Description: Homo sapiens NLR family, pyrin domain containing 2 (NLRP2), transcript variant 1, mRNA. RefSeq Summary (NM_001174083): This gene is a member of the nucleotide-binding and leucine-rich repeat receptor (NLR) family, and is predicted to contain an N-terminal pyrin effector domain (PYD), a centrally-located nucleotide-binding and oligomerization domain (NACHT) and C-terminal leucine-rich repeats (LRR). Members of this gene family are thought to be important regulators of immune responses. This gene product interacts with components of the IkB kinase (IKK) complex, and can regulate both caspase-1 and NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity. The pyrin domain is necessary and sufficient for suppression of NF-kB activity. An allelic variant (rs147585490) has been found that is incapable of blocking the transcriptional activity of NF-kB. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Dec 2016]. Transcript (Including UTRs) Position: hg19 chr19:55,477,711-55,512,510 Size: 34,800 Total Exon Count: 12 Strand: + Coding Region Position: hg19 chr19:55,481,384-55,512,266 Size: 30,883 Coding Exon Count: 11
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
SCOP Domains: 47986 - DEATH domain 52047 - RNI-like 52058 - L domain-like 52075 - Outer arm dynein light chain 1 52540 - P-loop containing nucleoside triphosphate hydrolases
ModBase Predicted Comparative 3D Structure on Q9NX02-4
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.