製品: NLRP3 Mouse monoclonal Antibody
カタログ: BF8029
タンパク質の説明: Mouse monoclonal antibody to NLRP3
アプリケーション: WB IHC
反応性: Human, Mouse, Rat
分子量: 80~120kD; 118kD(Calculated).
ユニプロット: Q96P20

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製品説明

ソース:
Mouse IgG1
アプリケーション:
WB 1:500-1:3000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

反応性:
Human,Mouse,Rat
クローナリティ:
Monoclonal [AFfirm8029(AFP21817)]
特異性:
NLRP3 Mouse monoclonal antibody detects endogenous levels of total NLRP3.
コンジュゲート:
Unconjugated.
精製:
Affinity-chromatography.
保存:
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
別名:

折りたたみ/展開

AGTAVPRL; AII/AVP; Angiotensin/vasopressin receptor AII/AVP like; Angiotensin/vasopressin receptor AII/AVP-like; C1orf7; Caterpiller protein 1.1; CIAS 1; CIAS1; CLR1.1; Cold autoinflammatory syndrome 1; Cold autoinflammatory syndrome 1 protein; Cryopyrin; Familial cold autoinflammatory syndrome; FCAS; FCU; LRR and PYD domains-containing protein 3; Muckle-Wells syndrome; MWS; NACHT; NACHT LRR and PYD containing protein 3; NALP 3; NALP3; NALP3_HUMAN; NLR family pyrin domain containing 3; NLRP3; PYPAF 1; PYPAF1; PYRIN containing APAF1 like protein 1; PYRIN-containing APAF1-like protein 1;

免疫原

免疫原:

A synthesized peptide derived from Human NLRP3.

Uniprot:
遺伝子(ID):
発現特異性:
Q96P20 NLRP3_HUMAN:

Predominantly expressed in macrophages. Also expressed in dendritic cells, B- and T-cells (at protein level) (PubMed:11786556) (PubMed:17164409). Expressed in LPS-treated granulocytes, but not in resting cells (at protein level) (PubMed:17164409). Expression in monocytes is very weak (at protein level) (PubMed:17164409). Expressed in stratified non-keratinizing squamous epithelium, including oral, esophageal and ectocervical mucosa and in the Hassall's corpuscles in the thymus. Also, detected in the stratified epithelium covering the bladder and ureter (transitional mucosa) (at protein level) (PubMed:17164409). Expressed in lung epithelial cells (at protein level) (PubMed:23229815). Expressed in chondrocytes (PubMed:12032915). Expressed at low levels in resting osteoblasts (PubMed:17907925).

タンパク質配列:
MKMASTRCKLARYLEDLEDVDLKKFKMHLEDYPPQKGCIPLPRGQTEKADHVDLATLMIDFNGEEKAWAMAVWIFAAINRRDLYEKAKRDEPKWGSDNARVSNPTVICQEDSIEEEWMGLLEYLSRISICKMKKDYRKKYRKYVRSRFQCIEDRNARLGESVSLNKRYTRLRLIKEHRSQQEREQELLAIGKTKTCESPVSPIKMELLFDPDDEHSEPVHTVVFQGAAGIGKTILARKMMLDWASGTLYQDRFDYLFYIHCREVSLVTQRSLGDLIMSCCPDPNPPIHKIVRKPSRILFLMDGFDELQGAFDEHIGPLCTDWQKAERGDILLSSLIRKKLLPEASLLITTRPVALEKLQHLLDHPRHVEILGFSEAKRKEYFFKYFSDEAQARAAFSLIQENEVLFTMCFIPLVCWIVCTGLKQQMESGKSLAQTSKTTTAVYVFFLSSLLQPRGGSQEHGLCAHLWGLCSLAADGIWNQKILFEESDLRNHGLQKADVSAFLRMNLFQKEVDCEKFYSFIHMTFQEFFAAMYYLLEEEKEGRTNVPGSRLKLPSRDVTVLLENYGKFEKGYLIFVVRFLFGLVNQERTSYLEKKLSCKISQQIRLELLKWIEVKAKAKKLQIQPSQLELFYCLYEMQEEDFVQRAMDYFPKIEINLSTRMDHMVSSFCIENCHRVESLSLGFLHNMPKEEEEEEKEGRHLDMVQCVLPSSSHAACSHGLVNSHLTSSFCRGLFSVLSTSQSLTELDLSDNSLGDPGMRVLCETLQHPGCNIRRLWLGRCGLSHECCFDISLVLSSNQKLVELDLSDNALGDFGIRLLCVGLKHLLCNLKKLWLVSCCLTSACCQDLASVLSTSHSLTRLYVGENALGDSGVAILCEKAKNPQCNLQKLGLVNSGLTSVCCSALSSVLSTNQNLTHLYLRGNTLGDKGIKLLCEGLLHPDCKLQVLELDNCNLTSHCCWDLSTLLTSSQSLRKLSLGNNDLGDLGVMMFCEVLKQQSCLLQNLGLSEMYFNYETKSALETLQEEKPELTVVFEPSW

PTMs - Q96P20 基板として

Site PTM Type Enzyme
Ubiquitination
S5 Phosphorylation
Y13 Phosphorylation
S161 Phosphorylation
S163 Phosphorylation
S198 Phosphorylation
T233 Phosphorylation
S295 Phosphorylation
S334 Phosphorylation
S387 Phosphorylation
S436 Phosphorylation
K496 Ubiquitination
S728 Phosphorylation
Y861 Phosphorylation
S975 Phosphorylation

研究背景

機能:

As the sensor component of the NLRP3 inflammasome, plays a crucial role in innate immunity and inflammation. In response to pathogens and other damage-associated signals, initiates the formation of the inflammasome polymeric complex, made of NLRP3, PYCARD and CASP1 (and possibly CASP4 and CASP5). Recruitment of proCASP1 to the inflammasome promotes its activation and CASP1-catalyzed IL1B and IL18 maturation and secretion in the extracellular milieu. Activation of NLRP3 inflammasome is also required for HMGB1 secretion. The active cytokines and HMGB1 stimulate inflammatory responses. Inflammasomes can also induce pyroptosis, an inflammatory form of programmed cell death. Under resting conditions, NLRP3 is autoinhibited. NLRP3 activation stimuli include extracellular ATP, reactive oxygen species, K(+) efflux, crystals of monosodium urate or cholesterol, amyloid-beta fibers, environmental or industrial particles and nanoparticles, cytosolic dsRNA, etc. However, it is unclear what constitutes the direct NLRP3 activator. Activation in presence of cytosolic dsRNA is mediated by DHX33. Independently of inflammasome activation, regulates the differentiation of T helper 2 (Th2) cells and has a role in Th2 cell-dependent asthma and tumor growth (By similarity). During Th2 differentiation, required for optimal IRF4 binding to IL4 promoter and for IRF4-dependent IL4 transcription. Binds to the consensus DNA sequence 5'-GRRGGNRGAG-3'. May also participate in the transcription of IL5, IL13, GATA3, CCR3, CCR4 and MAF (By similarity).

PTMs:

The disulfide bond in the pyrin domain might play a role in reactive oxygen species-mediated activation.

Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. Ubiquitination does not lead to degradation, but inhibits inflammasome activation (By similarity). Deubiquitination is catalyzed by BRCC3 and associated with NLRP3 activation and inflammasome assembly. This process can be induced by the activation of Toll-like receptors (by LPS), through a non-transcriptional pathway dependent on the mitochondrial production of reactive oxygen species, and by ATP.

細胞の位置付け:

Cytoplasm>Cytosol. Inflammasome. Endoplasmic reticulum. Secreted. Nucleus.
Note: In macrophages, under resting conditions, mainly located in the cytosol, on the endoplasmic reticulum. After stimulation with inducers of the NLRP3 inflammasome, mitochondria redistribute in the vicinity of the endoplasmic reticulum in the perinuclear region, which results in colocalization of NLRP3 on the endoplasmic reticulum and PYCARD on mitochondria, allowing the activation of inflammasome assembly. After the induction of pyroptosis, inflammasome specks are released into the extracellular space where they can further promote IL1B processing and where they can be engulfed by macrophages. Phagocytosis induces lysosomal damage and inflammasome activation in the recipient cells (PubMed:24952504). In the Th2 subset of CD4(+) helper T-cells, mainly located in the nucleus. Nuclear localization depends upon KPNA2. In the Th1 subset of CD4(+) helper T-cells, mainly cytoplasmic (By similarity).

Golgi apparatus membrane.
Note: (Microbial infection) Upon HRSV infection, the protein is mainly located in lipid rafts in the Golgi membrane.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
組織特異性:

Predominantly expressed in macrophages. Also expressed in dendritic cells, B- and T-cells (at protein level). Expressed in LPS-treated granulocytes, but not in resting cells (at protein level). Expression in monocytes is very weak (at protein level). Expressed in stratified non-keratinizing squamous epithelium, including oral, esophageal and ectocervical mucosa and in the Hassall's corpuscles in the thymus. Also, detected in the stratified epithelium covering the bladder and ureter (transitional mucosa) (at protein level). Expressed in lung epithelial cells (at protein level). Expressed in chondrocytes. Expressed at low levels in resting osteoblasts.

サブユニット構造:

Sensor component of NLRP3 inflammasomes. 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. The core of NLRP3 inflammasomes consists of a signal sensor component (NLRP3), an adapter (ASC/PYCARD), which recruits an effector proinflammatory caspase (CASP1 and, possibly, CASP4 and CASP5). Within the complex, NLRP3 and PYCARD interact via their respective DAPIN/pyrin domains. This interaction initiates speck formation (nucleation) which greatly enhances further addition of soluble PYCARD molecules to the speck in a prion-like polymerization process. NLRP3 localizes at the end of each PYCARD filament. Clustered PYCARD nucleates the formation of CASP1 filaments through the interaction of their respective CARD domains, acting as a platform for CASP1 polymerization. CASP1 filament formation increases local enzyme concentration, resulting in trans-autocleavage and activation. Active CASP1 then processes IL1B and IL18 precursors, leading to the release of mature cytokines in the extracellular milieu and inflammatory response. Reconstituted ternary inflammasomes show star-shaped structures, in which multiple filaments, containing CASP1, protrude radially from a single central hub, containing the sensor protein and PYCARD. In this complex, the sensor protein is sub-stoichiometric to PYCARD, and PYCARD is further substoichiometric to CASP1, suggesting amplifications of signal transduction from the sensor, via the adapter, to the effector. Interacts with MEFV; this interaction targets NLRP3 to degradation by autophagy, hence preventing excessive IL1B- and IL18-mediated inflammation. Interacts with GBP5 (via DAPIN domain); this interaction promotes inflammasome assembly in response to microbial and soluble, but not crystalline, agents. Interacts with EIF2AK2/PKR; this interaction requires EIF2AK2 activity, is accompanied by EIF2AK2 autophosphorylation and promotes inflammasome assembly in response to specific stimuli. Interacts with PML (isoform PML-1) (via the leucine-rich repeat (LRR) domain); PML-mediated increase in NLRP3 inflammasome activation does not depend upon this interaction. Directly interacts with IRF4 (via the LRR domain); this interaction is required for optimal IRF4 binding to IL4 promoter and efficient IL4 transactivation during differentiation of Th2 helper T-cells (By similarity). Interacts (via NACHT domain) with DHX33 (via DEAH box). Interacts with PYDC5.

タンパク質ファミリー:

The pyrin domain (also called DAPIN domain or PYD) is involved in PYCARD-binding.

The LRR domain mediates the interaction with IRF4 and PML.

Intramolecular interactions between NACHT and leucine-rich repeat (LRR) domains may be important for autoinhibition in the absence of activating signal.

Belongs to the NLRP family.

研究領域

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

参考文献

1). Artesunate inhibits macrophage-like phenotype switching of vascular smooth muscle cells and attenuates vascular inflammatory injury in atherosclerosis via NLRP3. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38325261) [IF=7.5]

Application: WB    Species: Human    Sample: HVSMCs

Fig. 4. The anti-inflammatory effects of artesunate. (A) Immunofluorescence for NLRP3 and IL-1β expression in vitro. (B) Relative protein expression of NLRP3, Cleaved-CASP1, and Cleaved-IL-1β in vitro. *P 

Application: IF/ICC    Species: Mouse    Sample:

Fig. 2. Effects of artesunate on the expression of NLRP3, IL-1β, and NF-κB in the aorta. (A) Atherosclerosis and Artemisia annua L. related target genes and intersecting genes. (B) Pathway enrichment analysis of intersecting genes. (C) Relationship diagram of enrichment pathways and related genes. (D) Serum concentrations of TNF-α and IL-1β in the mice. (E) Immunohistochemistry for NF-κB and IL-1β expression in the aorta. (F) Immunofluorescence for NLRP3 expression in the aorta. **P 

2). Flavonoids from Smilax china L. Rhizome improve chronic pelvic inflammatory disease by promoting macrophage reprogramming via the NLRP3 inflammasome-autophagy pathway. Journal of Functional Foods, 2023 [IF=5.6]

Application: WB    Species: Rat    Sample:

Fig. 3. Effect of FSCR on the NLRP3 inflammasome-related autophagy signaling pathway in uterine tissue of CPID rats. Detection of mRNA expression in NLRP3 inflammatory bodies by RT-PCR: NLRP3, CASP1, ASC, IL-1β, and IL-18 (A). Western blot detection of proteins in the NLRP3 inflammatory body: NLRP3, cleaved-CASP1, and cleaved-IL-1β (B). Western blot detection of proteins in the autophagy pathway: Beclin1, p-VPS34, and p62 (C). The expression of NLRP3 inflammatory bodies and autophagic vesicles in uterine tissues was observed by IF: NLRP3 was labeled with red fluorescence, VPS34 was labeled with green fluorescence, and nuclei were labeled with DAPI with blue fluorescence (D). Western blot detection of proteins in the lysosomal pathway: LAMP2, Ubiquitin and LC3 Ⅱ. (E). Results are presented as the mean ± S.E.M.

Application: IF/ICC    Species: Rat    Sample:

Fig. 3. Effect of FSCR on the NLRP3 inflammasome-related autophagy signaling pathway in uterine tissue of CPID rats. Detection of mRNA expression in NLRP3 inflammatory bodies by RT-PCR: NLRP3, CASP1, ASC, IL-1β, and IL-18 (A). Western blot detection of proteins in the NLRP3 inflammatory body: NLRP3, cleaved-CASP1, and cleaved-IL-1β (B). Western blot detection of proteins in the autophagy pathway: Beclin1, p-VPS34, and p62 (C). The expression of NLRP3 inflammatory bodies and autophagic vesicles in uterine tissues was observed by IF: NLRP3 was labeled with red fluorescence, VPS34 was labeled with green fluorescence, and nuclei were labeled with DAPI with blue fluorescence (D). Western blot detection of proteins in the lysosomal pathway: LAMP2, Ubiquitin and LC3 Ⅱ. (E). Results are presented as the mean ± S.E.M.

3). Inhibition of HDAC6 alleviates cancer‑induced bone pain by reducing the activation of NLRP3 inflammasome. International journal of molecular medicine, 2024 (PubMed: 37997785) [IF=5.4]

Application: WB    Species: Rat    Sample: spinal cord

Figure 5 Effect of TSA on NLRP3 inflammasome activation and NF-κB. (A) Representative immunofluorescence staining images and (B) quantitative analysis for NLRP3, caspase-1 and NF-κB in the spinal cord. Scale bar, 20 μm. (C) Representative western blot bands and (E) quantitative analysis of NLRP3, caspase-1 and NF-κB proteins in spinal cord. (D and F) HDAC6 interaction with NLRP3 detected by immunoprecipitation assay. Spinal tissue lysates were immunoprecipitated with anti-HDAC6 and anti-NLRP3 antibodies and immunoblots were probed with anti-NLRP3 and anti-HDAC6 antibodies. The input panel showed target proteins prior to immunoprecipitation in the extracts. Data were presented as mean ± SD (n=3). *P

Application: IF/ICC    Species: Rat    Sample: spinal cord

Figure 5 Effect of TSA on NLRP3 inflammasome activation and NF-κB. (A) Representative immunofluorescence staining images and (B) quantitative analysis for NLRP3, caspase-1 and NF-κB in the spinal cord. Scale bar, 20 μm. (C) Representative western blot bands and (E) quantitative analysis of NLRP3, caspase-1 and NF-κB proteins in spinal cord. (D and F) HDAC6 interaction with NLRP3 detected by immunoprecipitation assay. Spinal tissue lysates were immunoprecipitated with anti-HDAC6 and anti-NLRP3 antibodies and immunoblots were probed with anti-NLRP3 and anti-HDAC6 antibodies. The input panel showed target proteins prior to immunoprecipitation in the extracts. Data were presented as mean ± SD (n=3). *P

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