Product nameAnti-NLRP3 antibody
See all NLRP3 primary antibodies
DescriptionGoat polyclonal to NLRP3
Tested applicationsSuitable for: Flow Cyt, IHC-FoFr, ICC/IFmore details
Species reactivityReacts with: Mouse, Human
Predicted to work with: Rat, Cow
No signal has been obtained in Western blot but low background has observed in Daudi, A431, Jurkat, U937 and MOLT-4 lysates at up to 1µg/ml. We would appreciate any feedback from people in the field.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 0.5% BSA, Tris buffered saline
Concentration information loading...
PurityImmunogen affinity purified
Purification notesPurified from goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide.
Our Abpromise guarantee covers the use of ab4207 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Flow Cyt||Use at an assay dependent concentration.
ab37373 - Goat polyclonal IgG, is suitable for use as an isotype control with this antibody.
|IHC-FoFr||Use at an assay dependent concentration. PubMed: 28726778|
|ICC/IF||Use at an assay dependent concentration.|
FunctionMay function as an inducer of apoptosis. Interacts selectively with ASC and this complex may function as an upstream activator of NF-kappa-B signaling. Inhibits TNF-alpha induced activation and nuclear translocation of RELA/NF-KB p65. Also inhibits transcriptional activity of RELA. Activates caspase-1 in response to a number of triggers including bacterial or viral infection which leads to processing and release of IL1B and IL18.
Tissue specificityExpressed in blood leukocytes. Strongly expressed in polymorphonuclear cells and osteoblasts. Undetectable or expressed at a lower magnitude in B- and T-lymphoblasts, respectively. High level of expression detected in chondrocytes. Detected in non-keratinizing epithelia of oropharynx, esophagus and ectocervix and in the urothelial layer of the bladder.
Involvement in diseaseDefects in NLRP3 are the cause of familial cold autoinflammatory syndrome type 1 (FCAS1) [MIM:120100]; also known as familial cold urticaria. FCAS are rare autosomal dominant systemic inflammatory diseases characterized by episodes of rash, arthralgia, fever and conjunctivitis after generalized exposure to cold.
Defects in NLRP3 are a cause of Muckle-Wells syndrome (MWS) [MIM:191900]; also known as urticaria-deafness-amyloidosis syndrome. MWS is a hereditary periodic fever syndrome characterized by fever, chronic recurrent urticaria, arthralgias, progressive sensorineural deafness, and reactive renal amyloidosis. The disease may be severe if generalized amyloidosis occurs.
Defects in NLRP3 are the cause of chronic infantile neurologic cutaneous and articular syndrome (CINCA) [MIM:607115]; also known as neonatal onset multisystem inflammatory disease (NOMID). CINCA is a rare congenital inflammatory disorder characterized by a triad of neonatal onset of cutaneous symptoms, chronic meningitis and joint manifestations with recurrent fever and inflammation.
Sequence similaritiesBelongs to the NLRP family.
Contains 1 DAPIN domain.
Contains 9 LRR (leucine-rich) repeats.
Contains 1 NACHT domain.
- Information by UniProt
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Effects of ATP, cholesterol crystals and 7-Ketocholesterol on Nlrp3 inflammasome formation in Asc+/+and Asc−/− BMMs
Representative confocal fluorescence images depicting the effects of cholesterol crystals (CHC, 0.5 mg/ml, 16 h), 7-ketocholesterol (7-Ket, 10 µg/ml, 16 h), or ATP (2.5 mM, 16 h) on the colocalization between Nlrp3 and Asc from Asc+/+ and Asc−/− BMMs.
4% paraformaldehyde-fixed, 0.1% Triton X-100 permeabilized mouse bone marrow macrophages were stained for NLRP3 using ab4207 at 1/200 dilution in ICC/IF.
(From Figure 2A of Li et al)
Paraformaldehyde-fixed, 0.15% Triton X-100 permeabilized U937 (human histiocytic lymphoma cell line) cells stained for NLRP3 (green) using ab4207 at 10 μg/ml in ICC/IF. (green). The nuclear counterstain is DAPI (blue). The negative control is unimmunized goaet IgG at 10 μug/ml, followed by the secndary antibody.
Flow cytometric analysis of paraformaldehyde-fixed, 0.5% Triton X-100 permeabilized human PBMCs labeling NLRP3 with ab4207 at 10 μg/ml (blue) compared to an unimmunized control IgG (black). Gated on granulocytes.
ab4207 staining NLRP3 in the Human White Blood Cells (Mixed Population) by Flow Cytometry. WBC were isolated spinning Blood on Ficoll Gradient after removal of RBC's and permeabilized with 0.1% Triton-X100 in 2% BSA for 15 minutes. The sample was incubated with the primary antibody (1/100 in PBS + 2% BSA in PBS) for 16 hours at 4°C. An Alexa Flour488 Donkey Anti Goat IgG (H+L) (1/250) was used as the secondary antibody.
Gating Strategy: Monocytes
ab4207 staining CIAS1 / NALP3 in murine RAW 264.7 cells by Immunocytochemistry/ Immunofluorescence.Cells were fixed in paraformaldehyde, permeabilized using 0.1% Triton-X100 in 2% BSA for 15 minutes, blocked with 2% BSA for 1 hour at 22°C and then incubated with ab4207 at a 1/200 dilution for 16 hours at 4°C. The secondary used was an Alexa Fluor® 488 conjugated donkey anti-goat (H+L) polyclonal used at a 1/500 dilution.WGA: Alexa Fluor® 568 Wheat Germ Agglutinin.
Immunofluorescence analysis of Human MDM cells, staining CIAS1 / NALP3 with ab4207.
Cells were fixed with paraformaldehyde, permeabilized with 0.1% Triton X-100 and blocked with 5% goat serum for 1 hour at room temp. Samples were incubated with primary antibody (1/200 in 1% BSA in PBS) for 12 hours at 4°C. A Cy5® conjugated donkey anti-goat polyclonal IgG (1/400) was used as the secondary antibody.
This product has been referenced in:
- Luan J et al. NOD-Like Receptor Protein 3 Inflammasome-Dependent IL-1ß Accelerated ConA-Induced Hepatitis. Front Immunol 9:758 (2018). Read more (PubMed: 29692782) »
- Peng S et al. Atorvastatin Inhibits Inflammatory Response, Attenuates Lipid Deposition, and Improves the Stability of Vulnerable Atherosclerotic Plaques by Modulating Autophagy. Front Pharmacol 9:438 (2018). Read more (PubMed: 29773990) »