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Western blot analysis of Cleaved Caspase-1 (Asp296) using Jurkat whole cell lysates.

AF4005 at 1/100 staining Rat heart tissue by IHC-P.

AF4005 at 1/100 staining Rat skin tissue by IHC-P.

Fig.

$Fig.2 NaAsO2 induced autophagy, activation of NLRP3 inflammasome and 662 hepatic stellate cell in vivo. (A) The expression level of LC3 and p62 in rat livers 663 following exposure to NaAsO2. The protein fraction was analyzed by Western blot. (B) 664 The expression level of cytoplasmic CTSB in rat livers following exposure to NaAsO2. 665 The protein fraction was analyzed by Western blot. (C) The expression level of NLRP3 inflammasome-associated proteins in rat livers following exposure to NaAsO2. 667 The protein fraction was analyzed by Western blot. (D) The expression level of 668 Collagen- , α-SMA, MMP-1, and TIMP-1in rat livers following exposure to NaAsO2. 669 The protein fraction was analyzed by Western blot. (E) α-SMA was detected by IF. 670 White arrows indicate positive staining. Values are mean ± SD, and n = 5. *p < 0.05, 671 **p < 0.01 compared with the control group; Scale bar = 100 µm$

Fig.

FIGURE 4 BRD4 inhibition alleviated NLRP3 inflammasome activity in NP cells.

$Fig.3 NaAsO2 impairs insulin signaling via activation of NLRP3 inflammasome in HepG2 cells. HepG2 cells were pretreated with 1 μg/ml LPS for 4 hours, 5 μM MCC950, for 4 hours, and were then treated with 4 μM NaAsO2 for 24 hours. Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The efficiency of MCC950, and its effect on NLRP3, caspase-1 activation, IL-1β and IL- 18 production in NaAsO2-treated HepG2 cells (A-E). HepG2 cells were stimulated with 100 nM insulin for 10 min at the end of treatment. Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The efficiency of MCC950, and its effect on p-IRS (Ser 307)/IRS1 and p-AKT (Ser473)/AKT1 ratio in NaAsO2-treated HepG2 cells (F-H). Insulin‐ stimulated glucose uptake in HepG2 cells was measured using a glucose assay kit (I). Results are mean ± SEM (n = 3). *P < 0.05 compare with the LPS group. #P<0.05 compare with 4 μM NaAsO2 group.$

Fig.

FIGURE 3 Overexpression of miR-302c-3p reverses ox-LDL-induced pyroptosis in HUVECs.

Fig.

Figure 5 ORY attenuated HMGB1/NLRP3 inflammasome during HIRI.

Figure 6 YSPDF treatment regulated the expressions of TGF-β1, p-Smad2, Smad2, p-Smad3, Smad3, α-SMA, E-cadherin, Nrf2, HO-1, NQO1, NLRP3, ASC, caspase-1, and cleaved caspase-1 in the kidneys of db/db mice.

FIGURE 3 Melatonin decreased the expression of NLRP3 inflammasome‐related proteins in the EAP mice model.

FIGURE 4 Melatonin decreased the expression of the NLRP3 inflammasome‐related proteins, IL‐1β, and activated the Sirt1 signaling pathway in the EAP model.

Fig.

$Fig. 3 Deletion of Osbpl2 reduces the β-catenin level in 3T3-L1 preadipocytes. A, B Lysates of WT and KO cells were immunoblotted for β-catenin, phospho-β-catenin, PPAR-γ, OSBPL2, and ERK1/2 (n = 3). The data are normalized to the ERK1/2 control. C WT cells and KO cells at day 0 were fixed and immune-stained with anti-β-catenin (red). Scale bar, 50 μm (inserts, 10 μm). D, E Reduced nuclear localization of β-catenin (imaged by confocal microscope and detected by ZEN software, where a mask is created within the nucleus and the mean pixel intensity of β-catenin within the nucleus is compared to that within the entire cell) related to C. Scale bar, 50 μm (inserts, 10 μm). F WT cells and KO cells were lysed, and the lysates were separated into cytosol and nucleus fractions. The abundance of β-catenin in the two fractions was assessed by western blotting. HISTONE H3 acted as internal nucleus control, and GAPDH acted as internal cytoplasm control (n = 3). G β-Catenin were IP with anti-β-catenin antibody in WT preadipocytes or KO preadipocytes and lysates were immunoblotted for ubiquitin detection (n = 3). H Lysates of 3T3-L1 preadipocytes transfected with empty vector or FLAG-tagged Osbpl2 plasmid for 48 h were immunoblotted for β-catenin and ERK1/2 detection (n = 3). OE = OSBPL2 overexpression. Data are normalized to the ERK1/2 control. All data are from three independent experiments. The data are presented as the mean ± SD values (n ≥ 3). *P < 0.05; **P < 0.01, ***P < 0.001, ns: not significant.$

Fig.

FIGURE 4 Hypercholesterolemia induces IDD and pyroptosis-associated molecular changes, which were attenuated by atorvastatin.

FIGURE 3 Cholesterol triggers pyroptosis in rat NP cells.

Figure 2 BMSC-Exos inhibit the pyroptosis and maintain chondrocyte homeostasis of OA chondrocytes.

Fig.

Figure 12 LGZGD regulates protein expressions of NLRP3, Caspase-1, and GSDMD in AMI rats: (a) NLRP3, Caspase-1, and GSDMD pictures of Western spots; (b) NLRP3; (c) Caspase-1 p20; (d) GSDMD.

FIGURE 4 Caspase-1–dependent canonical pathway activated RTEC pyroptosis.

Figure 10 The expressions of cleaved caspase 1/caspase 1 and cleaved caspase 3/caspase 3 in lung tissues were detected by western blot.

Figure 6 XFZYD decreased pyroptosis in rat models with CPB-induced ALI.

Figure 7 XFZYD inhibited the IKBα/NF-κB signaling in rat models with CPB-induced ALI.

Figure 4.

Figure 5 Vav1 knockdown represses inflammation in the ischemic penumbra of MCAO/R rats.

Figure 4 The knockdown of CEBPB inhibited the activation of NLRP3 inflammasomes in MRL/lpr mice.

Figure 6.

Fig.

Figure 1.

Figure 3 Capsaicin alleviates LPS-induced pyroptosis in HK-2 cells by activating TRPV1/UCP2 axis.

Fig.

产品:	Cleaved-Caspase 1 (Asp296), p20 抗体
货号:	AF4005
描述:	Rabbit polyclonal antibody to Cleaved-Caspase 1 (Asp296), p20
应用:	WB IHC
反应:	Human, Mouse, Rat
分子量:	20kD(p20), 35~50kD(precursor); 45kD(Calculated).
蛋白号:	P29466
RRID:	AB_2845463

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阻断肽(封闭肽)是特异性结合目标抗体和阻断抗体结合的多肽。这些多肽包含抗体识别的抗原表位。与阻断肽结合的抗体不再与靶蛋白上的表位结合。例如，在免疫印迹(WB)和免疫组化(IHC)中，通过比较被阻断抗体和未阻断抗体的染色，可以看到哪种染色是特异性的。

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说明书

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IHC Protocol

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产品描述

来源:

Rabbit

应用:

WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:

Human,Mouse,Rat

克隆:

Polyclonal

特异性:

Cleaved-Caspase-1 (Asp296,p20) Antibody detects endogenous levels of fragment of activated Caspase-1 resulting from cleavage adjacent to Asp296.

RRID:

AB_2845463
引用格式: Affinity Biosciences Cat# AF4005, RRID:AB_2845463.

偶联:

Unconjugated.

纯化:

The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).

保存:

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

别名:

展开/折叠

CASP-1; CASP1; CASP1_HUMAN; Caspase 1; Caspase-1 subunit p10; ICE; IL-1 beta-converting enzyme; IL-1BC; IL1 beta converting enzyme; IL1B convertase; Interleukin 1 beta convertase; Interleukin 1B converting enzyme; Interleukin-1 beta convertase; Interleukin-1 beta-converting enzyme; p45;

抗原和靶标

免疫原:

Uniprot:

P29466(CASP1_HUMAN) >>Visit HPA database.

基因/基因ID:

CASP1(834)

表达:

P29466 CASP1_HUMAN:

Expressed in larger amounts in spleen and lung. Detected in liver, heart, small intestine, colon, thymus, prostate, skeletal muscle, peripheral blood leukocytes, kidney and testis. No expression in the brain.

序列:

P29466 CASP1_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MADKVLKEKRKLFIRSMGEGTINGLLDELLQTRVLNKEEMEKVKRENATVMDKTRALIDSVIPKGAQACQICITYICEEDSYLAGTLGLSADQTSGNYLNMQDSQGVLSSFPAPQAVQDNPAMPTSSGSEGNVKLCSLEEAQRIWKQKSAEIYPIMDKSSRTRLALIICNEEFDSIPRRTGAEVDITGMTMLLQNLGYSVDVKKNLTASDMTTELEAFAHRPEHKTSDSTFLVFMSHGIREGICGKKHSEQVPDILQLNAIFNMLNTKNCPSLKDKPKVIIIQACRGDSPGVVWFKDSVGVSGNLSLPTTEEFEDDAIKKAHIEKDFIAFCSSTPDNVSWRHPTMGSVFIGRLIEHMQEYACSCDVEEIFRKVRFSFEQPDGRAQMPTTERVTLTRCFYLFPGH

翻译修饰 - P29466 作为底物

P29466

Site	PTM Type	Source
S16	Phosphorylation	Uniprot
T21	Phosphorylation	Uniprot
T32	Phosphorylation	Uniprot
K37	Ubiquitination	Uniprot
K44	Ubiquitination	Uniprot
T49	Phosphorylation	Uniprot
K53	Ubiquitination	Uniprot
K134	Ubiquitination	Uniprot
K148	Ubiquitination	Uniprot
S149	Phosphorylation	Uniprot
K158	Ubiquitination	Uniprot
K204	Ubiquitination	Uniprot
T226	Phosphorylation	Uniprot
S227	Phosphorylation	Uniprot
K268	Ubiquitination	Uniprot
K274	Ubiquitination	Uniprot
K278	Ubiquitination	Uniprot
S306	Phosphorylation	Uniprot
K319	Ubiquitination	Uniprot
K320	Ubiquitination	Uniprot
K325	Ubiquitination	Uniprot
S376	Phosphorylation	Uniprot

研究背景

P29466_CASP1_HUMAN

功能:

Thiol protease that cleaves IL-1 beta between an Asp and an Ala, releasing the mature cytokine which is involved in a variety of inflammatory processes. Important for defense against pathogens. Cleaves and activates sterol regulatory element binding proteins (SREBPs). Can also promote apoptosis. Upon inflammasome activation, during DNA virus infection but not RNA virus challenge, controls antiviral immunity through the cleavage of CGAS, rendering it inactive. In apoptotic cells, cleaves SPHK2 which is released from cells and remains enzymatically active extracellularly.

翻译修饰:

The two subunits are derived from the precursor sequence by an autocatalytic mechanism.

细胞定位:

Cytoplasm. Cell membrane.

组织特异性:

亚基结构:

Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 20 kDa (p20) and a 10 kDa (p10) subunit. The p20 subunit can also form a heterodimer with the epsilon isoform which then has an inhibitory effect. May be a component of the inflammasome, a protein complex which also includes PYCARD, CARD8 and NALP2 and whose function would be the activation of proinflammatory caspases. Both the p10 and p20 subunits interact with MEFV. Interacts with CARD17/INCA and CARD18. Interacts with SERPINB1; this interaction regulates CASP1 activity.

蛋白家族:

Belongs to the peptidase C14A family.

研究领域

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

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

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

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

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway. (View pathway)

文献引用

1). Arsenic induces hepatic insulin resistance via mtROS-NLRP3 inflammasome pathway. JOURNAL OF HAZARDOUS MATERIALS (PubMed: 32544768) [IF=13.6]

Application: WB Species: Human Sample: HepG2 cells

Fig.3 NaAsO2 impairs insulin signaling via activation of NLRP3 inflammasome in HepG2 cells. HepG2 cells were pretreated with 1 μg/ml LPS for 4 hours, 5 μM MCC950, for 4 hours, and were then treated with 4 μM NaAsO2 for 24 hours. Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The efficiency of MCC950, and its effect on NLRP3, caspase-1 activation, IL-1β and IL- 18 production in NaAsO2-treated HepG2 cells (A-E). HepG2 cells were stimulated with 100 nM insulin for 10 min at the end of treatment. Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The efficiency of MCC950, and its effect on p-IRS (Ser 307)/IRS1 and p-AKT (Ser473)/AKT1 ratio in NaAsO2-treated HepG2 cells (F-H). Insulin‐ stimulated glucose uptake in HepG2 cells was measured using a glucose assay kit (I). Results are mean ± SEM (n = 3). *P < 0.05 compare with the LPS group. #P<0.05 compare with 4 μM NaAsO2 group.

2). SGLT2 inhibitor canagliflozin alleviates vascular calcification through suppression of NLRP3 inflammasome. Cardiovascular Research (PubMed: 37523743) [IF=10.8]

3). Sodium-glucose cotransporter 2 inhibitor canagliflozin alleviates vascular calcification through suppression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome. Cardiovascular research (PubMed: 37523743) [IF=10.8]

4). Hair follicle-MSC-derived small extracellular vesicles as a novel remedy for acute pancreatitis. JOURNAL OF CONTROLLED RELEASE (PubMed: 36402231) [IF=10.8]

5). A unique death pathway keeps RIPK1 D325A mutant mice in check at embryonic day 10.5. PLOS Biology (PubMed: 34437534) [IF=9.8]

6). Activating cGAS–STING axis contributes to neuroinflammation in CVST mouse model and induces inflammasome activation and microglia pyroptosis. Journal of Neuroinflammation (PubMed: 35689216) [IF=9.3]

Application: IHC Species: Mouse Sample:

Fig. 7Effects of RU.521 on NLRP3 inflammasome and pyroptosis post-CVST. A Western blot assay for NLRP3, caspase-1 p20, pro-IL-1β, cleaved-IL-1β, GSDMD and GSDMD-C expressions from the impaired cortex at 3 days post-CVST. B Typical immunohistochemical staining for NLRP3, caspase-1 p20, IL-1β and GSDMD at diverse groups after CVST. Scale bar = 50 μm. C, D Quantitative analysis of western blot assay. *P < 0.05, **P < 0.01. n = 6. E Representative co-localization staining for IL-1β (green) and microglia (IBA-1, red) in the injured cortex as shown by white arrows, at 3 days after CVST. Scale bar = 50 μm

7). Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway. International Journal of Biological Sciences (PubMed: 36632449) [IF=9.2]

8). ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway. Cell Death & Disease (PubMed: 32829380) [IF=9.0]

Application: IF/ICC Species: mouse Sample: HK2 cells

Fig. 7 Effects of ELA on the ROS production and NLRP3 imflammasome activation are independent of APJ. APJ knockdown was conducted by the transfection of plasmid pWHAPJg into HK2 cells and confirmed by RT-PCR. Then the HK2 cells with APJ knockdown were pretreated with ELA peptide (1 nM) for 1 h and then treated by Aldosterone (0.1 µM) for 24 h. a Representative immunoblots of APJ in renal cortex and medulla and summarized intensities of blots. b mRNA levels of APJ in HK2 cells with or without APJ knockdown. c ROS production in HK2 cells with APJ knockdown. d, e Representative confocal fluorescent images of co-localization (yellow) between Nlrp3 (green)/Caspase-1 (red) and summarized colocalization coefficient in HK2 cells with APJ knockdown. Scale bar, 10 µm. N = 6 per group. *P < 0.05 versus Ctrl group; #P < 0.05 versus DOCA/ salt group

9). Autophagic-CTSB-inflammasome axis modulates hepatic stellate cells activation in arsenic-induced liver fibrosis. Chemosphere (PubMed: 31669990) [IF=8.8]

Application: WB Species: rat Sample: HSC-t6 cells

Fig.4 |NaAsO2-induced HSCs activation was dependent on the activation of NLRP3 inflammasome. (A, B) HSC-t6 cells were pretreated with or without MCC950 for 2h and then treated with NaAsO2 for 24 h. The expression level of caspase-1 p20, IL-1β, Collagen-, a-SMA, MMP-1, and TIMP-1 were determined by Western blot.

Application: WB Species: rat Sample: livers

Fig.2 NaAsO2 induced autophagy, activation of NLRP3 inflammasome and 662 hepatic stellate cell in vivo. (A) The expression level of LC3 and p62 in rat livers 663 following exposure to NaAsO2. The protein fraction was analyzed by Western blot. (B) 664 The expression level of cytoplasmic CTSB in rat livers following exposure to NaAsO2. 665 The protein fraction was analyzed by Western blot. (C) The expression level of NLRP3 inflammasome-associated proteins in rat livers following exposure to NaAsO2. 667 The protein fraction was analyzed by Western blot. (D) The expression level of 668 Collagen- , α-SMA, MMP-1, and TIMP-1in rat livers following exposure to NaAsO2. 669 The protein fraction was analyzed by Western blot. (E) α-SMA was detected by IF. 670 White arrows indicate positive staining. Values are mean ± SD, and n = 5. *p < 0.05, 671 **p < 0.01 compared with the control group; Scale bar = 100 µm

10). Mesenchymal stem cells protect against TBI-induced pyroptosis in vivo and in vitro through TSG-6. Cell Communication and Signaling (PubMed: 35982465) [IF=8.4]

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Cleaved-Caspase 1 (Asp296), p20 Antibody - #AF4005

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抗原和靶标

翻译修饰 - P29466 作为底物

研究背景

研究领域

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