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  1. Article ; Online: A [(M

    Liu, Li-Hua / Liu, Lin / Chi, Hao-Ran / Li, Chen-Ning / Han, Zheng-Bo

    Chemical communications (Cambridge, England)

    2022  Volume 58, Issue 44, Page(s) 6417–6420

    Abstract: A new metal-organic polyhedron with a high surface area of 407 m ...

    Abstract A new metal-organic polyhedron with a high surface area of 407 m
    Language English
    Publishing date 2022-05-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 1472881-3
    ISSN 1364-548X ; 1359-7345 ; 0009-241X
    ISSN (online) 1364-548X
    ISSN 1359-7345 ; 0009-241X
    DOI 10.1039/d2cc01734b
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: m

    Yang, Xia / Bai, Qiaorui / Chen, Weizhong / Liang, Jiaer / Wang, Fang / Gu, Weiqi / Liu, Lei / Li, Quanfeng / Chen, Zishuo / Zhou, Anni / Long, Jianting / Tian, Han / Wu, Jueheng / Ding, Xiaofan / Zhou, Ningning / Li, Mengfeng / Yang, Yi / Cai, Junchao

    Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    2023  Volume 10, Issue 20, Page(s) e2206744

    Abstract: The importance of mRNA N6-methyladenosine (m ...

    Abstract The importance of mRNA N6-methyladenosine (m
    MeSH term(s) Humans ; Adenocarcinoma ; Adenocarcinoma of Lung ; Adenosine ; Cell Cycle Proteins ; Lung Neoplasms/genetics ; RNA, Messenger
    Chemical Substances Adenosine (K72T3FS567) ; Cell Cycle Proteins ; MCM5 protein, human ; RNA, Messenger ; IGF2BP3 protein, human
    Language English
    Publishing date 2023-05-12
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2808093-2
    ISSN 2198-3844 ; 2198-3844
    ISSN (online) 2198-3844
    ISSN 2198-3844
    DOI 10.1002/advs.202206744
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: M

    He, Mingyu / Wang, Yang / Xie, Jiajie / Pu, Jiaying / Shen, Zhihua / Wang, Ao / Li, Tao / Wang, Tong / Li, Guanghui / Liu, Ying / Mei, Zhongting / Ren, Zijing / Wang, Wenbo / Liu, Xiaoyan / Hong, Jinhuan / Liu, Qian / Lei, Hong / He, Xiaoqi / Du, Weijie /
    Yuan, Ye / Yang, Lei

    Oncogene

    2023  Volume 43, Issue 5, Page(s) 341–353

    Abstract: Doxorubicin and platinum are widely used in the frontline treatment of osteosarcoma, but resistance to chemotherapy limits its curative effect. Here, we have identified that METTL1 mediated ... ...

    Abstract Doxorubicin and platinum are widely used in the frontline treatment of osteosarcoma, but resistance to chemotherapy limits its curative effect. Here, we have identified that METTL1 mediated N
    MeSH term(s) Humans ; Ferroptosis/genetics ; MicroRNAs/metabolism ; Osteosarcoma/drug therapy ; Osteosarcoma/genetics ; Bone Neoplasms/drug therapy ; Bone Neoplasms/genetics ; RNA, Messenger ; Ferritins ; Oxidoreductases/metabolism
    Chemical Substances MicroRNAs ; RNA, Messenger ; FTH1 protein, human (EC 1.-) ; Ferritins (9007-73-2) ; Oxidoreductases (EC 1.-) ; MIRN98 microRNA, human
    Language English
    Publishing date 2023-12-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-023-02882-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2218: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: m

    Shen, Min / Guo, Mei / Li, Yujia / Wang, Yingqian / Qiu, Yangling / Shao, Jiangjuan / Zhang, Feng / Xu, Xuefen / Yin, Guoping / Wang, Shijun / Chen, Anping / Zhang, Zili / Zheng, Shizhong

    Free radical biology & medicine

    2022  Volume 182, Page(s) 246–259

    Abstract: ... dramatically abolished the DHA-induced ferroptosis in HSCs. Mechanistically, the up-regulated m ...

    Abstract Activation of hepatic stellate cells (HSCs) is a central event in the development of liver fibrosis, and the elimination of activated HSCs is considered to be an effective anti-fibrotic strategy. Here, we report that dihydroartemisinin (DHA) prevented the activation of HSCs via ferroptosis pathway. Importantly, DHA treatment increased the level of autophagy in HSCs. The inhibition of autophagy by 3-MA dramatically abolished the DHA-induced ferroptosis in HSCs. Mechanistically, the up-regulated m
    MeSH term(s) Animals ; Artemisinins ; Autophagy ; Ferroptosis/genetics ; Hepatic Stellate Cells ; Liver/metabolism ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/genetics ; Methylation ; Mice ; Signal Transduction
    Chemical Substances Artemisinins ; artenimol (6A9O50735X)
    Language English
    Publishing date 2022-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2022.02.028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2109: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: m

    Zhang, Ting / Ding, Chenbo / Chen, Huifang / Zhao, Jun / Chen, Zhejun / Chen, Baiwen / Mao, Kaiqiong / Hao, Yajuan / Roulis, Manolis / Xu, Hao / Kluger, Yuval / Zou, Qiang / Ye, Youqiong / Zhan, Meixiao / Flavell, Richard A / Li, Hua-Bing

    Science advances

    2022  Volume 8, Issue 12, Page(s) eabl5723

    Abstract: Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). However, the mechanisms underlying mucosal barrier dysfunction are poorly understood. ...

    Abstract Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). However, the mechanisms underlying mucosal barrier dysfunction are poorly understood.
    MeSH term(s) Animals ; Apoptosis/genetics ; Colon/metabolism ; Colon/pathology ; Epithelial Cells/metabolism ; Homeostasis ; Mice ; NF-kappa B/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
    Chemical Substances NF-kappa B ; RNA, Messenger
    Language English
    Publishing date 2022-03-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abl5723
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: m

    Zhou, Yuan / Pei, Zhengda / Maimaiti, Aizezi / Zheng, Linyi / Zhu, Zhongcheng / Tian, Mengxiang / Zhou, Zhongyi / Tan, Fengbo / Pei, Qian / Li, Yuqiang / Liu, Wenxue

    Cell death discovery

    2022  Volume 8, Issue 1, Page(s) 83

    Abstract: N6-methyladenosine (m6A) modifications of RNAs are involved in various aspects of colorectal carcinogenesis via regulation of mRNA stability, splicing, and translation. KIAA1429, an m6A methyltransferase, was found deregulated in multiple cancer types. ... ...

    Abstract N6-methyladenosine (m6A) modifications of RNAs are involved in various aspects of colorectal carcinogenesis via regulation of mRNA stability, splicing, and translation. KIAA1429, an m6A methyltransferase, was found deregulated in multiple cancer types. However, its role in colorectal cancer remains elusive. By analyzing TCGA and GEPIA database, we found that KIAA1429 in colorectal cancer was highly expressed. In addition, we used immunohistochemistry, western blotting, and QRT-PCR to detect the expression of KIAA1429 in colorectal cancer samples and cell lines, and we found that KIAA1429 was overexpressed in colorectal cancer sample and cell line. Functionally, silencing of KIAA1429 by shRNA in colorectal cancer cell lines resulted in decreased cell proliferation, colony formation, and migration. On the contrary, overexpression of KIAA1429 increased cell proliferation, colony formation, and migration. Further mechanism analysis demonstrated that KIAA1429 increased the expression of SIRT1 via regulating its mRNA stability in an m6A-dependent manner. More importantly, in vivo experiment showed that depletion of KIAA1429 significantly inhibited colorectal tumor growth. In conclusion, our results suggested that the m6A methyltransferase KIAA1429 promotes the growth and motility of colorectal cancer and could be a potent therapeutic target.
    Language English
    Publishing date 2022-02-25
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-022-00878-w
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  7. Article: [m

    Zhao, G / Li, H / Zhang, H / Xiao, K / Yang, H / Li, Z / Fu, C

    Nan fang yi ke da xue xue bao = Journal of Southern Medical University

    2024  Volume 43, Issue 12, Page(s) 2035–2042

    Abstract: Objective: To investigate the expression of WTAP, a m: Methods: Sixteen C57BL/6 mice with renal ...

    Abstract Objective: To investigate the expression of WTAP, a m
    Methods: Sixteen C57BL/6 mice with renal I/R injury or sham operation (
    Results: Compared with sham-operated mice, the mice with renal I/R injury showed significantly increased Scr and BUN levels (
    Conclusion: WTAP expression is up-regulated in the kidneys of mice with renal I/R injury and in HK-2 cells with H/R exposure. Inhibition of WTAP alleviates H/R-induced apoptotic damage in HK-2 cells possibly by inhibiting FOXO1 expression.
    MeSH term(s) Humans ; Animals ; Mice ; Mice, Inbred C57BL ; Cell Survival ; Epithelial Cells ; Kidney ; Methyltransferases ; RNA, Messenger ; Forkhead Box Protein O1 ; RNA Splicing Factors ; Cell Cycle Proteins
    Chemical Substances Methyltransferases (EC 2.1.1.-) ; RNA, Messenger ; FOXO1 protein, human ; Forkhead Box Protein O1 ; WTAP protein, human ; RNA Splicing Factors ; Cell Cycle Proteins
    Language Chinese
    Publishing date 2024-01-08
    Publishing country China
    Document type English Abstract ; Journal Article
    ZDB-ID 2250951-3
    ISSN 1673-4254
    ISSN 1673-4254
    DOI 10.12122/j.issn.1673-4254.2023.12.07
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6344: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: The m

    He, Yichen / Chen, Yimeng / Li, Zhengsheng / Wu, Changping

    Journal of cancer research and clinical oncology

    2024  Volume 150, Issue 2, Page(s) 30

    Abstract: Background and aim: As the first identified m: Methods: We initially assessed the expression ... m: Conclusion: FTO could potentially serve as a diagnostic marker for ccRCC. FTO promotes ... the progression of ccRCC by regulating m ...

    Abstract Background and aim: As the first identified m
    Methods: We initially assessed the expression of FTO in tumor and adjacent tissues using TCGA database, RT-qPCR, and Western blot. We then conducted CCK-8, cell cycle analysis, and colony formation assay to investigate the impact of FTO on ccRCC cell proliferation. MeRIP-seq and RNA-seq were employed to identify potential downstream targets of FTO in ccRCC, and these findings were further validated through dual-luciferase reporter assays and MeRIP-qPCR. Then, DNA damage and cell death were assessed separately through gammaH2AX immunofluorescence detection and the LIVE/DEAD Fixable Dead Cell Stain assay, respectively. Subsequently, we identified downstream pathways influenced by FTO's regulation of POLQ through TCGA database analysis and GSEA enrichment analysis. Validation was carried out through Western blot.
    Results: FTO is highly expressed in ccRCC tissues and cell lines. Furthermore, ROC curve demonstrates that FTO contributes to the diagnosis of ccRCC. FTO modulates m
    Conclusion: FTO could potentially serve as a diagnostic marker for ccRCC. FTO promotes the progression of ccRCC by regulating m
    MeSH term(s) Humans ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics ; Blotting, Western ; Carcinoma ; Carcinoma, Renal Cell/genetics ; Cell Proliferation/genetics ; Kidney Neoplasms/genetics ; Cell Line, Tumor ; DNA Polymerase theta/genetics
    Chemical Substances Alpha-Ketoglutarate-Dependent Dioxygenase FTO (EC 1.14.11.33) ; FTO protein, human (EC 1.14.11.33) ; POLQ protein, human (EC 2.7.7.-) ; DNA Polymerase theta (EC 2.7.7.-)
    Language English
    Publishing date 2024-01-25
    Publishing country Germany
    Document type Journal Article
    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/s00432-023-05541-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.10: Show issues Location:
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  9. Article ; Online: The m

    Zhang, Shaoqiong / Cui, Kaile / Li, Yuanyuan / Fan, Yiting / Wang, Dongxu / Yao, Xingen / Fang, Bo

    Stem cell research & therapy

    2024  Volume 15, Issue 1, Page(s) 43

    Abstract: ... activation remain unclear, and the role of N6-methyladenosine (m: Methods: NSCs were subjected to hypoxia ... reoxygenation (H/R) to simulate ischemia-reperfusion in vivo. m: Results: Overall of m: Conclusion ... The biological behaviors of NSCs after H/R are closely related to m ...

    Abstract Background: Ischemia-reperfusion injury to the central nervous system often causes severe complications. The activation of endogenous neural stem cells (NSCs) is considered a promising therapeutic strategy for nerve repair. However, the specific biological processes and molecular mechanisms of NSC activation remain unclear, and the role of N6-methyladenosine (m
    Methods: NSCs were subjected to hypoxia/reoxygenation (H/R) to simulate ischemia-reperfusion in vivo. m
    Results: Overall of m
    Conclusion: The biological behaviors of NSCs after H/R are closely related to m
    MeSH term(s) Mice ; Animals ; Methylation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Cell Differentiation/genetics ; Hypoxia/metabolism ; Neural Stem Cells
    Chemical Substances RNA, Messenger
    Language English
    Publishing date 2024-02-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 2548671-8
    ISSN 1757-6512 ; 1757-6512
    ISSN (online) 1757-6512
    ISSN 1757-6512
    DOI 10.1186/s13287-024-03658-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: m

    Li, Yan / Lou, Shenghan / Zhang, Jian / Zhao, Shilu / Lou, Ge

    Journal of translational medicine

    2024  Volume 22, Issue 1, Page(s) 113

    Abstract: ... were carried out to explore the m: Results: In this study, we discovered that MEG3 was downregulated ... by recognizing METTL3‑mediated m: Conclusion: We demonstrated that MEG3 is influenced by METTL3/YTHDF2 ...

    Abstract Background: Ovarian cancer poses a serious threat to women's health. Due to the difficulty of early detection, most patients are diagnosed with advanced-stage disease or peritoneal metastasis. We found that LncRNA MEG3 is a novel tumor suppressor, but its role in tumor occurrence and development is still unclear.
    Methods: We investigated the expression level of MEG3 in pan-cancer through bioinformatics analysis, especially in gynecological tumors. Function assays were used to detect the effect of MEG3 on the malignant phenotype of ovarian cancer. RIP, RNA pull-down, MeRIP-qPCR, actinomycin D test were carried out to explore the m
    Results: In this study, we discovered that MEG3 was downregulated in various cancers, with the most apparent downregulation in ovarian cancer. MEG3 inhibited the proliferation, migration, and invasion of ovarian cancer cells. Overexpression of MEG3 suppressed the degradation of VASH1 by negatively regulating miR-885-5p, inhibiting the ovarian cancer malignant phenotype. Furthermore, we demonstrated that MEG3 was regulated at the posttranscriptional level. YTHDF2 facilitated MEG3 decay by recognizing METTL3‑mediated m
    Conclusion: We demonstrated that MEG3 is influenced by METTL3/YTHDF2 methylation and restrains ovarian cancer proliferation and metastasis by binding miR-885-5p to increase VASH1 expression. MEG3 is expected to become a therapeutic target for ovarian cancer.
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic ; Methylation ; Methyltransferases/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
    Chemical Substances Cell Cycle Proteins ; Methyltransferases (EC 2.1.1.-) ; METTL3 protein, human (EC 2.1.1.62) ; MicroRNAs ; MIRN885 microRNA, human ; RNA, Long Noncoding ; VASH1 protein, human ; MEG3 non-coding RNA, human
    Language English
    Publishing date 2024-01-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2118570-0
    ISSN 1479-5876 ; 1479-5876
    ISSN (online) 1479-5876
    ISSN 1479-5876
    DOI 10.1186/s12967-024-04929-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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