Evidence map›Paper›PMID 29290984›Full record

ArticleOncotarget2017

Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson's disease models.

Hyojung Kim, Sangwoo Ham, Joon Yeop Lee, Areum Jo, Gum Hwa Lee, Yun-Song Lee, MyoungLae Cho, Heung-Mook Shin, Donghoon Kim, Olga Pletnikova and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Oral co-administration ofJournal of virology · 2024
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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

14 authors at 7 institutions in 2 countries.

Hyojung KimDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
Sangwoo HamDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
Joon Yeop LeeNational Development Institute of Korean Medicine, Gyeongsan 38540, Republic of Korea.
Areum JoDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
Gum Hwa LeeCollege of Pharmacy, Chosun University, Gwangju 501-759, Republic of Korea.
Yun-Song LeeDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
MyoungLae ChoNational Development Institute of Korean Medicine, Gyeongsan 38540, Republic of Korea.
Heung-Mook ShinNational Development Institute of Korean Medicine, Gyeongsan 38540, Republic of Korea.
Donghoon KimDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Olga PletnikovaDepartment of Pathology, Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Juan C TroncosoDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Joo-Ho ShinDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
Yun-Il LeeWell Aging Research Center, Daegu Geongbuk Institute of Science and Technology, Daegu 42988, South Korea.
Yunjong LeeDivision of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Republic of Korea.
National Development Institute of Korean Medicine · KRSamsung (South Korea) · KRDaegu Gyeongbuk Institute of Science and Technology · KRJohns Hopkins Medicine · USSungkyunkwan University · KRChosun University · KRJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNF146 is an E3 ubiquitin ligase that specifically recognizes and polyubiquitinates poly (ADP-ribose) (PAR)-conjugated substrates for proteasomal degradation. RNF146 has been shown to be neuroprotective against PAR polymerase-1 (PARP1)-induced cell death during stroke. Here we report that RNF146 expression and RNF146 inducers can prevent cell death elicited by Parkinson's disease (PD)-associated and PARP1-activating stimuli. In SH-SY5Y cells, RNF146 expression conferred resistance to toxic stimuli that lead to PARP1 activation. High-throughput screen using a luciferase construct harboring the RNF146 promoter identified liquiritigenin as an RNF146 inducer. We found that RNF146 expression by liquiritigenin was mediated by estrogen receptor activation and contributed to cytoprotective effect of liquiritigenin. Finally, RNF146 expression by liquiritigenin in mouse brains provided dopaminergic neuroprotection in a 6-hydroxydopamine PD mouse model. Given the presence of PARP1 activity and RNF146 deficits in PD, it could be a potential therapeutic strategy to restore RNF146 expression by natural compounds or estrogen receptor activation.

Indexed as

AIMP2luciferase screenPARP1-dependent cell deathpreconditioningRNF146

Identifiers

PMID29290984
PMCPMC5739769
OpenAlexW2762533813

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.