Evidence map›Paper›PMID 20194963›Full record

ArticleGenetics2010

Transformation/transcription domain-associated protein (TRRAP)-mediated regulation of Wee1.

Teresa M Calonge, Majid Eshaghi, Jianhua Liu, Ze'ev Ronai, Matthew J O'Connell

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2010. 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
2.0field-weighted citation impact, top 14% 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, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Regulatory motifs in Chk1.Cell cycle (Georgetown, Tex.) · 2013
    Article
  5. Connecting chromatin modifying factors to DNA damage response.International journal of molecular sciences · 2013
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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 3 institutions in 2 countries.

Teresa M CalongeDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
Majid Eshaghi
Jianhua Liu
Ze'ev Ronai
Matthew J O'Connell
Genome Institute of Singapore · SGIcahn School of Medicine at Mount Sinai · USInstitute for Medical Research · US

Funding

ATF2 in DNA damage response.R01CA117927 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI RONAI, ZEEV A. · 2006 to 2010
$2.2M
Chk1 signaling in the G2 DNA damage checkpointR01CA100076 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI O'CONNELL, MATTHEW J · 2003 to 2007
$1.7M
Chk1 signaling in the G2 DNA damage checkpointR56CA100076 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI O'CONNELL, MATTHEW J · 2009 to 2009
$336k
NCI NIH HHS CA100076NCI NIH HHS CA117927NCI NIH HHS R01 CA100076NCI NIH HHS R01 CA117927NCI NIH HHS R56 CA100076
6 · The paper itself

Abstract

The G2 DNA damage checkpoint inhibits Cdc2 and mitotic entry through the dual regulation of Wee1 and Cdc25 by the Chk1 effector kinase. Upregulation of Chk1 by mutation or overexpression bypasses the requirement for upstream regulators or DNA damage to promote a G2 cell cycle arrest. We screened in fission yeast for mutations that rendered cells resistant to overexpressed chk1(+). We identified a mutation in tra1, which encodes one of two homologs of transformation/transcription domain-associated protein (TRRAP), an ATM/R-related pseudokinase that scaffolds several histone acetyltransferase (HAT) complexes. Inhibition of histone deacetylases reverts the resistance to overexpressed chk1(+), suggesting this phenotype is due to a HAT activity, although expression of checkpoint and cell cycle genes is not greatly affected. Cells with mutant or deleted tra1 activate Chk1 normally and are checkpoint proficient. However, these cells are semi-wee even when overexpressing chk1(+) and accumulate inactive Wee1 protein. The changed division response (Cdr) kinases Cdr1 and Cdr2 are negative regulators of Wee1, and we show that they are required for the Tra1-dependent alterations to Wee1 function. This identifies Tra1 as another component controlling the timing of entry into mitosis via Cdc2 activation.

Indexed as

Adaptor Proteins, Signal TransducingCell Cycle ProteinsCheckpoint Kinase 1Enzyme ActivationG2 PhaseGene DeletionGene Expression ProfilingGene Expression Regulation, FungalHistone Deacetylase InhibitorsHydroxamic AcidsMitosisMutationNuclear ProteinsProtein KinasesProtein-Tyrosine KinasesSchizosaccharomycesAdaptor Proteins, Signal TransducingCell Cycle ProteinsCheckpoint Kinase 1Chk1 protein, S pombeHistone Deacetylase InhibitorsHydroxamic AcidsNuclear ProteinsProtein KinasesProtein-Tyrosine KinasesSchizosaccharomyces pombe Proteinstransformation-transcription domain-associated proteintrichostatin Awee1 protein, S pombe

Identifiers

PMID20194963
PMCPMC2870978
OpenAlexW2124876195

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.