Evidence map›Paper›PMID 31753025›Full record

ReviewCancer communications (London, England)2019

Post-translational modification of Parkin and its research progress in cancer.

Dan Ding, Xiang Ao, Ying Liu, Yuan-Yong Wang, Hong-Ge Fa, Meng-Yu Wang, Yu-Qi He, Jian-Xun Wang

Open access · goldAbstract readReview
In one paragraph

Review in Cancer communications (London, England), 2019. 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
2.6field-weighted citation impact, top 10% 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, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. PTEN: a new dawn in Parkinson's disease treatment.Frontiers in cellular neuroscience · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. The regulation of PBXs and their emerging role in cancer.Journal of cellular and molecular medicine · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

8 authors at 3 institutions in 1 country.

Dan DingSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Xiang AoSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Ying LiuSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Yuan-Yong WangSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Hong-Ge FaSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Meng-Yu WangSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
Yu-Qi HeDepartment of Gastroenterology, The Seventh Medical Center of PLA General Hospital, Beijing, 100700, China. endohe@163.com.
Jian-Xun WangSchool of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China. wangjx@qdu.edu.cn.
Qingdao University · CNAffiliated Hospital of Qingdao University · CNChinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical practice has shown that Parkin is the major causative gene found in an autosomal recessive juvenile parkinsonism (AR-JP) via Parkin mutations and that the Parkin protein is the core expression product of the Parkin gene, which itself belongs to an E3 ubiquitin ligase. Since the discovery of the Parkin gene in the late 1990s, researchers in many countries have begun extensive research on this gene and found that in addition to AR-JP, the Parkin gene is associated with many diseases, including type 2 diabetes, leprosy, Alzheimer's, autism, and cancer. Recent studies have found that the loss or dysfunction of Parkin has a certain relationship with tumorigenesis. In general, the Parkin gene, a well-established tumor suppressor, is deficient and mutated in a variety of malignancies. Parkin overexpression inhibits tumor cell growth and promotes apoptosis. However, the functions of Parkin in tumorigenesis and its regulatory mechanisms are still not fully understood. This article describes the structure, functions, and post-translational modifications of Parkin, and summarizes the recent advances in the tumor suppressive function of Parkin and its underlying mechanisms.

Indexed as

HumansNeoplasmsProtein Processing, Post-TranslationalUbiquitin-Protein Ligasesparkin proteinUbiquitin-Protein LigasesCancerE3 ubiquitin ligaseNeddylationNIP3-like protein XParkinParkin/PTEN-induced kinase 1 (PINK1)PhosphorylationPost-translational modificationSumoylationUbiquitination

Identifiers

PMID31753025
PMCPMC6873554
OpenAlexW2990541855

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.