ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Cutting edge: SHARPIN is required for optimal NLRP3 inflammasome activation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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Who cites it
37 citing papers in PubMed.
- Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026Review
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Deciphering Key Regulatory Roles of Linear Ubiquitination in Cell Fate Determination and Disease.Research (Washington, D.C.) · 2025Review
- SHARPIN contributes to sevoflurane-induced neonatal neurotoxicity through up-regulating HMGB1 to repress M2 like-macrophage polarization.Metabolic brain disease · 2024Article
- Biallelic human SHARPIN loss of function induces autoinflammation and immunodeficiency.Nature immunology · 2024Article
- The discovery of NLRP3 and its function in cryopyrin-associated periodic syndromes and innate immunity.Immunological reviews · 2024Review
- HOIL1 Regulates Group 3 Innate Lymphoid Cells in the Colon and Protects against Systemic Dissemination, Colonic Ulceration, and Lethality from Citrobacter rodentium Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The mechanism of linear ubiquitination in regulating cell death and correlative diseases.Cell death & disease · 2023Review
- SHARPIN: Role in Finding NEMO and in Amyloid-Beta Clearance and Degradation (ABCD) Pathway in Alzheimer's Disease?Cellular and molecular neurobiology · 2022Review
- Crosstalk Between the NLRP3 Inflammasome/ASC Speck and Amyloid Protein Aggregates Drives Disease Progression in Alzheimer's and Parkinson's Disease.Frontiers in molecular neuroscience · 2022Review
- IKKβ is required for the formation of the NLRP3 inflammasome.EMBO reports · 2021Article
- NLRP3 Ubiquitination-A New Approach to Target NLRP3 Inflammasome Activation.International journal of molecular sciences · 2021Review
- NLRP3 inflammasome in cancer and metabolic diseases.Nature immunology · 2021Review
- Targeting RIP Kinases in Chronic Inflammatory Disease.Biomolecules · 2021Review
- Inflammasome activation controlled by the interplay between post-translational modifications: emerging drug target opportunities.Cell communication and signaling : CCS · 2021Review
- Met1-linked ubiquitin signalling in health and disease: inflammation, immunity, cancer, and beyond.Cell death and differentiation · 2021Review
- Importance of Deubiquitination in Macrophage-Mediated Viral Response and Inflammation.International journal of molecular sciences · 2020Review
- Caspases in Cell Death, Inflammation, and Pyroptosis.Annual review of immunology · 2020Review
- Control of the inflammasome by the ubiquitin system.The FEBS journal · 2020Review
- Keratinocyte-specific deletion of SHARPIN induces atopic dermatitis-like inflammation in mice.PloS one · 2020Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The NLRP3 inflammasome is a multimeric protein complex that is assembled in response to a wide array of pathogens and danger-associated molecular patterns. Despite the ability of NLRP3 to respond to diverse cues, the mechanisms controlling the assembly of this complex are contested. Recently published studies showed that HOIL-1, a member of the linear ubiquitin chain assembly complex, contributes to activation of the NLRP3 inflammasome. SHARPIN, along with HOIP and HOIL-1, constitute the linear ubiquitin chain assembly complex. In this study, we examined whether SHARPIN is required for the activation of the NLRP3 inflammasome. Using Sharpin(cpdm) macrophages (deficient in SHARPIN expression), we demonstrate that SHARPIN is required for optimal activation of the NLRP3 inflammasome by both canonical and noncanonical stimuli. Furthermore, Sharpin(cpdm) macrophages had dramatic defects on both the NF-κB and MAPK pathways, suggesting a role in transcriptional priming of the NLRP3 inflammasome. In conclusion, our study identified SHARPIN as a novel regulator of the NLRP3 inflammasome.
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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.