NLRP1

NLRP1
Dostupne strukture
PDB	Pretraga ortologa: PDBe RCSB
Spisak PDB ID kodova
	1PN5, 3KAT, 4IFP, 4IM6
Identifikatori
Aliasi	NLRP1
Vanjski ID-jevi	OMIM: 606636 MGI: 3582959 HomoloGene: 19080 GeneCards: NLRP1
Lokacija gena (čovjek)
Hrom.	Hromosom 17 (čovjek)
Kraj	5,619,424 bp
Lokacija gena (miš)
Hrom.	Hromosom 11 (miš)
Kraj	71,121,559 bp
Obrazac RNK ekspresije
	; ; ; ;
	Više referentnih podataka o ekspresiji
Ontologija gena
Molekularna funkcija	• protein domain specific binding; • nucleotide binding; • cysteine-type endopeptidase activator activity involved in apoptotic process; • ATP binding; • vezivanje enzima; • GO:0001948, GO:0016582 vezivanje za proteine;
Ćelijska komponenta	• citoplazma; • Inflamasom; • jedro; • intracellular anatomical structure; • nukleoplazma; • citosol; • NLRP1 inflammasome complex;
Biološki proces	• neuron apoptotic process; • regulation of apoptotic process; • activation of cysteine-type endopeptidase activity involved in apoptotic process; • response to muramyl dipeptide; • GO:0097285 apoptoza; • defense response to bacterium; • regulation of inflammatory response; • immune system process; • inflammatory response; • Urođeni imunski sistem; • GO:0022415 viral process; • NLRP1 inflammasome complex assembly; • positive regulation of cysteine-type endopeptidase activity involved in apoptotic process;
	Izvori:Amigo / QuickGO
Ortolozi
	22861
	637515
	ENSG00000091592
	ENSMUSG00000070390
	Q9C000
	Q2LKV5; Q2LKV2; Q2LKW6; Q0GKD5
	NM_033007; NM_001033053; NM_014922; NM_033004; NM_033006
	NM_001039680; NM_001040696; NM_001162414
	NP_001028225; NP_055737; NP_127497; NP_127499; NP_127500
	NP_001035786; NP_001155886
	Wikipodaci
Pogledaj/uredi – čovjek	Pogledaj/uredi – miš

NLRP1 je protein koji ljudi kodira NACHT, LRR, FIIND, CARD domen i protein 1 sa domenima PYD sa hromosoma 17^[5]^[6]^[7] NLRP1 je bio prvi protein za koji je pokazano da formira inflamasom.^[8] NLRP1 se eksprimira u raznim tipovima ćelija, koji su pretežno epitelne ili hematopoetske. Ekspresija se također vidi unutar žljezdanih epitelnih struktura uključujući sluznicu tankog crijeva, želuca, epitel dišnih puteva i u koži bez dlake ili goloj koži.^[9] > NLRP1 polimorfizmi su povezani sa kožnim ekstra-intestinalnim manifestacijama u CD-u.^[9] Njegova najveća ekspresija je otkrivena u ljudskoj koži, psorijazi i vitiligu. Polimorfizmi NLRP1 pronađeni su kod lupus erythematosus i dijabetesa tipa 1.^[10] Utvrđeno je da se varijante mišjeg NLRP1 aktiviraju nakon cijepanja N-terminala pomoću smrtonosnog faktora proteaza u antraksu.^[8]

Aminokiselinska sekvenca[uredi | uredi izvor]

Dužina polipeptidnog lanca je 1.473 aminokiseline, a molekulska težina 165.866 Da.^[7]

C: Cistein

D: Asparaginska kiselina

E: Glutaminska kiselina

F: Fenilalanin

G: Glicin

H: Histidin

I: Izoleucin

K: Lizin

L: Leucin

M: Metionin

N: Asparagin

P: Prolin

Q: Glutamin

R: Arginin

S: Serin

T: Treonin

V: Valin

W: Triptofan

Y: Tirozin

10	20	30	40	50
MAGGAWGRLA	CYLEFLKKEE	LKEFQLLLAN	KAHSRSSSGE	TPAQPEKTSG
MEVASYLVAQ	YGEQRAWDLA	LHTWEQMGLR	SLCAQAQEGA	GHSPSFPYSP
SEPHLGSPSQ	PTSTAVLMPW	IHELPAGCTQ	GSERRVLRQL	PDTSGRRWRE
ISASLLYQAL	PSSPDHESPS	QESPNAPTST	AVLGSWGSPP	QPSLAPREQE
APGTQWPLDE	TSGIYYTEIR	EREREKSEKG	RPPWAAVVGT	PPQAHTSLQP
HHHPWEPSVR	ESLCSTWPWK	NEDFNQKFTQ	LLLLQRPHPR	SQDPLVKRSW
PDYVEENRGH	LIEIRDLFGP	GLDTQEPRIV	ILQGAAGIGK	STLARQVKEA
WGRGQLYGDR	FQHVFYFSCR	ELAQSKVVSL	AELIGKDGTA	TPAPIRQILS
RPERLLFILD	GVDEPGWVLQ	EPSSELCLHW	SQPQPADALL	GSLLGKTILP
EASFLITART	TALQNLIPSL	EQARWVEVLG	FSESSRKEYF	YRYFTDERQA
IRAFRLVKSN	KELWALCLVP	WVSWLACTCL	MQQMKRKEKL	TLTSKTTTTL
CLHYLAQALQ	AQPLGPQLRD	LCSLAAEGIW	QKKTLFSPDD	LRKHGLDGAI
ISTFLKMGIL	QEHPIPLSYS	FIHLCFQEFF	AAMSYVLEDE	KGRGKHSNCI
IDLEKTLEAY	GIHGLFGAST	TRFLLGLLSD	EGEREMENIF	HCRLSQGRNL
MQWVPSLQLL	LQPHSLESLH	CLYETRNKTF	LTQVMAHFEE	MGMCVETDME
LLVCTFCIKF	SRHVKKLQLI	EGRQHRSTWS	PTMVVLFRWV	PVTDAYWQIL
FSVLKVTRNL	KELDLSGNSL	SHSAVKSLCK	TLRRPRCLLE	TLRLAGCGLT
AEDCKDLAFG	LRANQTLTEL	DLSFNVLTDA	GAKHLCQRLR	QPSCKLQRLQ
LVSCGLTSDC	CQDLASVLSA	SPSLKELDLQ	QNNLDDVGVR	LLCEGLRHPA
CKLIRLGLDQ	TTLSDEMRQE	LRALEQEKPQ	LLIFSRRKPS	VMTPTEGLDT
GEMSNSTSSL	KRQRLGSERA	ASHVAQANLK	LLDVSKIFPI	AEIAEESSPE
VVPVELLCVP	SPASQGDLHT	KPLGTDDDFW	GPTGPVATEV	VDKEKNLYRV
HFPVAGSYRW	PNTGLCFVMR	EAVTVEIEFC	VWDQFLGEIN	PQHSWMVAGP
LLDIKAEPGA	VEAVHLPHFV	ALQGGHVDTS	LFQMAHFKEE	GMLLEKPARV
ELHHIVLENP	SFSPLGVLLK	MIHNALRFIP	VTSVVLLYHR	VHPEEVTFHL
YLIPSDCSIR	KAIDDLEMKF	QFVRIHKPPP	LTPLYMGCRY	TVSGSGSGML
EILPKELELC	YRSPGEDQLF	SEFYVGHLGS	GIRLQVKDKK	DETLVWEALV
KPGDLMPATT	LIPPARIAVP	SPLDAPQLLH	FVDQYREQLI	ARVTSVEVVL
DKLHGQVLSQ	EQYERVLAEN	TRPSQMRKLF	SLSQSWDRKC	KDGLYQALKE
THPHLIMELW	EKGSKKGLLP	LSS

Funkcija[uredi | uredi izvor]

Ovaj gen kodira člana Ced-4 porodice apoptoznih proteina. Članovi Ced porodice sadrže domen regrutacije kaspaze (CARD) i poznato je da su ključni posrednici programirane ćelijske smrti. Kodirani protein sadrži poseban N-terminalni pirin-oliki motiv, koji je možda uključen u interajcije protein-protein. Protein NLRP1 snažno reaguje sa kaspazom 2 i slabo sa kaspazom 9. Pokazalo se da prekomjerna ekspresija ovog gena u ćelijama izaziva piroptozu. Višestruke alternativno prerađene varijante transkripta koje kodiraju različite izoforme su pronađene za ovaj gen, ali biološka valjanost nekih varijanti nije utvrđena.^[7]

Mehanizam aktivacije[uredi | uredi izvor]

NLRP1 aktivira antibakterijski ili antivirusni imunski odgovor. Antibakterijski imunski odgovor nadoknađuje gubitak MAP kinaznog odgovora. Ljudi proizvode NLRP1, ali ljudski NLRP1 nije aktiviran smrtonosnim faktorom.^[8] NLRP1 bi se mogao aktivirati proteoliskim cijepanjem, što rezultira uklanjanjem autoinhibitornog PYD i oslobađanjem CARD domena, odgovornog za regrutovanje i aktivacija prokapaze-1 u aktivnom obliku kaspaze-1.^[8] Ljudska aktivacija NLRP1 može se izazvati na nekoliko načina uključujući enterovirusnu 3C- proteaze.^[11] njegov funkdcija je u munsti tek je počela da se shvata.^[8]

Interakcije[uredi | uredi izvor]

Pokazano je da NLRP1 reaguje sa kaspazom 9^[12]^[13] i APAF1.^[12] Preko svog FIIND domena, NLRP1 je u direktnoj interakciji sa DPP9 i DPP8, koji su potrebni za sprečavanje aktivacije NLRP1.^[14]

Gubitak DPP9 kod ljudi i miševa dovodi do aktivacije NLRP1.^[15]

Varijante NLRP1 kod ljudi[uredi | uredi izvor]

Kako su objavili Bruno Reversade i kolege, opisano je nekoliko mendelovskih bolesti uzrokovanih mutacijama zametne linije NLRP1.^[16] To uključuje višestruki samoizlječivi palmoplantarni karcinom, porodičnu Nikamovu bolest i autoupaluđu s artritisom i diskeratozom. Mutacije u NLRP1, bilo da su dominantne ili recesivne, imaju tendenciju da budu aleli pojačanja funkcije koji pokreću inflamasomnu signalizaciju sa IL1B i IL18.

Varijante NLRP1 kod miševa[uredi | uredi izvor]

Miševi imaju tri paraloga gena Nlrp1 (Nlrp1a, b, c). Nlrp1c je pseudogen.^[17] Mišji NLRP1B se ne aktivira mehanizmom tipa receptor-ligand. NLRP1B varijante određenih inbred sojeva miševa, BALB/c i 129, mogu se aktivirati smrtonosnim faktorom (LF) proteaza. Smrtonosni faktor proteaza proizvodi i luči Bacillus anthracis, agens antraksa.^[18] Zajedno sa zaštitnim antigenom (PA), LF formira bipartitni toksin, smrtonosni toksin. Uloga PA je da formira hromosomski translocacijski kanal koji isporučuje LF u citosol ćelije domaćina gdje LF ima ulogu u imunskom odgovoru, cijepanjem i inaktivacijom MAP kinaza.^[19]^[20] LF takođe direktno ciepa NLRP1B proksimalno do njegovog N-terminala, što je neophodno i dovoljno za formiranje NLRP1B inflamasoma i aktivaciju CASP1.^[21] Aktivacija NLRP1B-ovisnih inflamafomskih odgovora pojavljuje se u odbrani domaćina s mehanizmom poput IL-1β i neutrofila.^[22]^[23] NLRP1B može funkcionirati kao senzor bakterijskih proteaza, imunski odgovori su specifično aktivirani faktorima virulencija.^[24]^[25]

Nije jasno koji bi stimulansi mogli aktivirati NLRP1A, drugi poznati funkcionalni mišji paralog NLRP1. Studija je identifikovala miša koji je nosio misens mutacijsko pojačanje funkcije u NLRP1A (Q593P) koji aktivira inflamasomne odgovore. Mehanizam aktivacije divljeg tips NLRP1A ---nije jasan.^[26]

Reference[uredi | uredi izvor]

^ ^a ^b ^c GRCh38: Ensembl release 89: ENSG00000091592 - Ensembl, maj 2017
^ ^a ^b ^c GRCm38: Ensembl release 89: ENSMUSG00000070390 - Ensembl, maj 2017
^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ Thorpe KL, Abdulla S, Kaufman J, Trowsdale J, Beck S (Oct 1996). "Phylogeny and structure of the RING3 gene". Immunogenetics. 44 (5): 391–6. doi:10.1007/BF02602785. PMID 8781126. S2CID 44613743.
^ Tschopp J, Martinon F, Burns K (februar 2003). "NALPs: a novel protein family involved in inflammation". Nature Reviews. Molecular Cell Biology. 4 (2): 95–104. doi:10.1038/nrm1019. PMID 12563287. S2CID 31417018.
^ ^a ^b ^c "Entrez Gene: NLRP1 NLR family, pyrin domain containing 1".
^ ^a ^b ^c ^d ^e Chavarría-Smith J, Mitchell PS, Ho AM, Daugherty MD, Vance RE (decembar 2016). "Functional and Evolutionary Analyses Identify Proteolysis as a General Mechanism for NLRP1 Inflammasome Activation". PLOS Pathogens. 12 (12): e1006052. doi:10.1371/journal.ppat.1006052. PMC 5142783. PMID 27926929. Materijal je kopiran iz ovog izvora, koji je dostupan na linku Creative Commons Attribution 4.0 International License. Greška kod citiranja: Neispravna oznaka <ref>; naziv ":0" definiran je nekoliko puta s različitim sadržajem
^ ^a ^b Kummer JA, Broekhuizen R, Everett H, Agostini L, Kuijk L, Martinon F, et al. (maj 2007). "Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response". The Journal of Histochemistry and Cytochemistry. 55 (5): 443–52. doi:10.1369/jhc.6A7101.2006. PMID 17164409.
^ Grandemange S, Sanchez E, Louis-Plence P, Tran Mau-Them F, Bessis D, Coubes C, et al. (juli 2017). "NLRP1-associated autoinflammation with arthritis and dyskeratosis)". Annals of the Rheumatic Diseases. 76 (7): 1191–1198. doi:10.1136/annrheumdis-2016-210021. PMID 27965258. S2CID 206852426.
^ Robinson KS, Teo DE, Tan KS, Toh GA, Ong HH, Lim CK, et al. (decembar 2020). "Enteroviral 3C protease activates the human NLRP1 inflammasome in airway epithelia". Science. 370 (6521): eaay2002. doi:10.1126/science.aay2002. PMID 33093214. S2CID 225052810.
^ ^a ^b Chu ZL, Pio F, Xie Z, Welsh K, Krajewska M, Krajewski S, et al. (mart 2001). "A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis". The Journal of Biological Chemistry. 276 (12): 9239–45. doi:10.1074/jbc.M006309200. PMID 11113115.
^ Hlaing T, Guo RF, Dilley KA, Loussia JM, Morrish TA, Shi MM, et al. (mart 2001). "Molecular cloning and characterization of DEFCAP-L and -S, two isoforms of a novel member of the mammalian Ced-4 family of apoptosis proteins". The Journal of Biological Chemistry. 276 (12): 9230–8. doi:10.1074/jbc.M009853200. PMID 11076957.
^ Zhong FL, Robinson K, Teo DE, Tan KY, Lim C, Harapas CR, et al. (decembar 2018). "Human DPP9 represses NLRP1 inflammasome and protects against autoinflammatory diseases via both peptidase activity and FIIND domain binding". The Journal of Biological Chemistry. 293 (49): 18864–18878. doi:10.1074/jbc.RA118.004350. PMC 6295727. PMID 30291141.
^ Harapas CR, Robinson KS, Lay K, Wong J, Moreno Traspas R, Nabavizadeh N, et al. (3. 2. 2021). "DPP9 deficiency: an Inflammasomopathy which can be rescued by lowering NLRP1/IL-1 signaling". medRxiv. doi:10.1101/2021.01.31.21250067. S2CID 231775569.
^ Zhong FL, Mamaï O, Sborgi L, Boussofara L, Hopkins R, Robinson K, et al. (septembar 2016). "Germline NLRP1 Mutations Cause Skin Inflammatory and Cancer Susceptibility Syndromes via Inflammasome Activation". Cell. 167 (1): 187–202.e17. doi:10.1016/j.cell.2016.09.001. PMID 27662089.
^ Sastalla I, Crown D, Masters SL, McKenzie A, Leppla SH, Moayeri M (mart 2013). "Transcriptional analysis of the three Nlrp1 paralogs in mice". BMC Genomics. 14 (1): 188. doi:10.1186/1471-2164-14-188. PMC 3641005. PMID 23506131.
^ Boyden ED, Dietrich WF (februar 2006). "Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin". Nature Genetics. 38 (2): 240–4. doi:10.1038/ng1724. PMID 16429160. S2CID 23316987.
^ Turk BE (mart 2007). "Manipulation of host signalling pathways by anthrax toxins". The Biochemical Journal. 402 (3): 405–17. doi:10.1042/BJ20061891. PMID 17313374.
^ Moayeri M, Leppla SH (decembar 2009). "Cellular and systemic effects of anthrax lethal toxin and edema toxin". Molecular Aspects of Medicine. 30 (6): 439–55. doi:10.1016/j.mam.2009.07.003. PMC 2784088. PMID 19638283.
^ Chavarría-Smith J, Vance RE (2013). "Direct proteolytic cleavage of NLRP1B is necessary and sufficient for inflammasome activation by anthrax lethal factor". PLOS Pathogens. 9 (6): e1003452. doi:10.1371/journal.ppat.1003452. PMC 3688554. PMID 23818853.
^ Terra JK, Cote CK, France B, Jenkins AL, Bozue JA, Welkos SL, et al. (januar 2010). "Cutting edge: resistance to Bacillus anthracis infection mediated by a lethal toxin sensitive allele of Nalp1b/Nlrp1b". Journal of Immunology. 184 (1): 17–20. doi:10.4049/jimmunol.0903114. PMC 2811128. PMID 19949100.
^ Moayeri M, Crown D, Newman ZL, Okugawa S, Eckhaus M, Cataisson C, et al. (decembar 2010). "Inflammasome sensor Nlrp1b-dependent resistance to anthrax is mediated by caspase-1, IL-1 signaling and neutrophil recruitment". PLOS Pathogens. 6 (12): e1001222. doi:10.1371/journal.ppat.1001222. PMC 3000361. PMID 21170303.
^ de Zoete MR, Bouwman LI, Keestra AM, van Putten JP (mart 2011). "Cleavage and activation of a Toll-like receptor by microbial proteases". Proceedings of the National Academy of Sciences of the United States of America. 108 (12): 4968–73. Bibcode:2011PNAS..108.4968D. doi:10.1073/pnas.1018135108. PMC 3064367. PMID 21383168.
^ Sarris PF, Duxbury Z, Huh SU, Ma Y, Segonzac C, Sklenar J, et al. (maj 2015). "A Plant Immune Receptor Detects Pathogen Effectors that Target WRKY Transcription Factors". Cell (jezik: engleski). 161 (5): 1089–1100. doi:10.1016/j.cell.2015.04.024. PMID 26000484.
^ Masters SL, Gerlic M, Metcalf D, Preston S, Pellegrini M, O'Donnell JA, et al. (decembar 2012). "NLRP1 inflammasome activation induces pyroptosis of hematopoietic progenitor cells". Immunity (jezik: engleski). 37 (6): 1009–23. doi:10.1016/j.immuni.2012.08.027. PMC 4275304. PMID 23219391.

Doipunska literatura[uredi | uredi izvor]

Bertin J, DiStefano PS (decembar 2000). "The PYRIN domain: a novel motif found in apoptosis and inflammation proteins". Cell Death and Differentiation. 7 (12): 1273–4. doi:10.1038/sj.cdd.4400774. PMID 11270363.
Andersson B, Wentland MA, Ricafrente JY, Liu W, Gibbs RA (april 1996). "A "double adaptor" method for improved shotgun library construction". Analytical Biochemistry. 236 (1): 107–13. doi:10.1006/abio.1996.0138. PMID 8619474.
Yu W, Andersson B, Worley KC, Muzny DM, Ding Y, Liu W, et al. (april 1997). "Large-scale concatenation cDNA sequencing". Genome Research. 7 (4): 353–8. doi:10.1101/gr.7.4.353. PMC 139146. PMID 9110174.
Nagase T, Ishikawa K, Suyama M, Kikuno R, Hirosawa M, Miyajima N, et al. (februar 1999). "Prediction of the coding sequences of unidentified human genes. XIII. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Research. 6 (1): 63–70. doi:10.1093/dnares/6.1.63. PMID 10231032.
Hlaing T, Guo RF, Dilley KA, Loussia JM, Morrish TA, Shi MM, et al. (mart 2001). "Molecular cloning and characterization of DEFCAP-L and -S, two isoforms of a novel member of the mammalian Ced-4 family of apoptosis proteins". The Journal of Biological Chemistry. 276 (12): 9230–8. doi:10.1074/jbc.M009853200. PMID 11076957.
Chu ZL, Pio F, Xie Z, Welsh K, Krajewska M, Krajewski S, et al. (mart 2001). "A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis". The Journal of Biological Chemistry. 276 (12): 9239–45. doi:10.1074/jbc.M006309200. PMID 11113115.
Martinon F, Hofmann K, Tschopp J (februar 2001). "The pyrin domain: a possible member of the death domain-fold family implicated in apoptosis and inflammation". Current Biology. 11 (4): R118-20. doi:10.1016/S0960-9822(01)00056-2. PMID 11250163. S2CID 18564343.
Damiano JS, Stehlik C, Pio F, Godzik A, Reed JC (juli 2001). "CLAN, a novel human CED-4-like gene". Genomics. 75 (1–3): 77–83. doi:10.1006/geno.2001.6579. PMID 11472070.
Nath SK, Kelly JA, Namjou B, Lam T, Bruner GR, Scofield RH, et al. (decembar 2001). "Evidence for a susceptibility gene, SLEV1, on chromosome 17p13 in families with vitiligo-related systemic lupus erythematosus". American Journal of Human Genetics. 69 (6): 1401–6. doi:10.1086/324470. PMC 1235552. PMID 11592035.
Martinon F, Burns K, Tschopp J (august 2002). "The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta". Molecular Cell. 10 (2): 417–26. doi:10.1016/S1097-2765(02)00599-3. PMID 12191486.
Hiller S, Kohl A, Fiorito F, Herrmann T, Wider G, Tschopp J, et al. (oktobar 2003). "NMR structure of the apoptosis- and inflammation-related NALP1 pyrin domain" (PDF). Structure. 11 (10): 1199–205. doi:10.1016/j.str.2003.08.009. PMID 14527388.
Spritz RA, Gowan K, Bennett DC, Fain PR (januar 2004). "Novel vitiligo susceptibility loci on chromosomes 7 (AIS2) and 8 (AIS3), confirmation of SLEV1 on chromosome 17, and their roles in an autoimmune diathesis". American Journal of Human Genetics. 74 (1): 188–91. doi:10.1086/381134. PMC 1181907. PMID 14691733.
Damiano JS, Oliveira V, Welsh K, Reed JC (juli 2004). "Heterotypic interactions among NACHT domains: implications for regulation of innate immune responses". The Biochemical Journal. 381 (Pt 1): 213–9. doi:10.1042/BJ20031506. PMC 1133779. PMID 15107016.
Liu F, Lo CF, Ning X, Kajkowski EM, Jin M, Chiriac C, et al. (septembar 2004). "Expression of NALP1 in cerebellar granule neurons stimulates apoptosis". Cellular Signalling. 16 (9): 1013–21. doi:10.1016/j.cellsig.2004.02.006. PMID 15212762.

Vanjski linkovi[uredi | uredi izvor]

Q9C000

Šablon:NOD-liki receptori

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000091592 - Ensembl, maj 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000070390 - Ensembl, maj 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[pmid8781126-5] Thorpe KL, Abdulla S, Kaufman J, Trowsdale J, Beck S (Oct 1996). "Phylogeny and structure of the RING3 gene". Immunogenetics. 44 (5): 391–6. doi:10.1007/BF02602785. PMID 8781126. S2CID 44613743.

[pmid12563287-6] Tschopp J, Martinon F, Burns K (februar 2003). "NALPs: a novel protein family involved in inflammation". Nature Reviews. Molecular Cell Biology. 4 (2): 95–104. doi:10.1038/nrm1019. PMID 12563287. S2CID 31417018.

[entrez-7] "Entrez Gene: NLRP1 NLR family, pyrin domain containing 1".

[:0-8] Chavarría-Smith J, Mitchell PS, Ho AM, Daugherty MD, Vance RE (decembar 2016). "Functional and Evolutionary Analyses Identify Proteolysis as a General Mechanism for NLRP1 Inflammasome Activation". PLOS Pathogens. 12 (12): e1006052. doi:10.1371/journal.ppat.1006052. PMC 5142783. PMID 27926929. Materijal je kopiran iz ovog izvora, koji je dostupan na linku Creative Commons Attribution 4.0 International License. Greška kod citiranja: Neispravna oznaka <ref>; naziv ":0" definiran je nekoliko puta s različitim sadržajem

[:1-9] Kummer JA, Broekhuizen R, Everett H, Agostini L, Kuijk L, Martinon F, et al. (maj 2007). "Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response". The Journal of Histochemistry and Cytochemistry. 55 (5): 443–52. doi:10.1369/jhc.6A7101.2006. PMID 17164409.

[10] Grandemange S, Sanchez E, Louis-Plence P, Tran Mau-Them F, Bessis D, Coubes C, et al. (juli 2017). "NLRP1-associated autoinflammation with arthritis and dyskeratosis)". Annals of the Rheumatic Diseases. 76 (7): 1191–1198. doi:10.1136/annrheumdis-2016-210021. PMID 27965258. S2CID 206852426.

[11] Robinson KS, Teo DE, Tan KS, Toh GA, Ong HH, Lim CK, et al. (decembar 2020). "Enteroviral 3C protease activates the human NLRP1 inflammasome in airway epithelia". Science. 370 (6521): eaay2002. doi:10.1126/science.aay2002. PMID 33093214. S2CID 225052810.

[pmid11113115-12] Chu ZL, Pio F, Xie Z, Welsh K, Krajewska M, Krajewski S, et al. (mart 2001). "A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis". The Journal of Biological Chemistry. 276 (12): 9239–45. doi:10.1074/jbc.M006309200. PMID 11113115.

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