Evidence map›Paper›PMID 25460043›Full record

ArticleCellular signalling2015

Regulation of DNA damage responses and cell cycle progression by hMOB2.

Valenti Gomez, Ramazan Gundogdu, Marta Gomez, Lily Hoa, Neelam Panchal, Mark O'Driscoll, Alexander Hergovich

Open access · bronzeAbstract read
In one paragraph

Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024
    Review
  6. Article
  7. Mosaic Chromosomal Alterations Are Associated With Increased Lung Cancer Risk: Insight From the INTEGRAL-ILCCO Cohort Analysis.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. The STK38-XPO1 axis, a new actor in physiology and cancer.Cellular and molecular life sciences : CMLS · 2021
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Lycorine: A prospective natural lead for anticancer drug discovery.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
    Review
  18. Article
  19. Article
  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

7 authors at 3 institutions in 1 country.

Valenti GomezUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom.
Ramazan GundogduUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom.
Marta GomezUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom.
Lily HoaUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom.
Neelam PanchalUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom.
Mark O'DriscollGenome Damage and Stability Centre, University of Sussex, BN1 9RH, Brighton, United Kingdom.
Alexander HergovichUCL Cancer Institute, University College London, WC1E 6BT, London, United Kingdom. Electronic address: a.hergovich@ucl.ac.uk.
University College London · GBCRUK Lung Cancer Centre of Excellence · GBUniversity of Sussex · GB

Funding

Biotechnology and Biological Sciences Research Council (BB/I021248/1Cancer Research UK 15394Wellcome Trust 090090Wellcome Trust 090090/Z/09/ZWorldwide Cancer Research 11-0634
6 · The paper itself

Abstract

Mps one binder proteins (MOBs) are conserved regulators of essential signalling pathways. Biochemically, human MOB2 (hMOB2) can inhibit NDR kinases by competing with hMOB1 for binding to NDRs. However, biological roles of hMOB2 have remained enigmatic. Here, we describe novel functions of hMOB2 in the DNA damage response (DDR) and cell cycle regulation. hMOB2 promotes DDR signalling, cell survival and cell cycle arrest after exogenously induced DNA damage. Under normal growth conditions in the absence of exogenously induced DNA damage hMOB2 plays a role in preventing the accumulation of endogenous DNA damage and a subsequent p53/p21-dependent G1/S cell cycle arrest. Unexpectedly, these molecular and cellular phenotypes are not observed upon NDR manipulations, indicating that hMOB2 performs these functions independent of NDR signalling. Thus, to gain mechanistic insight, we screened for novel binding partners of hMOB2, revealing that hMOB2 interacts with RAD50, facilitating the recruitment of the MRE11-RAD50-NBS1 (MRN) DNA damage sensor complex and activated ATM to DNA damaged chromatin. Taken together, we conclude that hMOB2 supports the DDR and cell cycle progression.

Indexed as

DNA DamageAnimalsAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorChlorocebus aethiopsChromosomal Proteins, Non-HistoneCOS CellsCyclin-Dependent Kinase Inhibitor p21DoxorubicinG1 Phase Cell Cycle CheckpointsHumansNerve Tissue ProteinsNuclear ProteinsPhosphorylationAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneCyclin-Dependent Kinase Inhibitor p21DoxorubicinMOB2 protein, humanNBN protein, humanNerve Tissue ProteinsNuclear ProteinsRNA, Small InterferingStructural Maintenance of Chromosome Protein 1TP53 protein, humanTumor Suppressor Protein p53Cell cycle checkpoint activationCell cycle progressionDNA damage response signallingMps one binder 2MRE11–RAD50–NBS1 protein complexp53 tumour suppressor protein

Identifiers

PMID25460043
PMCPMC4276419
OpenAlexW1984351774

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.