Evidence map›Paper›PMID 18625723›Full record

ArticleMolecular and cellular biology2008

A novel Tel1/ATM N-terminal motif, TAN, is essential for telomere length maintenance and a DNA damage response.

Jeffrey J Seidel, Carol M Anderson, Elizabeth H Blackburn

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular basis of human ATM kinase inhibition.Nature structural & molecular biology · 2021
    Article
  4. Article
  5. Unpicking the Roles of DNA Damage Protein Kinases in Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  6. Progress towards a clinically-successful ATR inhibitor for cancer therapy.Current research in pharmacology and drug discovery · 2021
    Review
  7. Review
  8. Article
  9. ATM, radiation, and the risk of second primary breast cancer.International journal of radiation biology · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. ATM protein kinase: the linchpin of cellular defenses to stress.Cellular and molecular life sciences : CMLS · 2011
    Review
  14. Article
  15. Review
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Jeffrey J SeidelDepartment of Biochemistry and Biophysics, 600 16th Street, Room S316, University of California, San Francisco, San Francisco, CA 94158-2517, USA.
Carol M Anderson
Elizabeth H Blackburn
University of California, San Francisco · US

Funding

THE FUNCTION OF TELOMERASE AND TELOMERESR01GM026259 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BLACKBURN, ELIZABETH H · 1985 to 2014
$8.9M
STRUCTURE AND FUNCTION OF TELOMERESR37GM026259 · NIGMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BLACKBURN, ELIZABETH H · 1989 to 1998
–
NIGMS NIH HHS GM26259NIGMS NIH HHS R01 GM026259NIGMS NIH HHS R37 GM026259
6 · The paper itself

Abstract

Tel1/ATM, a conserved phosphatidylinositol 3-kinase-related kinase (PIKK), acts in the response to DNA damage and regulates telomere maintenance. PIKK family members share an extended N-terminal region of low sequence homology. Sequence alignment of the N terminus of Tel1/ATM orthologs revealed a conserved, novel motif we term TAN (for Tel1/ATM N-terminal motif). Point mutations in conserved residues of the TAN motif resulted in telomere shortening, and its deletion caused the same short telomere phenotype as complete deletion of Tel1 did. Overexpressing Tel1 TAN mutants did not rescue telomere shortening. The TAN motif was also essential for the function of Tel1 in the response to DNA damage, as TAN-deleted Tel1 was indistinguishable from the complete lack of Tel1 in causing reduced viability and signaling through Rad53 upon DNA damage. Strikingly, TAN deletion reduced recruitment of Tel1 to a double-strand DNA break. Together, these results define a conserved sequence motif within an otherwise poorly defined region of the Tel1/ATM kinase family proteins that is essential for normal Tel1 function in Saccharomyces cerevisiae.

Indexed as

Amino Acid SequenceDNA DamageIntracellular Signaling Peptides and ProteinsSaccharomyces cerevisiaeAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell NucleusDNA-Binding ProteinsDNA RepairDNA Repair EnzymesHumansMolecular Sequence DataProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsSequence AlignmentAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsTEL1 protein, S cerevisiaeTumor Suppressor ProteinsXRS2 protein, S cerevisiae

Identifiers

PMID18625723
PMCPMC2546937
OpenAlexW2115080180

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.