Evidence map›Paper›PMID 33546351›Full record

ReviewBiomolecules2021

Role of Small GTPase RhoA in DNA Damage Response.

Chibin Cheng, Daniel Seen, Chunwen Zheng, Ruijie Zeng, Enmin Li

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Alternative splicing of transposable elements in human breast cancer.bioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Rac1, A Potential Target for Tumor Therapy.Frontiers in oncology · 2021
    Review
  19. Review
  20. HIF2 Regulates Intestinal Wnt5a Expression.Frontiers in oncology · 2021
    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.

Chibin ChengDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515031, Guangdong, China.ORCID 0000-0003-4017-9175
Daniel SeenDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515031, Guangdong, China.
Chunwen ZhengDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515031, Guangdong, China.
Ruijie ZengDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515031, Guangdong, China.
Enmin LiDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515031, Guangdong, China.ORCID 0000-0001-6375-3614
Shantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has suggested a role of the small GTPase Ras homolog gene family member A (RhoA) in DNA damage response (DDR) in addition to its traditional function of regulating cell morphology. In DDR, 2 key components of DNA repair, ataxia telangiectasia-mutated (ATM) and flap structure-specific endonuclease 1 (FEN1), along with intracellular reactive oxygen species (ROS) have been shown to regulate RhoA activation. In addition, Rho-specific guanine exchange factors (GEFs), neuroepithelial transforming gene 1 (Net1) and epithelial cell transforming sequence 2 (Ect2), have specific functions in DDR, and they also participate in Ras-related C3 botulinum toxin substrate 1 (Rac1)/RhoA interaction, a process which is largely unappreciated yet possibly of significance in DDR. Downstream of RhoA, current evidence has highlighted its role in mediating cell cycle arrest, which is an important step in DNA repair. Unraveling the mechanism by which RhoA modulates DDR may provide more insight into DDR itself and may aid in the future development of cancer therapies.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsCell CycleCell SurvivalDNA RepairFlap EndonucleasesHumansMonomeric GTP-Binding ProteinsOncogene ProteinsProtein BindingProto-Oncogene Proteinsrac1 GTP-Binding ProteinrhoA GTP-Binding ProteinSignal TransductionAtaxia Telangiectasia Mutated ProteinsATM protein, humanECT2 protein, humanFEN1 protein, humanFlap EndonucleasesMonomeric GTP-Binding ProteinsNET1 protein, humanOncogene ProteinsProto-Oncogene Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanrhoA GTP-Binding ProteinRHOA protein, humancell cycle arrestDNA damage responseDNA repairEct2Net1Rac1RhoA

Identifiers

PMID33546351
PMCPMC7913530
OpenAlexW3127906466

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.