Evidence map›Paper›PMID 31750563›Full record

ArticleThe EMBO journal2019

LIN28A loss of function is associated with Parkinson's disease pathogenesis.

Mi-Yoon Chang, Boram Oh, Jang-Eun Choi, Yanuar Alan Sulistio, Hye-Ji Woo, Ayoung Jo, Jinil Kim, Eun-Hee Kim, Seung Won Kim, Jungwook Hwang and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

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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

23 authors at 6 institutions in 1 country.

Mi-Yoon ChangDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Boram OhDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Jang-Eun ChoiDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Yanuar Alan SulistioDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Hye-Ji WooDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Ayoung JoDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Jinil KimDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Eun-Hee KimDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Seung Won KimDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Jungwook HwangHanyang Biomedical Research Institute, Hanyang University, Seoul, Korea.
Jungyun ParkHanyang Biomedical Research Institute, Hanyang University, Seoul, Korea.
Jae-Jin SongDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Oh-Chan KwonDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.
Hyongbum Henry KimDepartment of Pharmacology, College of Medicine, Yonsei University, Seoul, Korea.
Young-Hoon KimDepartment of Pharmacology, College of Medicine, Yonsei University, Seoul, Korea.
Joo Yeon KoDepartment of Dermatology and Research Institute of Dermatology, University of Hanyang College of Medicine, Hanyang Medical Center, Seoul, Korea.
Jun Young HeoDepartment of Biochemistry, Department of Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.
Min Joung LeeDepartment of Biochemistry, Department of Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.
Moses LeeDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Murim ChoiDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Sun Ju ChungDepartment of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Hyun-Seob LeeGenomic Core Facility, Transdisciplinary Research & Collaboration Division, Translational Research Institute, Seoul National University Hospital, Seoul, Korea.ORCID 0000-0001-6230-1405
Sang-Hun LeeDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea.ORCID 0000-0001-7553-8188
Hanyang University Medical Center · KRSeoul National University · KRYonsei University · KRChungnam National University · KRSeoul National University Hospital · KRUlsan College · KR

Funding

National Research Foundation of Korea Ministry of Science and ICT, Republic of Korea 2017M3A9B4062401National Research Foundation of Korea Ministry of Science and ICT, Republic of Korea 2017R1A5A2015395National Research Foundation of Korea Ministry of Science and ICT, Republic of Korea NRF-2016R1A2B4016342National Research Foundation of Korea Ministry of Science and ICT, Republic of Korea NRF-2017R1A2B2002220
6 · The paper itself

Abstract

Parkinson's disease (PD) is neurodegenerative movement disorder characterized by degeneration of midbrain-type dopamine (mDA) neurons in the substantia nigra (SN). The RNA-binding protein Lin28 plays a role in neuronal stem cell development and neuronal differentiation. In this study, we reveal that Lin28 conditional knockout (cKO) mice show degeneration of mDA neurons in the SN, as well as PD-related behavioral deficits. We identify a loss-of-function variant of LIN28A (R192G substitution) in two early-onset PD patients. Using an isogenic human embryonic stem cell (hESC)/human induced pluripotent stem cell (hiPSC)-based disease model, we find that the Lin28 R192G variant leads to developmental defects and PD-related phenotypes in mDA neuronal cells that can be rescued by expression of wild-type Lin28A. Cell transplantation experiments in PD model rats show that correction of the LIN28A variant in the donor patient (pt)-hiPSCs leads to improved behavioral phenotypes. Our data link LIN28A to PD pathogenesis and suggest future personalized medicine targeting this variant in patients.

Indexed as

AnimalsBehavior, AnimalCell TransplantationDisease Models, AnimalDopamineDopaminergic NeuronsEmbryonic Stem CellsGene EditingGenetic Predisposition to DiseaseHumansInduced Pluripotent Stem CellsMiceMice, KnockoutMutationNeural Stem CellsParkinson DiseaseDopamineLIN28B protein, humanRNA-Binding Proteinshuman disease modelhuman pluripotent stem cellsLin28loss-of-function mutationParkinson's disease

Identifiers

PMID31750563
PMCPMC6912061
OpenAlexW2991171330

What OpenQuestion holds

Textmetadata
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.