ArticleCell reports2019
LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting the UPR with Small Molecules: Emerging Strategies for Immune Regulation.Molecules (Basel, Switzerland) · 2026Review
- Serum LACC1 level is a predictor of response to upadacitinib treatment in patients with rheumatoid arthritis: a prospective observational cohort study.European journal of medical research · 2025Observational
- A novel LACC1 variant c.658G>A (p. Asp220Asn) in familial juvenile arthritis: identification and functional analysis.Human genomics · 2025Article
- NOD1 deficiency promotes inflammation via autophagic degradation of ASK1.Communications biology · 2025Article
- Crohn's Disease-associated variant in laccase domain containing 1 (LACC1) modulates T cell gene expression, metabolism and T cell function.Nature communications · 2025Article
- The research progress of LACC1.Frontiers in immunology · 2025Review
- ER-phagy restrains inflammatory responses through its receptor UBAC2.The EMBO journal · 2024Article
- Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation.International journal of molecular sciences · 2024Review
- Control of immune cell function by the unfolded protein response.Nature reviews. Immunology · 2023Review
- Clinical characteristics and genotype analysis of a Chinese patient with juvenile arthritis due to novel LACC1 frameshift mutation and literature review.Molecular genetics & genomic medicine · 2023Review
- Insights of Endocytosis Signaling in Health and Disease.International journal of molecular sciences · 2023Review
- Long-term presence of autoantibodies in plasma of cured leprosy patients.Scientific reports · 2023Article
- Valosin-containing protein-regulated endoplasmic reticulum stress causes NOD2-dependent inflammatory responses.Scientific reports · 2022Article
- Tidy up - The unfolded protein response in sepsis.Frontiers in immunology · 2022Review
- Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response.The Journal of clinical investigation · 2021Article
- LACC1 deficiency links juvenile arthritis with autophagy and metabolism in macrophages.The Journal of experimental medicine · 2021Article
- Mediators of Metabolism: An Unconventional Role for NOD1 and NOD2.International journal of molecular sciences · 2021Review
- Monogenic autoinflammatory disorders: Conceptual overview, phenotype, and clinical approach.The Journal of allergy and clinical immunology · 2020Review
- Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation.Gastroenterology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
LACC1 genetic variants are associated with multiple immune-mediated diseases. However, laccase domain containing-1 (LACC1) functions are incompletely defined. We find that upon stimulation of the pattern-recognition receptor (PRR) NOD2, LACC1 localizes to the endoplasmic reticulum (ER) and forms a complex with ER-stress sensors. All three ER-stress branches, PERK, IRE1α, and ATF6, are required for NOD2-induced signaling, cytokines, and antimicrobial pathways in human macrophages. LACC1, and its localization to the ER, is required for these outcomes. Relative to wild-type (WT) LACC1, transfection of the common Val254 and rare Arg284 immune-mediated disease-risk LACC1 variants into HeLa cells and macrophages, as well as macrophages from LACC1 Val254 carriers, shows reduced NOD2-induced ER stress-associated outcomes; these downstream outcomes are restored by rescuing ER stress. Therefore, we identify ER stress to be essential in PRR-induced outcomes in macrophages, define a critical role for LACC1 in these ER stress-dependent events, and elucidate how LACC1 disease-risk variants mediate these outcomes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.