Evidence map›Paper›PMID 18180189›Full record

ArticleMolecular genetics and metabolism2008

Mammalian SNM1 is required for genome stability.

A W Hemphill, D Bruun, L Thrun, Y Akkari, Y Torimaru, K Hejna, P M Jakobs, J Hejna, S Jones, S B Olson and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular genetics and metabolism, 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
1.8field-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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. The multifunctional SNM1 gene family: not just nucleases.Future oncology (London, England) · 2010
    Review
  13. DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010
    Review
  14. Article
  15. DNA interstrand crosslink repair in mammalian cells.Journal of cellular physiology · 2009
    Review
  16. Article
  17. ERCC1 is required for FANCD2 focus formation.Molecular genetics and metabolism
    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

11 authors at 1 institution in 1 country.

A W HemphillDepartment of Molecular and Medical Genetics, Oregon Health & Sciences University, 3181 Sam Jackson Park Road, Portland, OR 97239, USA.
D Bruun
L Thrun
Y Akkari
Y Torimaru
K Hejna
P M Jakobs
J Hejna
S Jones
S B Olson
R E Moses
Oregon Health & Science University · US

Funding

Xenograft CoreP01HL048546 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI FLEMING, WILLIAM H · 1994 to 2020
$36.4M
NHLBI NIH HHS 1P01HL48546NHLBI NIH HHS P01 HL048546
6 · The paper itself

Abstract

The protein encoded by SNM1 in Saccharomyces cerevisiae has been shown to act specifically in DNA interstrand crosslinks (ICL) repair. There are five mammalian homologs of SNM1, including Artemis, which is involved in V(D)J recombination. Cells from mice constructed with a disruption in the Snm1 gene are sensitive to the DNA interstrand crosslinker, mitomycin (MMC), as indicated by increased radial formation following exposure. The mice reproduce normally and have normal life spans. However, a partial perinatal lethality, not seen in either homozygous mutant alone, can be noted when the Snm1 disruption is combined with a Fancd2 disruption. To explore the role of hSNM1 and its homologs in ICL repair in human cells, we used siRNA depletion in human fibroblasts, with cell survival and chromosome radials as the end points for sensitivity following treatment with MMC. Depletion of hSNM1 increases sensitivity to ICLs as detected by both end points, while depletion of Artemis does not. Thus hSNM1 is active in maintenance of genome stability following ICL formation. To evaluate the epistatic relationship between hSNM1 and other ICL repair pathways, we depleted hSNM1 in Fanconi anemia (FA) cells, which are inherently sensitive to ICLs. Depletion of hSNM1 in an FA cell line produces additive sensitivity for MMC. Further, mono-ubiquitination of FANCD2, an endpoint of the FA pathway, is not disturbed by depletion of hSNM1 in normal cells. Thus, hSNM1 appears to represent a second pathway for genome stability, distinct from the FA pathway.

Indexed as

Genomic InstabilityAnimalsCell Cycle ProteinsDNA RepairDNA Repair EnzymesEndodeoxyribonucleasesExodeoxyribonucleasesFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFibroblastsHumansMiceMice, TransgenicNuclear ProteinsRNA, Small InterferingTransfectionCell Cycle ProteinsDclre1a protein, mouseDCLRE1B protein, humanDNA Repair EnzymesEndodeoxyribonucleasesExodeoxyribonucleasesFanconi Anemia Complementation Group D2 ProteinNuclear ProteinsRNA, Small Interfering

Identifiers

PMID18180189
PMCPMC2413150
OpenAlexW2043340020

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.