Ask about this productRelated genes to: NLRP1 Blocking Peptide
- Gene:
- NLRP1 NIH gene
- Name:
- NLR family pyrin domain containing 1
- Previous symbol:
- NALP1, SLEV1
- Synonyms:
- KIAA0926, DKFZp586O1822, CARD7, NAC, CLR17.1, DEFCAP, VAMAS1
- Chromosome:
- 17p13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-28
- Date modifiied:
- 2016-06-01
Related products to: NLRP1 Blocking Peptide
Related articles to: NLRP1 Blocking Peptide
- SARS-CoV-2 portrays a public health threat because severe progression of infections can lead to hospitalization. Severity is often characterized by a systemic inflammatory response in later stages, along with disbalance in cytokine production, multi-organ failure, or acute respiratory distress syndrome (ARDS). As severe infections can be challenging due to limited treatment windows for direct-acting antivirals, host-targets, e.g., the Raf/MEK/ERK signaling cascade, came into focus. Specifically, MEK1/2 has been suggested as a target for antiviral and anti-inflammatory therapy. A recent phase II clinical trial showed the efficacy of the MEK1/2 inhibitor zapnometinib (ZMN/ATR-002) in hospitalized COVID-19 patients. The anti-inflammatory action of ATR-002 was only studied on some candidate cytokines. - Source: PubMed
Publication date: 2026/05/29
Rodner FranziskaSchughart KlausLudwig StephanSchreiber André - The NOD-like receptor (NLR) inflammasome system is an evolutionarily conserved intracellular surveillance network that responds to pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and metabolism-associated molecular patterns (MAMPs). Beyond the well-characterized NLRP3 inflammasome, accumulating evidence suggests that NLRP1, NLRP6, NLRC5, NLRP12, and NLRP2 are also implicated in metabolic disorders, including obesity, type 2 diabetes mellitus (T2DM), atherosclerosis, and metabolic dysfunction-associated steatotic liver disease (MASLD). This review summarizes the molecular mechanisms governing NLR inflammasome activation and discusses the divergent, context-dependent roles of selected NLR family members in metabolic inflammation. We distinguish established inflammasome-dependent pathways from emerging inflammasome-independent and PANoptosis-related mechanisms, with particular attention to species differences, disease context, and strength of evidence. Therapeutic strategies targeting inflammasome components or downstream effectors are critically evaluated, including small-molecule inhibitors, cytokine blockade, peptide-derived agents, and natural bioactive compounds. By integrating mechanistic findings with a translational evidence hierarchy spanning studies, animal models, human observational data, early clinical trials, randomized evidence, and approved or repurposed anti-inflammatory therapies, this review highlights both the promise and limitations of precision inflammasome modulation for metabolic disease intervention, providing an evidence-graded therapeutic perspective on NLR biology in metabolic disease. - Source: PubMed
Publication date: 2026/05/29
Zhou JunYang RuohaoZhu WanyuHe ZhilinMa YuekeFeng ZhiweiYu Lili - Systemic cervical cancer management continues to be challenging. Numerous chemotherapies have been approved, but predicting response is difficult due to the lack of biomarkers. Here, we analyze the genetic and protein profiles of 20 cervical cancer cell lines (CCCLs) and explore their correlation with drug response patterns to commonly used drugs, aiming to identify novel biomarkers of treatment response or resistance. - Source: PubMed
Scholl SuzyNery Elaine DelGestraud PierreHalladjian MaralGirard ElodieSoria AdèleAnthony ElodieDe Koning LeanneServant NicolasBerns ElsKamal Maud - - Source: PubMed
Publication date: 2026/06/08
Hossain ImranMolla Md Saifuddin - Beta amyloid diffuse plaques, neurofibrillary tangles and neuritic plaques, are increased in densities at the intermediate stage of Alzheimer's neuropathological change. These pathological changes releasing Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Associated Molecular Patterns (DAMPs). These molecules are sensed by pattern recognition receptors (PRRs) and trigger intracellular responses. One response is the activation of the inflammasome sensors NLRP1, NLRP3, and AIM2 to oligomerize with ASC speck to form the inflammasome complex and initiate the downstream signaling of GSDMD mediated pyroptosis. Another response is the increase in genes to manufacture proinflammatory cytokines, the inflammasome formation activates the cleavage of the proinflammatory cytokines to the activated forms, which are secreted into the extracellular environment and recruit a widespread inflammation. - Source: PubMed
Publication date: 2026/06/07
de Rivero Vaccari Juan PabloDavis David ASawaya Andrew PGaramszegi Susanna PSun XiaoyanBarreda AyledBramlett Helen MGultekin Sakir HumayunDietrich W DaltonKeane Robert WVontell Regina T