NLRP3 | NALP3/Cryopyrin Rabbit pAb (一抗) - WB | Bioss

bs-25913R

NLRP3 | NALP3/Cryopyrin Rabbit pAb

细胞凋亡诱导蛋白NALP3抗体

AGTAVPRL; AII; AVP; C1orf7; CIAS1; CLR1.1; DFNA34; FCAS; FCAS1; FCU; KEFH; MWS; NALP3; PYPAF1; AII/AVP; Mmig1; NLRP3_HUMAN; NLRP3; Angiotensin/vasopressin receptor AII/AVP-like; Caterpiller protein 1.1 (CLR1.1); Cold-induced autoinflammatory syndrome 1 protein; Cryopyrin; PYRIN-containing APAF1-like protein 1; 3.6.4.-; NLRP3_MOUSE; Cold autoinflammatory syndrome 1 protein homolog; Mast cell maturation-associated-inducible protein 1; NLR family pyrin domain containing 3; cold autoinflammatory syndrome 1; deafness, autosomal dominant 34; nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3; Cold-induced autoinflammatory syndrome 1 pr

Rabbit

KLH conjugated synthetic peptide derived from human NALP3: 371-470/1036

IgG

Liquid

affinity purified by Protein A

Polyclonal

114 kDa

125 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

May 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. Subcellular Location : Cytoplasm.

NLRP3

NACHT, LRR and PYD domains-containing protein 3

Cytoplasm.

Expressed 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.

Defects 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.

Belongs to the NLRP family.
Contains 1 DAPIN domain.
Contains 9 LRR (leucine-rich) repeats.
Contains 1 NACHT domain.

May 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.