ArticleScientific reports2016
Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Developing high-affinity decoy receptors to treat multiple myeloma and diffuse large B cell lymphoma.The Journal of experimental medicine · 2022Article
- Hypoxia-induced SETX links replication stress with the unfolded protein response.Nature communications · 2021Article
- Selective modulation by PARP-1 of HIF-1α-recruitment to chromatin during hypoxia is required for tumor adaptation to hypoxic conditions.Redox biology · 2021Article
- Tumor Hypoxia Drives Genomic Instability.Frontiers in cell and developmental biology · 2021Review
- Impact of hypoxia on DNA repair and genome integrity.Mutagenesis · 2020Review
- PPARγ Interaction with UBR5/ATMIN Promotes DNA Repair to Maintain Endothelial Homeostasis.Cell reports · 2019Article
- Ultra-High Dose Rate (FLASH) Radiotherapy: Silver Bullet or Fool's Gold?Frontiers in oncology · 2019Review
- Loss of PBRM1 rescues VHL dependent replication stress to promote renal carcinogenesis.Nature communications · 2017Article
- Article
- Ribonucleotide Reductase Requires Subunit Switching in Hypoxia to Maintain DNA Replication.Molecular cell · 2017Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Hypoxia-induced replication stress is one of the most physiologically relevant signals known to activate ATM in tumors. Recently, the ATM interactor (ATMIN) was identified as critical for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea. This suggests an essential role for ATMIN in ATM regulation during hypoxia, which induces replication stress. However, ATMIN also has a role in base excision repair, a process that has been demonstrated to be repressed and less efficient in hypoxic conditions. Here, we demonstrate that ATMIN is dispensable for ATM activation in hypoxia and in contrast to ATM, does not affect cell survival and radiosensitivity in hypoxia. Instead, we show that in hypoxic conditions ATMIN expression is repressed. Repression of ATMIN in hypoxia is mediated by both p53 and HIF-1α in an oxygen dependent manner. The biological consequence of ATMIN repression in hypoxia is decreased expression of the target gene, DYNLL1. An expression signature associated with p53 activity was negatively correlated with DYNLL1 expression in patient samples further supporting the p53 dependent repression of DYNLL1. Together, these data demonstrate multiple mechanisms of ATMIN repression in hypoxia with consequences including impaired BER and down regulation of the ATMIN transcriptional target, DYNLL1.
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