Evidence map›Paper›PMID 23149912›Full record

ArticleCancer research2013

DNA damage-specific control of cell death by cryptochrome in p53-mutant ras-transformed cells.

Jin Hyup Lee, Shobhan Gaddameedhi, Nuri Ozturk, Rui Ye, Aziz Sancar

Abstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Designing and Evaluating Circadian Experiments on Mouse Skin.The Journal of investigative dermatology · 2025
    Review
  5. Article
  6. Article
  7. Genetic Variations within the BovineAnimals : an open access journal from MDPI · 2022
    Article
  8. Review
  9. Review
  10. Cancer, hear my battle CRY.Journal of pineal research · 2020
    Review
  11. Article
  12. Article
  13. Cryptochrome 2 (CRY2) Suppresses Proliferation and Migration and Regulates Clock Gene Network in Osteosarcoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

5 authors at 1 institution in 1 country.

Jin Hyup LeeDepartment of Biochemistry and Biophysics, University of North Carolina, School of Medicine, Chapel Hill, North Carolina 27599, USA.
Shobhan Gaddameedhi
Nuri Ozturk
Rui Ye
Aziz Sancar
University of North Carolina at Chapel Hill · US

Funding

STRUCTURE AND FUNCTION OF UVRABC EXCISION NUCLEASER01GM032833 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1985 to 2015
$8.9M
STRUCTURE/FUNCTION OF DNA PHOTOLYASER01GM031082 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1985 to 2015
$4.9M
STRUCTURE/FUNCTION OF DNA PHOTOLYASER37GM031082 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1995 to 2004
$2.6M
NIGMS NIH HHS GM31082NIGMS NIH HHS GM32833NIGMS NIH HHS R01 GM031082NIGMS NIH HHS R01 GM032833NIGMS NIH HHS R37 GM031082
6 · The paper itself

Abstract

The main feedback loop driving circadian rhythm in mice is controlled, in part, by the genes encoding the cryptochromes Cry1 and Cry2. Targeted mutation of both Cry1 and Cry2 delay the early onset of tumor formation in p53-null mutant mice. Furthermore, Ras-transformed p53- and Cry-null mouse skin fibroblasts are more sensitive than p53 mutants to apoptotic cell death initiated by agents that activate either the intrinsic or the extrinsic apoptosis pathways. Here, we investigated the effect of Cry1 and Cry2 mutations on cell death by other genotoxic agents that generate alkylated bases, interstrand crosslinks, DNA-protein crosslinks, and double-strand breaks. Both ultraviolet (UV) and the UV mimetic compound oxaliplatin and the radiomimetic compound doxorubicin promoted apoptosis by upregulating the tumor suppressor p73. However, only the UV and oxaliplatin-induced upregulation of p73 mediated by the transcription factor Egr1, but not the doxorubicin-induced upregulation mediated by the transcription factor E2F1, was enhanced by Cry1/Cry2 double mutation. Accordingly, Egr1 downregulation reduced oxaliplatin-induced apoptosis, whereas E2F1 downregulation reduced doxorubicin-induced apoptosis. Our findings establish distinct roles for cryptochromes in intrinsic apoptosis induced by UV mimetic and radiomimetic agents.

Indexed as

DNA DamageAnimalsCell DeathCell LineCell Transformation, NeoplasticCircadian RhythmCryptochromesDNA-Binding ProteinsDoxorubicinMiceMice, Inbred C57BLMice, KnockoutMutagensMutationNuclear ProteinsOrganoplatinum CompoundsCRY1 protein, humanCRY2 protein, humanCryptochromesDNA-Binding ProteinsDoxorubicinMutagensNuclear ProteinsOrganoplatinum CompoundsOxaliplatinTP73 protein, humanTrp73 protein, mouseTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID23149912
PMCPMC3548992
OpenAlexW2096784028

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.