Evidence map›Paper›PMID 28553204›Full record

ArticleFrontiers in cellular neuroscience2017

Leucine-Rich Repeat Kinase 2 (LRRK2) Stimulates IL-1β-Mediated Inflammatory Signaling through Phosphorylation of RCAN1.

Kyung A Han, Lang Yoo, Jee Y Sung, Sun A Chung, Ji W Um, Hyeyoung Kim, Wongi Seol, Kwang C Chung

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 29% 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, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Ripks and Neuroinflammation.Molecular neurobiology · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. TheThyroid : official journal of the American Thyroid Association · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Leucine Rich Repeat Kinase 2 and Innate Immunity.Frontiers in neuroscience · 2020
    Review
  17. Review
  18. 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 4 institutions in 1 country.

Kyung A HanDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversitySeoul, South Korea.
Lang YooDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversitySeoul, South Korea.
Jee Y SungCenter for Pediatric Oncology, National Cancer CenterGoyang-si, South Korea.
Sun A ChungDepartment of Food and Nutrition, College of Human Ecology, Yonsei UniversitySeoul, South Korea.
Ji W UmDepartment of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST)Daegu, South Korea.
Hyeyoung KimDepartment of Food and Nutrition, College of Human Ecology, Yonsei UniversitySeoul, South Korea.
Wongi SeolInAm Neuroscience Research Center, Sanbon Medical Center, College of Medicine, Wonkwang UniversityGunpo-si, South Korea.
Kwang C ChungDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversitySeoul, South Korea.
Yonsei University · KRDaegu Gyeongbuk Institute of Science and Technology · KRNational Cancer Center · KRWonkwang University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leucine-rich repeat kinase 2 (LRRK2) is a Ser/Thr kinase having mixed lineage kinase-like and GTPase domains, controlling neurite outgrowth and neuronal cell death. Evidence suggests that LRRK2 is involved in innate immune response signaling, but the underlying mechanism is yet unknown. A novel protein inhibitor of phosphatase 3B, RCAN1, is known to positively regulate inflammatory signaling through modulation of several intracellular targets of interleukins in immune cells. In the present study, we report that LRRK2 phosphorylates RCAN1 (RCAN1-1S) and is markedly up-regulated during interleukin-1β (IL-1β) treatment. During IL-1β treatment, LRRK2-mediated phosphorylation of RCAN1 promoted the formation of protein complexes, including that between Tollip and RCAN1. LRRK2 decreased binding between Tollip and IRAK1, which was accompanied by increased formation of the IRAK1-TRAF6 complex. TAK1 activity was significantly enhanced by LRRK2. Furthermore, LRRK2 enhanced transcriptional activity of NF-κB and cytokine IL-8 production. These findings suggest that LRRK2 might be important in positively modulating IL-1β-mediated signaling through selective phosphorylation of RCAN1.

Indexed as

interleukin-1βLRRK2NF-κBParkinson’s diseasephosphorylationRCAN1

Identifiers

PMID28553204
PMCPMC5425608
OpenAlexW2613669496

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.