An increase in LRRK2 suppresses autophagy and enhances Dectin-1–induced immunity in a mouse model of colitis
Open accessAbstract
A LRRK2 inhibitor ameliorates intestinal inflammation in a mouse model of colitis.
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A more recent study demonstrated an induction of NFAT activity in HEK293T cells expressing LRRK2 or LRRK2 G2019S.
“A more recent study, on the other hand, demonstrated an induction of NFAT activity in HEK293T cells expressing LRRK2 or LRRK2 G2019S (38).”
From LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies (2020) · cites this paper as [38]
The Results section, “LRRK2 regulates NFAT transcriptional activity in mouse BMDCs” (page unavailable), reports increased NFAT reporter activity in HEK293T cells cotransfected with an LRRK2-expressing plasmid. It does not report the same result for LRRK2 G2019S; a search for G2019S found no relevant passage in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBone marrow-derived dendritic cells isolated from mice overexpressing Lrrk2 and treated with zymosan expressed more Il-2, an NFAT target gene, compared to that of non-transgenic mice.
“Moreover, bone marrow-derived dendritic cells isolated from mice overexpressing Lrrk2 and treated with zymosan expressed more Il-2, an NFAT target gene, compared to that of non-transgenic mice (38).”
From LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies (2020) · cites this paper as [38]
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LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies
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- Authors
- Takagawa, T., Kitani, A., Fuss, I., Levine, B., Brant, S. R., Peter, I., Tajima, M., Nakamura, S., & Strober, W.
- Affiliations
- National Institutes of Health (US)
- Howard Hughes Medical Institute (US)
- Johns Hopkins University (US)
- Icahn School of Medicine at Mount Sinai (US)
- Division of Internal Medicine, Department of Inflammatory Bowel Disease, Hyogo College of Medicine, Nishinomiya 663-8501, Japan.
- Corresponding author
- Strober, Warren
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2018-06-06
- Volume
- 10
- Issue
- 444
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6636639
- OpenAlex
- W2806366257
- Cited by
- 145
- References
- 5
- Citations by year
- 2026: 14 · 2025: 15 · 2024: 15 · 2023: 20 · 2022: 24 · 2021: 25 · 2020: 18 · 2019: 13 · 2018: 1
- FWCI
- 8.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- National Institutes of Health (U19AI109725-01)
- NIH Grant (DK062431)
- NIAID Intramural Program (AI000354-35)
- the New York Crohn’s Foundation and the Leona M. and Harry B. Helmsley Charitable Trust
- Grant-in-Aid for Researchers, Hyogo College of Medicine
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- LRRK2, LRRK2 inhibitors, autophagy, Dectin-1, innate immunity, intestinal inflammation, colitis, mouse colitis model
- MeSH terms
- Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Beclin-1, Dectin-1, Animals, Autophagy, Bone Marrow Cells, Colitis, Colon, Crohn Disease, Dendritic Cells, Disease Models, Animal, Humans, Immunity, Inflammation, Mice, Transgenic, Transcription, Genetic, Signal Transduction, Cytokines, Dextran Sulfate, NF-kappa B, Lectins, C-Type, NFATC Transcription Factors, Proteolysis
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