Evidence map›Paper›PMID 20647761›Full record

ArticleCell cycle (Georgetown, Tex.)2010

MCL-1 localizes to sites of DNA damage and regulates DNA damage response.

Sarwat Jamil, Cezar Stoica, Tillie-Louise Hackett, Vincent Duronio

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

47 citing papers in PubMed, 64 citations in OpenAlex.

  1. GET3 regulates apoptosis via tail-anchoring of MCL1.Cell death and differentiation · 2026
    Article
  2. Observational
  3. Saga of MCL1 inhibitors in multiple myeloma.Biochemical pharmacology · 2026
    Review
  4. Article
  5. MCL1 may not mediate chemoresistance.bioRxiv : the preprint server for biology · 2025
    Article
  6. Embryonic Stem Cell-Specific Responses to DNA Replication Stress.bioRxiv : the preprint server for biology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

4 authors at 2 institutions in 2 countries.

Sarwat JamilDepartment of Medicine, University of British Columbia and Vancouver Coastal Health Research Institute, Vancouver, BC, Canada.
Cezar Stoica
Tillie-Louise Hackett
Vincent Duronio
University of British Columbia · CAProvidence Health Care · CA

Funding

Canadian Institutes of Health Research MOP-74481
6 · The paper itself

Abstract

MCL-1, a pro-survival member of the BCL-2 family, was previously shown to have functions in ATR-dependent Chk1 phosphorylation following DNA damage. To further delineate these functions, we explored possible differences in DNA damage response caused by lack of MCL-1 in mouse embryo fibroblasts (MEFs). As expected, Mcl-1(-/-) MEFs had delayed Chk1 phosphorylation following etoposide treatment, compared to wild type MEFs. However, their response to hydroxyurea, which causes a G(1)/S checkpoint response, was not significantly different. In addition, appearance of gamma-H2AX was delayed in the Mcl-1(-/-) MEFs treated with etoposide. We next investigated whether MCL-1 is present, together with other DNA damage response proteins, at the sites of DNA damage. Immunoprecipitation of etoposide-treated extracts with anti-MCL-1 antibody showed association of MCL-1 with gamma-H2AX as well as NBS1. Immunofluorescent staining for MCL-1 further showed increased co-staining of MCL-1 and NBS1 following DNA damage. By using a system that creates DNA double strand breaks at specific sites in the genome, we demonstrated that MCL-1 is recruited directly adjacent to the sites of damage. Finally, in a direct demonstration of the importance of MCL-1 in allowing proper repair of DNA damage, we found that treatment for two brief exposures to etoposide , followed by periods of recovery, which mimics the clinical situation of etoposide use, resulted in greater accumulation of chromosomal abnormalities in the MEFs that lacked MCL-1. Together, these data indicate an important role for MCL-1 in coordinating DNA damage mediated checkpoint response, and have broad implications for the importance of MCL-1 in maintenance of genome integrity.

Indexed as

DNA Breaks, Double-StrandedDNA RepairAnimalsCell Cycle ProteinsCheckpoint Kinase 1EtoposideHeLa CellsHistonesHumansMiceMyeloid Cell Leukemia Sequence 1 ProteinNuclear ProteinsPhosphorylationProtein KinasesProto-Oncogene Proteins c-bcl-2RNA InterferenceCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanChek1 protein, mouseEtoposideHistonesMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinNBN protein, humanNuclear ProteinsProtein KinasesProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID20647761
PMCPMC3040962
OpenAlexW2092875419

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.