Evidence map›Paper›PMID 26381412›Full record

ArticleThe Journal of biological chemistry2015

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase.

Huibin Yang, Phillip L Palmbos, Lidong Wang, Evelyn H Kim, Gina M Ney, Chao Liu, Jayendra Prasad, David E Misek, Xiaochun Yu, Mats Ljungman and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Identification of a Novel Oncogenic Fusion GeneInternational journal of molecular sciences · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. RNF8 promotes epithelial-mesenchymal transition of breast cancer cells.Journal of experimental & clinical cancer research : CR · 2016
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Huibin YangDepartments of Surgery, University of Michigan, Ann Arbor, Michigan 48109; Departments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109.
Phillip L PalmbosDepartments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109; Departments of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109.
Lidong WangDepartments of Surgery, University of Michigan, Ann Arbor, Michigan 48109; Departments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109.
Evelyn H KimDepartments of Surgery, University of Michigan, Ann Arbor, Michigan 48109.
Gina M NeyDepartments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109; Departments of Pediatrics, University of Michigan, Ann Arbor, Michigan 48109.
Chao LiuDepartments of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109.
Jayendra PrasadDepartments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109; Departments of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109.
David E MisekDepartments of Surgery, University of Michigan, Ann Arbor, Michigan 48109.
Xiaochun YuDepartments of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109.
Mats LjungmanDepartments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109; Departments of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109.
Diane M SimeoneDepartments of Surgery, University of Michigan, Ann Arbor, Michigan 48109; Departments of Translational Oncology Program, University of Michigan, Ann Arbor, Michigan 48109; Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109. Electronic address: simeone@med.umich.edu.
University of Michigan–Ann Arbor · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
ONCOLOGY RESEARCH TRAINING GRANTT32CA009357 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Qing Li · 1987 to 2026
$8.6M
Regulation of Ionizing Radiation-Induced DNA Damage ResponseR01CA130899 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YILUN · 2009 to 2023
$5.5M
Molecular Mechanisms of BRCA1-Dependent DNA Damage Response and TumorogenesisR01CA132755 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHEN, BINGHUI · 2008 to 2019
$3.5M
Oncogenic Function of ATDC in Bladder CancerR01CA174836 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SIMEONE, DIANE M · 2014 to 2018
$2.3M
Functional analysis of BRCA1 in DNA damage response and tumor suppressionR01CA187209 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2014 to 2018
$1.7M
Functional analysis of the TET2/OGT complex in epigenetic modificationsR01GM108647 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2015 to 2018
$1.3M
NCI NIH HHS CA17483601A1NCI NIH HHS R01 CA130899NCI NIH HHS R01 CA13104505A1NCI NIH HHS R01 CA132755NCI NIH HHS R01 CA174836NCI NIH HHS R01 CA187209NCI NIH HHS T32 CA009357NIDDK NIH HHS P30 DK034933NIGMS NIH HHS R01 GM108647
6 · The paper itself

Abstract

Induction of DNA damage by ionizing radiation (IR) and/or cytotoxic chemotherapy is an essential component of cancer therapy. The ataxia telangiectasia group D complementing gene (ATDC, also called TRIM29) is highly expressed in many malignancies. It participates in the DNA damage response downstream of ataxia telangiectasia-mutated (ATM) and p38/MK2 and promotes cell survival after IR. To elucidate the downstream mechanisms of ATDC-induced IR protection, we performed a mass spectrometry screen to identify ATDC binding partners. We identified a direct physical interaction between ATDC and the E3 ubiquitin ligase and DNA damage response protein, RNF8, which is required for ATDC-induced radioresistance. This interaction was refined to the C-terminal portion (amino acids 348-588) of ATDC and the RING domain of RNF8 and was disrupted by mutation of ATDC Ser-550 to alanine. Mutations disrupting this interaction abrogated ATDC-induced radioresistance. The interaction between RNF8 and ATDC, which was increased by IR, also promoted downstream DNA damage responses such as IR-induced γ-H2AX ubiquitination, 53BP1 phosphorylation, and subsequent resolution of the DNA damage foci. These studies define a novel function for ATDC in the RNF8-mediated DNA damage response and implicate RNF8 binding as a key determinant of the radioprotective function of ATDC.

Indexed as

Active Transport, Cell NucleusAmino Acid SequenceAmino Acid SubstitutionBRCA1 ProteinCell Line, TumorDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA DamageDNA RepairHEK293 CellsHistonesHumansIntracellular Signaling Peptides and ProteinsMolecular Sequence DataMutagenesis, Site-DirectedPhosphorylationBRCA1 ProteinBRCA1 protein, humanDNA-Binding ProteinsH2AX protein, humanHistonesIntracellular Signaling Peptides and ProteinsRecombinant ProteinsRNF8 protein, humanTP53BP1 protein, humanTranscription FactorsTRIM29 protein, humanTumor Suppressor p53-Binding Protein 1Ubiquitin-Protein LigasesATDC (ataxia-telangiectasia group D complementing gene)chromatinDNA damage response (DDR)DNA repairDSB (double-strand break)E3 ubiquitin-protein ligase RNF8 (RNF8)IR (ionizing radiation)protein-protein interactionradiationTRIM29

Identifiers

PMID26381412
PMCPMC4646387
OpenAlexW2271026772

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.