The following text describes a protein:
Function:
Acts as the sensor component of the nlrp1 inflammasome, which mediates inflammasome activation in response to various pathogen-associated signals, leading to subsequent pyroptosis. Inflammasomes are supramolecular complexes that assemble in the cytosol in response to pathogens and other damage-associated signals and play critical roles in innate immunity and inflammation. Acts as a recognition receptor (PRR): recognizes specific pathogens and other damage-associated signals, and mediates the formation of the inflammasome polymeric complex (By similarity). In response to pathogen-associated signals, the N-terminal part of nlrp1 is degraded by the proteasome, releasing the cleaved C-terminal part of the protein (NACHT, LRR and PYD domains-containing protein 1, C-terminus), which polymerizes to initiate the formation of the inflammasome complex: the inflammasome recruits and activate pro-inflammatory caspases (caspa and/or caspb), leading to pyroptosis (By similarity); [NACHT, LRR and PYD domains-containing protein 1 homolog]: Constitutes the precursor of the nlrp1 inflammasome, which mediates autoproteolytic processing within the FIIND domain to generate the N-terminal and C-terminal parts, which are associated non-covalently in absence of pathogens and other damage-associated signals; [NACHT, LRR and PYD domains-containing protein 1, N-terminus]: Regulatory part that prevents formation of the nlrp1 inflammasome: in absence of pathogens and other damage-associated signals, interacts with the C-terminal part of nlrp1 (NACHT, LRR and PYD domains-containing protein 1, C-terminus), preventing activation of the nlrp1 inflammasome (By similarity). In response to pathogen-associated signals, this part is ubiquitinated and degraded by the proteasome, releasing the cleaved C-terminal part of the protein, which polymerizes and forms the nlrp1 inflammasome (By similarity); [NACHT, LRR and PYD domains-containing protein 1, C-terminus]: Constitutes the active part of the nlrp1 inflammasome (By similarity). In absence of pathogens and other damage-associated signals, interacts with the N-terminal part of nlrp1 (NACHT, LRR and PYD domains-containing protein 1, N-terminus), preventing activation of the nlrp1 inflammasome (By similarity). In response to pathogen-associated signals, the N-terminal part of nlrp1 is degraded by the proteasome, releasing this form, which polymerizes to form the nlrp1 inflammasome complex: the nlrp1 inflammasome complex then directly recruits and activates pro-inflammatory caspases (caspa and/or caspb) activation, leading to subsequent pyroptosis (By similarity).
Subcellular Localization:
Cytoplasm. Note=Co-localizes with pycard, caspa and caspb in the cytoplasm; [NACHT, LRR and PYD domains-containing protein 1, C-terminus]: Inflammasome.
Domain:
The CARD domain is involved in the interaction with pycard; [NACHT, LRR and PYD domains-containing protein 1, C-terminus]: The C-terminal part of nlrp1 oligomerizes to form the core of the nlrp1 inflammasome filament: in the filament, the CARD domains form a central helical filaments that are promoted by oligomerized, but flexibly linked, UPA regions surrounding the filaments.
Sequence:
MSSDYTDRNNLASAIKTLGDMLEKDEAFQRLMYNASTKGEINRGRVNKVFLKALLSAGDKVGEFLNELIDHLNLFKVLGDFSWNPPVLKEAELNERTSQLRTQQHKYVERVSGFSHYGFGETGTPARGDITSPRGPQVASIEEDLATSKLAELLLAVGDHLEKIEKKGQFLPENVERFSLDCFITSESVKLSSEAVELAPCYTEPVIIQRSKEQTEKYCQEYVRSPHTSSHLLSNDKTQSIRIGQLFSPDSDGNTPKTVILCGDSGRGKSFVLEKIILDWVHLEHHFENFDAVFLLKYEELKCLSEEMSLTELLSRSCSLTSDQISQILQLTPEKVLFLIDGIDDFSFNAHIQISSPTDPSQKAPVISIIHCLMRDLLLVESSVIVTTRYTAAAELSSLCKRPQRFTEIEGFSERRVQEYFQKFFQDEQLFKKAYESMKTNETLLTFCSVPLLCWMVCFCLKKDADQVMTELKTTTSIYVHFVSTLLEDHHQSQSFLRSLGQLAEEGMKNRQNLFDEKSVTRTGLDPATRVFMNKIYLKRKKKHELLFKFKHLSFQEFFAALYYIMLDEEESWCKVSELFNMMESEALIHRSPPIFRGRLSNPIPSVMMFLCGLFNKKVSSSLFEKMKSTFSHNVKLKKKELKKKLMKMIPAMIRQYGFELFALHCLYELQDERFVTKVLETHKFIDLSNVSLRSTDCLVLCYCLRLCPNIRELNFMNCDLTAAKLKILQPALGLCETLRFSVEHLSEIGDLIQILSESKILRELKVREDEYGVESPRWSFNLSVTRGDVLLTLSSSEKNPSFSSVLNIRLTCAQSQISRTDWTLFLQRLRKTGTLTEDSSADDDHVSLQLSSLHSVGLKSLDLTLVSLNESWASGIISLIQNCTSLQQLKVSVTGLLLEEGLKLLKKSLTDPHCTVIIEGRRNCSEPSEEHLRQSYEKVEIHFKPKLLEELAELSICNPGSSALNIHCQSCVDVADSDQWVQVEPSVCRGEGGTEFRITTPAGRFQCSRTRMRWVCDGDVTLHYRAVDGHFLNAELERLQCERVAPVLDVNVISGKLEEAHLPHYMCLAESDPALTNAVKLLSVEDEGISLESVELTRFHAKILQPMFSPKTVLVKLGIPVKVHCDLLIFMTHTCPIILNVYFFPSDSLVEENIKTEEKSSHQIKCSRPEAPLQMKKQHSLEVPDAVVQPEAIKLRGNMKPNFFQVKQPVVNDITMILSRVDDQKSVWTGTIWKKLIDIKLNKTESDLFQSGQKHKTSQPAHSFDKAQFFDTHWCNLIKSVENVDTVADKLLQKQIIHEQFYSEIIHHKSTSEESMRKICVIVRKGSAAVKEIFISILLQENPNLLNHLPSSDS