Evidence map›Paper›PMID 28395174›Full record

ArticleRedox biology2017

Loss of Parkin reduces inflammatory arthritis by inhibiting p53 degradation.

Yu Yeon Jung, Dong Ju Son, Hye Lim Lee, Dae Hwan Kim, Min Jong Song, Young Wan Ham, Youngsoo Kim, Sang Bae Han, Mi Hee Park, Jin Tae Hong

Open access · goldAbstract readComparative Study
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Autophagic Organelles in DNA Damage Response.Frontiers in cell and developmental biology · 2021
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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

10 authors at 4 institutions in 2 countries.

Yu Yeon JungCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea; Department of Dental Hygiene, Gwangyang Health Sciences University, Gwnagyang, Jeonnam 57764, Korea.
Dong Ju SonCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea.
Hye Lim LeeCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea.
Dae Hwan KimCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea.
Min Jong SongDepartment of Obstetrics and Gynecology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, Republic of Korea.
Young Wan HamDepartment of Chemistry and Biochemistry, Brigham Young University, Provo, UT, United States.
Youngsoo KimCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea.
Sang Bae HanCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea.
Mi Hee ParkCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea. Electronic address: pmh5205@hanmail.net.
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-31, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea. Electronic address: jinthong@chungbuk.ac.kr.
Chungbuk National University · KRBrigham Young University · USGwangyang Health College · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkin is associated with various inflammatory diseases, including Parkinson's disease (PD) and rheumatoid arthritis (RA). However, the precise role of Parkin in RA is unclear. The present study addressed this issue by comparing the development of RA between non-transgenic (non-Tg) mice and PARK2 knockout (KO) mice. We found that cyclooxygenase-2 and inducible nitric oxide synthase expression and nuclear factor-κB activity were reduced but p53 activation was increased in PARK2 KO as compared to non-Tg mice. These effects were associated with reduced p53 degradation. Parkin was found to interact with p53; however, this was abolished in Parkin KO mice, which prevented p53 degradation. Treatment of PARK2 KO mice with p53 inhibitor increased Parkin expression as well as inflammation and RA development while decreasing nuclear p53 translocation, demonstrating that PARK2 deficiency inhibits inflammation in RA via suppression of p53 degradation. These results suggest that RA development may be reduced in PD patients.

Indexed as

AnimalsArthritis, RheumatoidCell NucleusCyclooxygenase 2Disease Models, AnimalHEK293 CellsHumansLipopolysaccharidesMaleMiceMice, TransgenicNF-kappa BNitric Oxide Synthase Type IIProtein BindingProteolysisRAW 264.7 CellsCyclooxygenase 2LipopolysaccharidesNF-kappa BNitric Oxide Synthase Type IINOS2 protein, humanparkin proteinPTGS2 protein, humanTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein LigasesArthritisp53ParkinUbiquitination

Identifiers

PMID28395174
PMCPMC5388915
OpenAlexW2604719331

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.