We are analyzing https://link.springer.com/article/10.1186/s13045-022-01224-4.

Title:
RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential | Journal of Hematology & Oncology
Description:
RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
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Keywords {🔍}

alkbh, pubmed, cancer, article, google, scholar, cas, cell, central, rna, cells, expression, mrna, wang, tumor, demethylase, cancers, targeting, promotes, zhang, protein, demethylation, modification, methylation, binding, stem, liu, nmethyladenosine, human, gene, regulation, carcinoma, rnas, fig, target, chen, yang, functions, histone, res, role, regulates, breast, immune, nsclc, proliferation, therapeutic, potential, roles, dna,

Topics {✒️}

activating atm-chk2-p53/cdc25c signaling pre-mir-181b-1/yap signaling axis naturally-derived small-molecule inhibitors kdm4c-alkbh5-axl signaling axis mir-193a-3p promotes growth mir-193a-3p transfection results mrna-binding factor rbm15/spenito suppresses mir-193a-3p maturation oxygenase double-stranded β-helix programmable m6a-editing systems comprises arg–ser-rich regions cell-type-specific methylation patterns myb proto-oncogene c-myb dead-box rna helicase article download pdf n6-methyladenosine rna demethylase n6-methyladenosine-modified rna alkbh5-mediated post-transcriptional regulation controls sorafenib-induced autophagy mirna-193a-3p regulates rna n6-methyladenosine methyltransferase m6a-dependent epigenetic silencing transcriptional pre-mrna splicing circular rna-protein interactions full-length human alkbh5 primary mir-193a-3p alkbh5 post-transcriptionally regulates m6a-ck2alpha-mediated glycolysis m6a-ythdf2-dependent fashion crispr–cas13b-based tool m6a-guided epigenetic inhibition hypoxia-inducible factor 1alpha n6-methyladenosine alkbh5 promotes ctcf ccctc-binding factor n6-methyladenosine-dependent regulation crispr-based m6a targeting n6-methyladenosine binding protein post-transcriptionally regulating tacc3 n6-methyladenosine-independent manner single-nucleotide-resolution mapping small-molecule inhibitors targeting circrnas represent single-stranded double-stranded nucleic acids crispr-based gene therapy m6a-ythdf2-dependent manner mixed-lineage leukemia protein n6-methyladenosine binding induces arrows represent β-strands alkbh5-mediated m6a demethylation alkbh5-mediated m6a-demethylation

Schema {🗺️}

WebPage:
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         headline:RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential
         description:RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
         datePublished:2022-01-21T00:00:00Z
         dateModified:2022-01-21T00:00:00Z
         pageStart:1
         pageEnd:24
         license:http://creativecommons.org/publicdomain/zero/1.0/
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            ALKBH5
            RNA demethylation
            Cancer
            Gene regulation
            Therapeutic target
            Oncology
            Hematology
            Cancer Research
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ScholarlyArticle:
      headline:RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential
      description:RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
      datePublished:2022-01-21T00:00:00Z
      dateModified:2022-01-21T00:00:00Z
      pageStart:1
      pageEnd:24
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      sameAs:https://doi.org/10.1186/s13045-022-01224-4
      keywords:
         m6A modification
         ALKBH5
         RNA demethylation
         Cancer
         Gene regulation
         Therapeutic target
         Oncology
         Hematology
         Cancer Research
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PostalAddress:
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
      name:Institute of Hematology, Zhejiang University, Hangzhou, China

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