Biological Strategies: Western Blot: NLRP2/NALP2 Antibody [NB100-56155] - Analysis of NLRP2/NALP2 using antibody at 1:2000. HEK293T: mock transfected cells, HEK293T-NALP2:NALP2 transiently transfected cells; ...read more
Immunohistochemistry-Paraffin: NLRP2/NALP2 Antibody [NB100-56155] - NLRP2 was detected in immersion fixed paraffin-embedded sections of human placenta using Rabbit Anti-Human NLRP2 polyclonal Antibody (Catalog # ...read more
A synthetic peptide corresponding to amino acids 97-115 (LKSFNKRKPLSLGITRKER) of human NALP2/PAN1/PYPAF2 was used as immunogen; GenBank no. gi|8923473|ref|NP_060322.1
Isotype
IgG
Clonality
Polyclonal
Host
Rabbit
Gene
NLRP2
Purity
Unpurified
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Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
Buffer
Whole antisera
Preservative
0.02% Sodium Azide
Purity
Unpurified
Alternate Names for NLRP2/NALP2 Antibody
CLR19.9
FLJ20510
NACHT, leucine rich repeat and PYD containing 2
NACHT, LRR and PYD domains-containing protein 2
NALP2
NALP2NACHT, LRR and PYD containing protein 2
NBS1
NBS1PYRIN-containing APAF1-like protein 2
NLR family, pyrin domain containing 2
NLRP2
nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domaincontaining 2
PAN1
PAN1Nucleotide-binding site protein 1
PYPAF2
PYPAF2PYRIN domain and NACHT domain-containing protein 1
Background
NALP2 (also known as PAN1/PYPAF2) is a member of the NLR (NACHT-LRR) family which includes both NODs and NALPs (Bruey et al, 2004). Alternative names for the NLR family include CATERPILLER, NOD and NOD-LRR. NLR family members are thought to be intracellular pathogen-recognition receptors (PRRs) (reviewed in Martionon and Tschopp, 2005 and 2007; Creagh and O'Neill, 2006; Petrilli et al, 2005). PRRs are key components of immune systems and are involved in innate effector mechanisms and activation of adaptive immunity. Toll-like receptors (TLRs) are the most well studied PPRs and overlaps have been identified between the signaling pathways used by some NLRs and TLRs suggesting redundancy and cooperation between NLR and TLR pathways. At least fourteen NALPs have been identified in the human genome, and a common feature among NALPs 1-3, 6, and 12 is their ability to to recruit the adaptor protein ASC through a homotypic PYD-PYD interaction, which in turn recruits caspase-1 through a CARD-CARD interaction. The oligomerization of NALPs is thought to bring the inflammatory caspases into close proximity leading to their activation within the inflammasome. The inflammasome is a multiprotein complex of more than 700 kDa that is responsible for the activation of caspases 1 and 5, which leads to the processing and secretion of the pro-inflammatory cytokines IL-1b and IL-18. The NALP2/3 inflammasomes contain, in addition to NALP2 or NALP3, the caspase recruitment domain (CARD)-containing protein Cardinal, ASC and caspase 1. Processing of the pro-inflammatory cytokines IL-1b and IL-18 by caspases leads to to the secretion of active cytokines and elicits a potent inflammatory response. Similar to TLRs, activation of the inflammasome by NLRs occurs through the recognition of pathogen-associated molecular patterns (PAMPs) through their LRR (leucine rich) domains): TLR family members recognize bacteria, viruses, fungi and protoza, whereas NLRs with known functions recognize bacteria. The expression of NALP2 is upregulated in THP-1 macrophage cells by LPS and certain cytokines including interferon g and b, supporting a role for NALP2 in host-defense and inflammation (Bruey et al, 2004). Additionally, NALP2 is expressed in several human tumor cell lines. However, the endogenous expression of NALP2 varies widely among tumor cells lines, with the highest levels found in MCF-7 and MDA-MB-435 breast cancer, Caco2 colon cancer and UACC62 melanoma cells (Bruey et al, 2004). This antibody recognizes NALP2; human NALP2 is a 1062 amino acid protein.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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