Evidence map›Paper›PMID 11432841›Full record

ArticleThe EMBO journal2001

The ribonucleotide reductase inhibitor Sml1 is a new target of the Mec1/Rad53 kinase cascade during growth and in response to DNA damage.

X Zhao, A Chabes, V Domkin, L Thelander, R Rothstein

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

173 citing papers in PubMed, 286 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Rad53 arrests leading and lagging strand DNA synthesis via distinct mechanisms in response to DNA replication stress.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Article
  19. Review
  20. Article

113 more citing papers are in PubMed but not listed here.

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.

X ZhaoDepartment of Genetics and Development, Columbia University, College of Physicians and Surgeons, 701 West 168th Street, New York, NY 10032, USA.
A Chabes
V Domkin
L Thelander
R Rothstein
Columbia University · US

Funding

Mechanism of spontaneous and DSB-induced repairR37GM050237 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2005 to 2014
$6.0M
MECHANISM OF SPONTANEOUS AND DSB-INDUCED REPAIRR01GM050237 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI ROTHSTEIN, RODNEY J. · 1993 to 2016
$3.0M
NIGMS NIH HHS GM50237NIGMS NIH HHS R01 GM050237NIGMS NIH HHS R37 GM050237
6 · The paper itself

Abstract

The evolutionarily conserved protein kinases Mec1 and Rad53 are required for checkpoint response and growth. Here we show that their role in growth is to remove the ribonucleotide reductase inhibitor Sml1 to ensure DNA replication. Sml1 protein levels fluctuate during the cell cycle, being lowest during S phase. The disappearance of Sml1 protein in S phase is due to post-transcriptional regulation and is associated with protein phosphorylation. Both phosphorylation and diminution of Sml1 require MEC1 and RAD53. More over, failure to remove Sml1 in mec1 and rad53 mutants results in incomplete DNA replication, defective mitochondrial DNA propagation, decreased dNTP levels and cell death. Interestingly, similar regulation of Sml1 also occurs after DNA damage. In this case, the regulation requires MEC1 and RAD53, as well as other checkpoint genes. Therefore, Sml1 is a new target of the DNA damage checkpoint and its removal is a conserved function of Mec1 and Rad53 during growth and after damage.

Indexed as

Cell Cycle ProteinsDNA DamageDNA RepairDNA ReplicationEnzyme InhibitorsProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsCheckpoint Kinase 2DNA, FungalFungal ProteinsGamma RaysGenotypeHydroxyureaIntracellular Signaling Peptides and ProteinsProtein KinasesRibonucleotide ReductasesCell Cycle ProteinsCheckpoint Kinase 2DNA, FungalEnzyme InhibitorsFungal ProteinsHydroxyureaIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeProtein KinasesProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeRibonucleotide ReductasesSaccharomyces cerevisiae ProteinsSML1 protein, S cerevisiae

Identifiers

PMID11432841
PMCPMC125510
OpenAlexW1979544330

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.