Редактирование: NLRP1

NACHT, LRR and PYD domains-containing protein 1 (Caspase recruitment domain-containing protein 7) (Death effector filament-forming ced-4-like apoptosis protein) (Nucleotide-binding domain and caspase recruitment domain) [CARD7] [DEFCAP] [KIAA0926] [NAC] [NALP1]

==Publications==

{{medline-entry
|title=NADPH oxidase 2-mediated [[NLRP1]] inflammasome activation involves in neuronal senescence in hippocampal neurons in vitro.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30677569
|abstract=Oxidative stress and inflammation are closely related to neuron ageing. NADPH oxidase 2 (NOX2) is a major source of reactive oxygen species (ROS) generation in brain. The nucleotide-binding oligomerisation domain (NOD)-like receptor protein 1 ([[NLRP1]]) inflammasome is responsible for the formation of proinflammatory molecules in neurons. We hypothesize that NOX2-derived ROS accumulation mediates activation of [[NLRP1]] inflammasome, which is involved in age-related neuronal damage. In the present study, we investigated the changes of NOX2-[[NLRP1]] signaling pathway in primary hippocampal neurons cultured for different time (6, 9 and 12 days, d). Meanwhile, we further examined the effect of ROS inhibitor and [[NLRP1]]-siRNA on neuronal senescence. The results showed that, compared with 6 d group, the neuronal apoptosis and β-Galactosidase (β-Gal) expression were significantly increased, and the microtubule-associated protein 2 (MAP2) expression significantly decreased in primary hippocampal neurons cultured for 12 d. In addition, the results also showed that the production of ROS, the expressions of NOX2 and [[NLRP1]] inflammasome were significantly increased with the prolongation of culture time in hippocampal neurons. Moreover, the NOX inhibitor (apocynin) and ROS scavenger (tempol) significantly decreased ROS production and alleviated neuronal damage. Meanwhile, the tempol and apocynin treatment significantly decreased the expression of [[NLRP1]] inflammasome in hippocampal neurons. Furthermore, the [[NLRP1]]-siRNA and caspase-1 inhibitor treatment also alleviated neuronal damage. These results suggest that NOX2-derived ROS generation may induce brain inflammation via NLRP-1 inflammasome activation and lead to age-related neuronal damage. The NADPH oxidase and [[NLRP1]] inflammasome may be important therapeutic targets for age-related neuronal damage.
|mesh-terms=* Animals
* Apoptosis
* Cells, Cultured
* Cellular Senescence
* Gene Expression Regulation
* Hippocampus
* Inflammation
* NADPH Oxidase 2
* Nerve Tissue Proteins
* Neurons
* RNA, Small Interfering
* Rats
* Rats, Sprague-Dawley
* Reactive Oxygen Species
* Signal Transduction
|keywords=* NADPH oxidase
* NLRP1 inflammasome
* Neuroinflammation
* Neuronal senescence
* ROS oxidative stress
|full-text-url=https://sci-hub.do/10.1016/j.intimp.2019.01.025
}}
{{medline-entry
|title=Genetic analysis of long-lived families reveals novel variants influencing high density-lipoprotein cholesterol.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24917880
|abstract=The plasma levels of high-density lipoprotein cholesterol (HDL) have an inverse relationship to the risks of atherosclerosis and cardiovascular disease (CVD), and have also been associated with longevity. We sought to identify novel loci for HDL that could potentially provide new insights into biological regulation of HDL metabolism in healthy-longevous subjects. We performed a genome-wide association (GWA) scan on HDL using a mixed model approach to account for family structure using kinship coefficients. A total of 4114 subjects of European descent (480 families) were genotyped at ~2.3 million SNPs and ~38 million SNPs were imputed using the 1000 Genome Cosmopolitan reference panel in MACH. We identified novel variants near-[[NLRP1]] (17p13) associated with an increase of HDL levels at genome-wide significant level (p < 5.0E-08). Additionally, several [[CETP]] (16q21) and ZNF259-[[APOA5]]-A4-[[C3]]-A1 (11q23.3) variants associated with HDL were found, replicating those previously reported in the literature. A possible regulatory variant upstream of [[NLRP1]] that is associated with HDL in these elderly Long Life Family Study (LLFS) subjects may also contribute to their longevity and health. Our [[NLRP1]] intergenic SNPs show a potential regulatory function in Encyclopedia of DNA Elements (ENCODE); however, it is not clear whether they regulate [[NLRP1]] or other more remote gene. [[NLRP1]] plays an important role in the induction of apoptosis, and its inflammasome is critical for mediating innate immune responses. Nlrp1a (a mouse ortholog of human [[NLRP1]]) interacts with SREBP-1a (17p11) which has a fundamental role in lipid concentration and composition, and is involved in innate immune response in macrophages. The [[NLRP1]] region is conserved in mammals, but also has evolved adaptively showing signals of positive selection in European populations that might confer an advantage. [[NLRP1]] intergenic SNPs have also been associated with immunity/inflammasome disorders which highlights the biological importance of this chromosomal region. 

|keywords=* NALP1
* aging
* familial longevity
* family-based study
* genomewide association study
* lipids
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4042684
}}