Cited by 247DNA Repair MechanismsCancer, Hypoxia, and MetabolismGenomics and Chromatin Dynamics

HIF-1: A Target For Cancer, Ischemia and Inflammation—Too Good to be True?

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Melillo, Giovanni·2004·Cell Cycle

Abstract

The histone H2A variant, H2AX, is a core component of chromatin that is phosphorylated in chromatin flanking DNA double strand breaks (DSBs). Here, we summarize H2AX functions and outline a specific "anchoring" model, that can explain the translocation prone phenotype of H2AX-deficient and H2AX/p53-deficient mice. We also discuss how this model of H2AX function could account for some aspects of the genomic instability and cancer prone human phenotypes associated with Ataxia Telangiectasia (AT), Nijmegen Breakage Syndrome (NBS), Ataxia Telangiectasia Like Disorder (ATLD), and Bloom's Syndrome (BS).

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Research works printed but not linked: 18

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Authors
Melillo, G.
Affiliations
Leidos (United States) (US)
Corresponding author
Melillo, Giovanni
Venue
Cell Cycle
Published
2004-02
Volume
3
Issue
2
Pages
149-150
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W2016440796
Cited by
247
References
0
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 7 · 2020: 1 · 2019: 4 · 2018: 4 · 2017: 9 · 2016: 6 · 2015: 9 · 2014: 18 · 2013: 11 · 2012: 7
FWCI
11.39
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Health and Human Services
  • National Institutes of Health (N01-CO-12400)
  • U.S. Public Health Service (N01C012400)
  • National Cancer Institute (CO-12400, N01CO12400)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords
H2AX, histone H2A variant, DNA double-strand breaks, p53, genomic instability, cancer susceptibility, ataxia telangiectasia, NBS1, Nijmegen breakage syndrome, ataxia-telangiectasia-like disorder, Bloom syndrome, HIF-1
MeSH terms
Animals, Ataxia Telangiectasia, Cell Transformation, Neoplastic, Chromatin, DNA Damage, DNA-Binding Proteins, Histones, Humans, Models, Biological, Phosphorylation, Tumor Suppressor Protein p53, Protein Serine-Threonine Kinases, Mice, Knockout, Cell Cycle Proteins, Tumor Suppressor Proteins, Mice, Ataxia Telangiectasia Mutated Proteins

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