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Hypoxia reduces inflammatory processes and induces autophagy in Il-10−/− mice. a, b, c, d, e, f and g WT, Nrlp3−/−,Il-10−/−, and Il-10−/−Nrlp3−/−double knockout mice were subjected to normoxia (N, 21% O2) or hypoxia (H, 8% O2). After 18 h, mice were killed and colon biopsies were collected. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Results represent mean + s.e.m., WT mice under normoxia: n = 5, WT mice under hypoxia: n = 5; Nrlp3−/− mice under normoxia: n = 4; Nrlp3−/− mice under hypoxia: n = 5; Il-10−/− mice under hypoxia: n = 4; Il-10−/− mice under hypoxia: n = 4; Il-10−/−Nrlp3−/− mice under normoxia: n = 7; Il-10−/−Nrlp3−/− mice under hypoxia: n = 9, *P < 0.05; **P < 0.01; ***P < 0.001. h Total protein was isolated and western blot performed. LC3-I and LC3-II bands were quantified, and autophagy was measured by variations in the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)

DMOG reduces inflammation and induces autophagy in DSS-treated mice. a, b, c, d, e and f WT mice were administered with 2% DSS for 5 days and co-administered with 8 mg DMOG injected intraperitoneally every second day. Weight loss was monitored during the course of treatment a. After a recovery period, mice were killed at day 9 colon biopsies were collected and colon length was measured b. Mucosal damage was assessed by colonoscopy c and murine endoscopic score of colitis severity (MEICS) was calculated d. H&E staining of distal colon sections displayed a significant decrease in barrier breakdown and inflammatory infiltrate in DMOG-treated mice e. Scale bar, 100 µm. Total histological score at day 9 was calculated as the sum of epithelial damage and infiltration score f. g, h, i, j, k, l and m distal colon biopsies were collected and transcript analysis was performed. Statistical analysis was performed using Student t-test.Results represent mean + s.e.m., DSS-treated mice administered with PBS: n = 5; DSS-treated mice administered with DMOG: n = 5; *P < 0.05; **P < 0.01. n Total protein was isolated and Western blot performed. LC3-I and LC3-II bands were quantified, and autophagy was measured by variations in the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)

Hypoxia reduces inflammatory signaling pathways and NLRP3 expression and induces autophagy in IECs. a HT-29 cells were subjected to normoxia and hypoxia at the indicated times in the absence or presence of 10 µg/ml LPS. Autophagy was measured by variations in the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin. Results are representative of two independent experiments. b, c and d HT-29 cells were subjected to normoxia and hypoxia for the indicated periods in the absence or presence of 10 µg/ml LPS, followed by transcript analysis. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Results represent mean + s.e.m. of two independent experiments done in triplicate, *P < 0.05; **P < 0.01; ***P < 0.001; ns not significant. e HT-29 cells were subjected to normoxia or hypoxia in the presence and absence of 10 µg/ml LPS and 20 µM of MG132. Results are representative of two independent experiments. f and g Putative binding sites for HIF-1α and NF-κB were found in the p62 f and NLRP3 g promoters using Genomatix software tools. Numbers under the boxes indicate the distance from the transcription start site. HT-29 cells were subjected to normoxia (21% O2) or hypoxia (0.2% O2) for 6 h and 24 h. ChIP analysis was performed using antibodies against HIF-1α and NF-κB for immunoprecipitation. PCR was performed using the promoter-specific primers for the p62 f and NLRP3 g promoter binding sites of HIF-1α and NF-κB. Aliquots taken prior to immunoprecipitation were used as input control. PCR products were run on 2% agarose gel. The results are representative of three independent experiments.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)

Hypoxia reduces inflammatory processes and induces autophagy in the DSS mouse model of colitis. a, b, c, d, e, f and g WT and Nrlp3−/− mice were administered with DSS or DSS-free water and subjected to normoxia (N, 21% O2) or hypoxia (H, 8% O2). After 18 h, mice were killed and colon biopsies were collected. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Results represent mean + s.e.m., WT mice under normoxia: n = 5, WT mice under normoxia: n = 5, DSS-treated WT mice under normoxia: n = 6; Nrlp3−/− mice under normoxia: n = 5; DSS-treated Nrlp3−/− mice under normoxia: n = 6; WT mice under hypoxia: n = 4, DSS-treated WT mice under hypoxia: n = 5; Nrlp3−/− mice under hypoxia: n = 3; DSS-treated Nrlp3−/− mice under hypoxia: n = 3, *P < 0.05; **P < 0.01; ***P < 0.001. h Total protein was isolated and western blot performed. LC3-I and LC3-II bands were quantified, and autophagy was measured by variations in the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)

NLRP3 regulates autophagy through an inflammasome-independent mechanism via direct binding to mTOR. a HT-29 cells were transfected with NLRP3-specific siRNA or negative control siRNA using Lipofectamine RNAiMAX. Forty-eight hours after transfection, total protein was isolated and western blot performed. Quantification of the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin is presented. Statistical analysis was performed using Student t-test. Results represent mean + s.e.m. of three independent experiments, *P < 0.05. b HT-29 cells were subjected to normoxia (21% O2) or hypoxia (0.2% O2) for 24 h in the presence and absence of LPS. Co-IP using NLRP3 antibody was performed, followed by anti-mTOR immunoblotting. Quantification relative to cells subjected to normoxia in the absence of LPS after normalization to NLRP3 is presented. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Results represent mean of three independent experiments + s.e.m., **P < 0.01
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)

NLRP3 regulates autophagy through an inflammasome-independent mechanism via direct binding to mTOR. a HT-29 cells were transfected with NLRP3-specific siRNA or negative control siRNA using Lipofectamine RNAiMAX. Forty-eight hours after transfection, total protein was isolated and western blot performed. Quantification of the ratio of LC3-II/LC3-I and the total amount of LC3 (LC3-I plus LC3-II) relative to β-actin is presented. Statistical analysis was performed using Student t-test. Results represent mean + s.e.m. of three independent experiments, *P < 0.05. b HT-29 cells were subjected to normoxia (21% O2) or hypoxia (0.2% O2) for 24 h in the presence and absence of LPS. Co-IP using NLRP3 antibody was performed, followed by anti-mTOR immunoblotting. Quantification relative to cells subjected to normoxia in the absence of LPS after normalization to NLRP3 is presented. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Results represent mean of three independent experiments + s.e.m., **P < 0.01
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation. Nat Commun (2017)







Product Details
Alternative Name |
NACHT-, LRR- and PYD-containing protein 3, CIAS1, Cryopyrin, Cold autoinflammatory syndrome 1 protein, PYPAF1, PYRIN-containing APAF1-like protein 1 |
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Application |
IHC (FS), IP, WB |
Clone |
Nalpy3-b |
Formulation |
Liquid. In PBS containing 0.02% sodium azide. |
Host |
Mouse |
Immunogen |
Recombinant human NLRP3/NALP3 (NACHT-, LRR- and PYD-containing protein 3) (pyrin domain). |
Isotype |
IgG1 |
Recommendation Dilutions/Conditions |
Immunoprecipitation (1:50)Western Blot (1:1,000)Suggested dilutions/conditions may not be available for all applications.Optimal conditions must be determined individually for each application. |
Source |
Purified from concentrated hybridoma tissue culture supernatant. |
Species Reactivity |
Human |
Specificity |
Detects endogenous protein by IP and WB. |
UniProt ID |
Q96P20 |
Worry-free Guarantee |
This antibody is covered by our Worry-Free Guarantee. |
Handling & Storage
Handling |
Avoid freeze/thaw cycles. |
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Short Term Storage |
+4°C |
Long Term Storage |
-20°C |
Shipping |
Blue Ice |
Regulatory Status |
RUO – Research Use Only |
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- Macrophage IL-1β-positive microvesicles exhibit thrombo-inflammatory properties and are detectable in patients with active juvenile idiopathic arthritis: A. Cambon, et al.; Front. Immunol. 14, 1228122 (2023), Abstract
- Canagliflozin inhibits inflammasome activation in diabetic endothelial cells – Revealing a novel calcium-dependent anti-inflammatory effect of canagliflozin on human diabetic endothelial cells: X. Li, et al.; Biomed. Pharmacother. 159, 114228 (2023), Abstract
- Inflammasome assembly is required for intracellular formation of β2-microglobulin amyloid fibrils, leading to IL-1β secretion: N. Kaneko, et al.; Int. J. Immunopathol. Pharmacol. 36, 3946320221104550 (2022), Abstract
- K+ regulates relocation of Pellino-2 to the site of NLRP3 inflammasome activation in macrophages.: Cristea, I., Bruland, O., et al.; FEBS Lett. 595, 2437 (2021), Application(s): ICC-IF / Reactant(s): Human, Abstract
- Stimulation of Vibratory Urticaria-Associated Adhesion-GPCR, EMR2/ADGRE2, Triggers the NLRP3 Inflammasome Activation Signal in Human Monocytes.: Gordon, S., Lin, H. H., et al.; Front. Immunol. 11, 602016 (2021), Application(s): WB / Reactant(s): Human, Abstract
- Hemoglobin oxidation generates globin-derived peptides in atherosclerotic lesions and intraventricular hemorrhage of the brain, provoking endothelial dysfunction.: Balla, J., Méhes, G., et al.; Lab. Invest. 100, 986 (2020), Application(s): WB / Reactant(s): Human, Abstract
- SARS-Coronavirus Open Reading Frame-8b triggers intracellular stress pathways and activates NLRP3 inflammasomes.: Shi, C. S., Nabar, N. R., et al.; Cell Death Discov. 5, 101 (2019), Reactant(s): Human, Abstract
- ASC and NLRP3 maintain innate immune homeostasis in the airway through an inflammasome-independent mechanism: R. Fang, et al.; Mucosal Immunol. 12, 1092 (2019), Abstract
- IAPP/amylin deposition, which is correlated with expressions of ASC and IL-1β in β-cells of Langerhans’ islets, directly initiates NLRP3 inflammasome activation: Morikawa, S., Kaneko, N., et al.; Int. J. Immunopathol. Pharmacol. 32, 2058738418788749 (2018), Abstract
- Hypoxic expression of NLRP3 and VEGF in cultured retinal pigment epithelial cells: contribution of P2Y2 receptor signaling.: Bringmann, A., Wiedemann, P., et al.; Purinergic Signal. 14, 471 (2018), Reactant(s): Human, Abstract
- Issues with the Specificity of Immunological Reagents for NLRP3: Implications for Age-related Macular Degeneration: C. Kosmidou, et al.; Sci. Rep. 8, 61 (2018), Abstract — Full Text
- PTPN22 regulates NLRP3-mediated IL1B secretion in an autophagy-dependent manner: M.R. Spalinger, et al.; Autophagy 13, 1590 (2017), Abstract — Full Text
- Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation: J. Cosin-Roger, et al.; Nat. Commun. 8, 98 (2017), Application(s): WB / Reactant(s) Human, Mouse, Abstract — Full Text
- Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states: D. Furman, et al.; Nat. Med. 23, 174 (2017), Abstract — Full Text
- Sulforaphane exerts its anti-inflammatory effect against amyloid-β peptide via STAT-1 dephosphorylation and activation of Nrf2/HO-1 cascade in human THP-1 macrophages: Y.W. An, et al.; Neurobiol. Aging 38, 1 (2016), Application(s): Western blot, Abstract
- Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early-onset autoinflammatory disease: Q. Zhou, et al.; Nat. Genet. 48, 67 (2016), Application(s): Immunoblots of total cell lysates, Abstract
- Enhanced activity of NLRP3 inflammasome in peripheral blood cells of patients with active rheumatoid arthritis: C. Choulaki, et al.; Arthritis Res. Ther. 17, 257 (2015), Application(s): WB / Reactant(s) Human, Abstract — Full Text
- Dysregulated production of interleukin-1β upon activation of the NLRP3 inflammasome in patients with familial Mediterranean fever: A. Repa, et al.; Hum. Immunol. 76, 488 (2015), Application(s): Western Blot, Abstract
- Staphylococcus aureus Activates the NLRP3 Inflammasome in Human and Rat Conjunctival Goblet Cells: V. McGilligan, et al.; PLoS One 8, e74010 (2013), Application(s): WB, IHC, and Cell culture of rat and human cells, Abstract — Full Text
- Mechanism of hepatic inflammation during hepatitis C virus infection: A.A. Negash, et al.; , (2013), (Thesis paper), Application(s): WB, IHC of human liver cells, Abstract
- NLRP3 inflammasome activation in retinal pigment epithelial cells by lysosomal destabilization: implications for age-related macular degeneration: W.A. Tseng, et al.; Invest. Ophthalmol. Vis. Sci. 54, 110 (2013), Application(s): Immunohistochemistry of paraffin-embedded tissue, Abstract — Full Text
- Complement Protein C1q Directs Macrophage Polarization and Limits Inflammasome Activity during the Uptake of Apoptotic cells: M. Benoit, et al.; J. Immunol. 188, 5682 (2012), Application(s): WB, Cell culture of human lymphocytes and macrophages, Abstract — Full Text
- A comprehensive analysis of pattern recognition receptors in normal and inflamed human epidermis: upregulation of dectin-1 in psoriasis.: Schalkwijk, J., de Koning, H. D., et al.; J. Invest. Dermatol. 130, 2611 (2010), Application(s): IHC, Abstract
- Expression and function of the NALP3 inflammasome in rheumatoid synovium: Kolly, L., Busso, N., et al.; Immunology 129, 178 (2010), Abstract
- Malarial hemozoin activates the NLRP3 inflammasome through Lyn and Syk kinases: M.T. Shio, et al.; PLoS Pathog. 5, e1000559 (2009), Abstract
- Polymorphism in a gene coding for the inflammasome component NALP3 and recurrent vulvovaginal candidiasis in women with vulvar vestibulitis syndrome: A. Lev-Sagie, et al.; Am. J. Obstet. Gynecol. 200, 303 (2009), Application(s): Immunohistochemistry of paraffin-embedded tissue, Abstract
- Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response: J.A. Kummer, et al.; J. Histochem. Cytochem. 55, 443 (2007), Abstract
- NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder: L. Agostini, et al.; Immunity 20, 319 (2004), Abstract
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