Evidence map›Paper›PMID 18495871›Full record

ArticleMolecular biology of the cell2008

An essential role for MCL-1 in ATR-mediated CHK1 phosphorylation.

Sarwat Jamil, Shadi Mojtabavi, Payman Hojabrpour, Stefanie Cheah, Vincent Duronio

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

44 citing papers in PubMed, 74 citations in OpenAlex.

  1. Saga of MCL1 inhibitors in multiple myeloma.Biochemical pharmacology · 2026
    Review
  2. MCL1 may not mediate chemoresistance.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. ElevatedJournal of thoracic disease · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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  20. 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

5 authors at 1 institution in 1 country.

Sarwat JamilDepartment of Medicine, University of British Columbia and Vancouver Coastal Health Research Institute, Vancouver, BC, V6H 3Z6 Canada.
Shadi Mojtabavi
Payman Hojabrpour
Stefanie Cheah
Vincent Duronio
Vancouver Coastal Health · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here we report a novel role for myeloid cell leukemia 1 (Mcl-1), a Bcl-2 family member, in regulating phosphorylation and activation of DNA damage checkpoint kinase, Chk1. Increased expression of nuclear Mcl-1 and/or a previously reported short nuclear form of Mcl-1, snMcl-1, was observed in response to treatment with low concentrations of etoposide or low doses of UV irradiation. We showed that after etoposide treatment, Mcl-1 could coimmunoprecipitate with the regulatory kinase, Chk1. Chk1 is a known regulator of DNA damage response, and its phosphorylation is associated with activation of the kinase. Transient transfection with Mcl-1 resulted in an increase in the expression of phospho-Ser345 Chk1, in the absence of any evidence of DNA damage, and accumulation of cells in G2. Importantly, knockdown of Mcl-1 expression abolished Chk1 phosphorylation in response to DNA damage. Mcl-1 could induce Chk1 phosphorylation in ATM-negative (ataxia telangectasia mutated) cells, but this response was lost in ATR (AT mutated and Rad3 related)-defective cells. Low levels of UV treatment also caused transient increases in Mcl-1 levels and an ATR-dependent phosphorylation of Chk1. Together, our results strongly support an essential regulatory role for Mcl-1, perhaps acting as an adaptor protein, in controlling the ATR-mediated regulation of Chk1 phosphorylation.

Indexed as

Gene Expression RegulationAntineoplastic Agents, PhytogenicAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell NucleusCheckpoint Kinase 1DNA DamageEtoposideHeLa CellsHL-60 CellsHumansMyeloid Cell Leukemia Sequence 1 ProteinPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2Antineoplastic Agents, PhytogenicAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanEtoposideMyeloid Cell Leukemia Sequence 1 ProteinProtein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID18495871
PMCPMC2488305
OpenAlexW2140192991

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.