicate that SbIII might also be a promising agent to treat acute promyelocytic leukemia, in the same manner as As2O3.
    Type of Medium: Online Resource
    ISSN: 1756-5901 , 1756-591X
    URL: Article
    DOI: 10.1039/c9mt00102f
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2474317-3
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