• Product nameAnti-NLRP3 antibody
    See all NLRP3 primary antibodies
  • Description
    Rabbit polyclonal to NLRP3
  • Tested applicationsSuitable for: WBmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide corresponding to a region within amino acids 974 and 1036 of Human CIAS1/ NALP3 (NP_001073289).

  • Positive control
    • Raji cell lysate



Our Abpromise guarantee covers the use of ab98151 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/500 - 1/3000. Predicted molecular weight: 118 kDa.


  • 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.
  • Cellular localizationCytoplasm.
  • Information by UniProt
  • Database links
  • Alternative names
    • AGTAVPRL antibody
    • AII/AVP antibody
    • Angiotensin/vasopressin receptor AII/AVP like antibody
    • Angiotensin/vasopressin receptor AII/AVP-like antibody
    • C1orf7 antibody
    • Caterpiller protein 1.1 antibody
    • CIAS 1 antibody
    • CIAS1 antibody
    • CLR1.1 antibody
    • Cold autoinflammatory syndrome 1 antibody
    • Cold autoinflammatory syndrome 1 protein antibody
    • Cryopyrin antibody
    • Familial cold autoinflammatory syndrome antibody
    • FCAS antibody
    • FCU antibody
    • LRR and PYD domains-containing protein 3 antibody
    • Muckle-Wells syndrome antibody
    • MWS antibody
    • NACHT antibody
    • NACHT LRR and PYD containing protein 3 antibody
    • NALP 3 antibody
    • NALP3 antibody
    • NALP3_HUMAN antibody
    • NLRP3 antibody
    • PYPAF 1 antibody
    • PYPAF1 antibody
    • PYRIN containing APAF1 like protein 1 antibody
    • PYRIN-containing APAF1-like protein 1 antibody
    see all

Anti-NLRP3 antibody images

  • Anti-NLRP3 antibody (ab98151) at 1/1500 dilution + Raji whole cell lysate at 30 µg

    Predicted band size : 118 kDa
    7.5% SDS PAGE

References for Anti-NLRP3 antibody (ab98151)

ab98151 has not yet been referenced specifically in any publications.

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