ArticleScience advances2016
TIE2-mediated tyrosine phosphorylation of H4 regulates DNA damage response by recruiting ABL1.
Article in Science advances, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Modular FRET sensor for site-specific detection of protein arginine methylation in living cells.American journal of translational research · 2026Article
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- The Tie2 antagonist rebastinib reduces ovarian cancer growth in a syngeneic murine model.BMC cancer · 2025Article
- Positional distribution and conservation of major phosphorylated sites in the human kinome.Frontiers in molecular biosciences · 2025Article
- A high-throughputActa pharmaceutica Sinica. B · 2023Article
- Review
- Angiopoietin-1 Upregulates Cancer Cell Motility in Colorectal Cancer Liver Metastases through Actin-Related Protein 2/3.Cancers · 2022Article
- Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair.Frontiers in cell and developmental biology · 2022Review
- Review
- In silico molecular target prediction unveils mebendazole as a potent MAPK14 inhibitor.Molecular oncology · 2020Article
- ΔNp73/ETS2 complex drives glioblastoma pathogenesis- targeting downstream mediators by rebastinib prolongs survival in preclinical models of glioblastoma.Neuro-oncology · 2020Article
- The Histone Code of Senescence.Cells · 2020Review
- Ponatinib treatment promotes arterial thrombosis and hyperactive platelets.Blood advances · 2019Article
- The role of caveolin-1 in tumors of the brain - functional and clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- Preserving genome integrity and function: the DNA damage response and histone modifications.Critical reviews in biochemistry and molecular biology · 2019Review
- Protein phosphatases in chromatin structure and function.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Linking inflammation and cancer: the unexpected SYK world.Neuro-oncology · 2018Article
- The Selective Tie2 Inhibitor Rebastinib Blocks Recruitment and Function of Tie2Molecular cancer therapeutics · 2017Article
- TIE2 Associates with Caveolae and Regulates Caveolin-1 To Promote Their Nuclear Translocation.Molecular and cellular biology · 2017Article
- Signaling coupled epigenomic regulation of gene expression.Oncogene · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
DNA repair pathways enable cancer cells to survive DNA damage induced after genotoxic therapies. Tyrosine kinase receptors (TKRs) have been reported as regulators of the DNA repair machinery. TIE2 is a TKR overexpressed in human gliomas at levels that correlate with the degree of increasing malignancy. Following ionizing radiation, TIE2 translocates to the nucleus, conferring cells with an enhanced nonhomologous end-joining mechanism of DNA repair that results in a radioresistant phenotype. Nuclear TIE2 binds to key components of DNA repair and phosphorylates H4 at tyrosine 51, which, in turn, is recognized by the proto-oncogene ABL1, indicating a role for nuclear TIE2 as a sensor for genotoxic stress by action as a histone modifier. H4Y51 constitutes the first tyrosine phosphorylation of core histones recognized by ABL1, defining this histone modification as a direct signal to couple genotoxic stress with the DNA repair machinery.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.