ArticleNature communications2015
Small heterodimer partner interacts with NLRP3 and negatively regulates activation of the NLRP3 inflammasome.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Small heterodimer partner protects against osteoarthritis by inhibiting IKKβ/NF-κB-mediated matrix-degrading enzymes in chondrocytes.Nature communications · 2026Article
- Brain-Derived Neurotrophic Factor Deficiency Exacerbates Innate Immune Responses by Enhancing NLRP3 Inflammasome Activation and GSDMD-Mediated Pyroptosis in Mice.Medicina (Kaunas, Lithuania) · 2026Article
- Gout Inflammation Time Programming: Molecular Clock from Crystal Triggering to Tissue Remodeling.International journal of molecular sciences · 2026Review
- Enhanced nuclear localization of small heterodimer partner in metabolic dysfunction-associated steatohepatitis.JHEP reports : innovation in hepatology · 2026Article
- The Role of IL-6 in Ischemic Stroke.Biomolecules · 2025Review
- Bile acids and their receptors in hepatic immunity.Liver research (Beijing, China) · 2025Review
- Role of Protein Regulators of Cholesterol Homeostasis in Immune Modulation and Cancer Pathophysiology.Endocrinology · 2025Review
- Bile acid receptors regulate the role of intestinal macrophages in inflammatory bowel disease.Frontiers in immunology · 2025Review
- Revealing the dance of NLRP3: spatiotemporal patterns in inflammasome activation.Immunometabolism (Cobham, Surrey) · 2025Review
- Integrative bioinformatics analysis and experimental validation reveals key genes and regulatory mechanisms in the development of gout.Frontiers in genetics · 2025Article
- Selective activation of PPARα by pemafibrate mitigates peritoneal inflammation and fibrosis through suppression of NLRP3 inflammasome and modulation of inflammation.Scientific reports · 2024Article
- Progress in mass spectrometry approaches to profiling protein-protein interactions in the studies of the innate immune system.Journal of proteins and proteomics · 2024Article
- Development of NR0B2 as a therapeutic target for the re-education of tumor associated myeloid cells.Cancer letters · 2024Article
- NR0B2 re-educates myeloid immune cells to reduce regulatory T cell expansion and progression of breast and other solid tumors.Cancer letters · 2024Article
- Nuclear receptor coactivator 6 is a critical regulator of NLRP3 inflammasome activation and gouty arthritis.Cellular & molecular immunology · 2024Article
- Article
- Cilostazol protects against degenerative cervical myelopathy injury and cell pyroptosis via TXNIP-NLRP3 pathway.Cell division · 2024Article
- Bile acids as a key target: traditional Chinese medicine for precision management of insulin resistance in type 2 diabetes mellitus through the gut microbiota-bile acids axis.Frontiers in endocrinology · 2024Review
- A role of gut microbiota metabolites in HLA-E and NKG2 blockage immunotherapy against tumors: new insights for clinical application.Frontiers in immunology · 2024Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive activation of the NLRP3 inflammasome results in damaging inflammation, yet the regulators of this process remain poorly defined. Herein, we show that the orphan nuclear receptor small heterodimer partner (SHP) is a negative regulator of NLRP3 inflammasome activation. NLRP3 inflammasome activation leads to an interaction between SHP and NLRP3, proteins that are both recruited to mitochondria. Overexpression of SHP competitively inhibits binding of NLRP3 to apoptosis-associated speck-like protein containing a CARD (ASC). SHP deficiency results in increased secretion of proinflammatory cytokines IL-1β and IL-18, and excessive pathologic responses typically observed in mouse models of kidney tubular necrosis and peritoneal gout. Notably, the loss of SHP results in accumulation of damaged mitochondria and a sustained interaction between NLRP3 and ASC in the endoplasmic reticulum. These data are suggestive of a role for SHP in controlling NLRP3 inflammasome activation through a mechanism involving interaction with NLRP3 and maintenance of mitochondrial homeostasis.
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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.