Evidence map›Paper›PMID 24239288›Full record

ArticleMolecular cell2013

TopBP1 controls BLM protein level to maintain genome stability.

Jiadong Wang, Junjie Chen, Zihua Gong

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells.Oxidative medicine and cellular longevity · 2019
    Article
  18. Article
  19. Article
  20. A New BRCT Binding Mode in TopBP1-BLM Helicase Interaction.Structure (London, England : 1993) · 2017
    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

3 authors at 1 institution in 1 country.

Jiadong WangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Junjie ChenDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: jchen8@mdanderson.org.
Zihua GongDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: zgong@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Analysis of BRCA1 Function in DNA RepairR01CA089239 · NCI · YALE UNIVERSITY · PI CHEN, JUNJIE · 2001 to 2015
$3.7M
Study the Role of DNA Damage Responses in Tumorigenesis and SenescenceR01CA092312 · NCI · YALE UNIVERSITY · PI CHEN, JUNJIE · 2001 to 2015
$3.5M
NCI NIH HHS CA016672NCI NIH HHS CA089239NCI NIH HHS CA092312NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA089239NCI NIH HHS R01 CA092312
6 · The paper itself

Abstract

Human TopBP1 is a key mediator protein involved in DNA replication checkpoint control. In this study, we report a specific interaction between TopBP1 and Bloom syndrome helicase (BLM) that is phosphorylation and cell-cycle dependent. Interestingly, TopBP1 depletion led to decreased BLM protein level and increased sister chromatid exchange (SCE). Moreover, our data indicated that BLM was ubiquitinated by E3 ligase MIB1 and degraded in G1 cells but was stabilized by TopBP1 in S phase cells. Depletion of MIB1 restored BLM protein level and rescued the elevated SCE phenotype in TopBP1-depleted cells. In addition, cells expressing an undegradable BLM mutant showed radiation sensitivity, probably by triggering end resection and inhibiting the nonhomologous end-joining (NHEJ) pathway in G1 phase. Altogether, these data suggest that, although BLM is downregulated in G1 phase in order to promote NHEJ-mediated DNA repair, it is stabilized by TopBP1 in S phase cells in order to suppress SCE and thereby prevent genomic instability.

Indexed as

Genomic InstabilityCarrier ProteinsCell LineCell Line, TumorDNA-Binding ProteinsDNA End-Joining RepairDown-RegulationG1 PhaseHEK293 CellsHeLa CellsHumansNuclear ProteinsPhosphorylationRecQ HelicasesSister Chromatid ExchangeS PhaseBloom syndrome proteinCarrier ProteinsDNA-Binding ProteinsMIB1 ligase, humanNuclear ProteinsRecQ HelicasesTOPBP1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID24239288
PMCPMC3880544
OpenAlexW2080775404

What OpenQuestion holds

Textmetadata
LicenceTDM
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.