Evidence map›Paper›PMID 27159997›Full record

ArticleBMC molecular biology2016

A potential role for protein palmitoylation and zDHHC16 in DNA damage response.

Na Cao, Jia-Kai Li, Yu-Qing Rao, Huijuan Liu, Ji Wu, Baojie Li, Peiquan Zhao, Li Zeng, Jing Li

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  13. [Screening of drugs that selectively inhibit uveal melanoma cells with SF3B1 mutations].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  14. Article
  15. Article
  16. Protein S-Palmitoylation and Lung Diseases.Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. International journal of biological sciences · 2020
    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

9 authors at 3 institutions in 2 countries.

Na CaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Jia-Kai LiDepartment of Ophthalmology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu-Qing RaoDepartment of Ophthalmology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Huijuan LiuBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Ji WuBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Baojie LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Peiquan ZhaoDepartment of Ophthalmology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Li ZengNeural Stem Cell Research Lab, Research Department, National Neuroscience Institute, Singapore, 308433, Singapore. li_zeng@nni.com.sg.
Jing LiDepartment of Ophthalmology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. lj_xinhua@126.com.
Shanghai Jiao Tong University · CNXinHua Hospital · CNNational Neuroscience Institute · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCells respond to DNA damage by activating the phosphatidylinositol-3 kinase-related kinases, p53 and other pathways to promote cell cycle arrest, apoptosis, and/or DNA repair. Here we report that protein palmitoylation, a modification carried out by protein acyltransferases with zinc-finger and Asp-His-His-Cys domains (zDHHC), is required for proper DNA damage responses.

resultsInhibition of protein palmitoylation compromised DNA damage-induced activation of Atm, induction and activation of p53, cell cycle arrest at G2/M phase, and DNA damage foci assembly/disassembly in primary mouse embryonic fibroblasts. Furthermore, knockout of zDHHC16, a palmitoyltransferase gene identified as an interacting protein for c-Abl, a non-receptor tyrosine kinase involved in DNA damage response, reproduced most of the defects in DNA damage responses produced by the inhibition of protein palmitoylation.

conclusionsOur results revealed critical roles for protein palmitoylation and palmitoyltransferase zDHHC16 in early stages of DNA damage responses and in the regulation of Atm activation.

Indexed as

DNA DamageDNA RepairAcyltransferasesAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCell Cycle CheckpointsCells, CulturedFemaleFibroblastsGene DeletionGene Knockout TechniquesLipoylationMice, Inbred C57BLProtein Interaction MapsAcyltransferasesAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCarrier ProteinsProto-Oncogene Proteins c-ablTumor Suppressor Protein p53Zdhhc16 protein, mouseDNA damage responseProtein palmitoylationzDHHC16

Identifiers

PMID27159997
PMCPMC4862184
OpenAlexW2345437143

What OpenQuestion 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 OpenQuestion graph.