Caspase 4 Antibody
(Synonyms: ICH2, CASP4, Caspase-4, CASP-4, ICE and Ced-3 homolog 2, ICE(rel)-II, Mih1, Protease TX, ICH-2)Caspase 4 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Caspase 4.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH 7.4), containing 30% glycerol, and 0.01% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
|---|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:100-200 | 1:50-200 |
Product Details
Caspase 4 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Caspase 4.
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Host Rabbit
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Clonality Polyclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 45 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 43 kDa
Synthetic peptide corresponding to the center region of human Caspase 4.
Endogenous
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH 7.4), containing 30% glycerol, and 0.01% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Caspase 4 is an Inflammatory caspase that acts as the effector of the non-canonical inflammasome by mediating lipopolysaccharide (LPS)-induced pyroptosis. Also indirectly activates the NLRP3 and NLRP6 inflammasomes. Acts as a thiol protease that cleaves a tetrapeptide after an Asp residue at position P1: catalyzes cleavage of CGAS, GSDMD and IL18. Effector of the non-canonical inflammasome independently of NLRP3 inflammasome and CASP1: the non-canonical inflammasome promotes pyroptosis through GSDMD cleavage without involving secretion of cytokine IL1B. In the non-canonical inflammasome, CASP4 is activated by direct binding to the lipid A moiety of LPS without the need of an upstream sensor. LPS-binding promotes CASP4 activation and CASP4-mediated cleavage of GSDMD and IL18, followed by IL18 secretion through the GSDMD pore, pyroptosis of infected cells and their extrusion into the gut lumen. Also indirectly promotes secretion of mature cytokines (IL1A and HMGB1) downstream of GSDMD-mediated pyroptosis via activation of the NLRP3 and NLRP6 inflammasomes. Involved in NLRP3-dependent CASP1 activation and IL1B secretion in response to non-canonical activators, such as UVB radiation or cholera enterotoxin. Involved in NLRP6 inflammasome-dependent activation in response to lipoteichoic acid (LTA), a cell-wall component of Gram-positive bacteria, which leads to CASP1 activation and IL1B secretion. Involved in LPS-induced IL6 secretion; this activity may not require caspase enzymatic activity. The non-canonical inflammasome is required for innate immunity to cytosolic, but not vacuolar, bacteria (By similarity). Plays a crucial role in the restriction of S.typhimurium replication in colonic epithelial cells during infection. Activation of the non-canonical inflammasome in brain endothelial cells can lead to excessive pyroptosis, leading to blood-brain barrier breakdown (By similarity). Pyroptosis limits bacterial replication, while cytokine secretion promotes the recruitment and activation of immune cells and triggers mucosal inflammation. May also act as an activator of adaptive immunity in dendritic cells, following activation by oxidized phospholipid 1-palmitoyl-2-arachidonoyl- sn-glycero-3-phosphorylcholine, an oxidized phospholipid (oxPAPC) (By similarity). Involved in cell death induced by endoplasmic reticulum stress and by treatment with cytotoxic APP peptides found in Alzheimer's patient brains. Cleavage of GSDMD is not strictly dependent on the consensus cleavage site but depends on an exosite interface on CASP4 that recognizes and binds the Gasdermin-D, C-terminal (GSDMD-CT) part. Catalyzes cleavage and maturation of IL18; IL18 processing also depends of the exosite interface on CASP4. In contrast, it does not directly process IL1B. During non-canonical inflammasome activation, cuts CGAS and may play a role in the regulation of antiviral innate immune activation[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27].
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Subcellular Localization
Cytoplasm, cytosol; Endoplasmic reticulum membrane; Mitochondrion; Inflammasome; Secreted
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Expression
Tissue_Specificity: Widely expressed, including in keratinocytes and colonic and small intestinal epithelial cells (at protein level). Not detected in brain.
Induction: In peripheral blood mononuclear cells and purified monocytes, up-regulated by bacterial lipopolysaccharides (LPS) and interferon-beta/IFNB1 at the mRNA level. However, this increase is not observed at the protein level, which remains constant in monocytes and other cell types following LPS treatment. In monocyte-derived macrophages, some up-regulation at the protein level is observed following treatment with LPS and IFNB1. In SH-EP1 neuroblastoma cell line, up-regulated by NF-kappa-B RELA/p65 at both mRNA and protein levels. -
Isoforms & Post-Translational Modification
Caspase 4 has 5 isoforms, P49662-1: amino acid length is 377, molecular weight is 43262 Da (predicted); P49662-2: amino acid length is 321, molecular weight is 36705 Da (predicted); P49662-3: amino acid length is 116, molecular weight is 13264 Da (predicted); P49662-4: amino acid length is 263, molecular weight is 30000 Da (predicted); P49662-5: amino acid length is 157, molecular weight is 18111 Da (predicted).In response to activation signals, undergoes autoproteolytic cleavage and activation
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Subunit
Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 20 kDa (Caspase-4 subunit p20) and a 10 kDa (Caspase-4 subunit p10) subunit.
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SwissProt ID
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Synonyms
ICH2, CASP4, Caspase-4, CASP-4, ICE and Ced-3 homolog 2, ICE(rel)-II, Mih1, Protease TX, ICH-2
Documentation
[1]. Shi J, et al. Inflammatory caspases are innate immune receptors for intracellular LPS. Nature. 2014 Oct 9;514(7521):187-92. [Content Brief]
[2]. Shi J, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature. 2015 Oct 29;526(7575):660-5. [Content Brief]
[3]. Wang K, et al. Structural Mechanism for GSDMD Targeting by Autoprocessed Caspases in Pyroptosis. Cell. 2020 Mar 5;180(5):941-955.e20. [Content Brief]
[4]. Li Z, et al. Shigella evades pyroptosis by arginine ADP-riboxanation of caspase-11. Nature. 2021 Nov;599(7884):290-295. [Content Brief]
[5]. Zhu F, et al. The orphan receptor Nur77 binds cytoplasmic LPS to activate the non-canonical NLRP3 inflammasome. Immunity. 2023 Apr 11;56(4):753-767.e8. [Content Brief]
[6]. Devant P, et al. Structural insights into cytokine cleavage by inflammatory caspase-4. Nature. 2023 Dec;624(7991):451-459. [Content Brief]
[7]. Shi X, et al. Recognition and maturation of IL-18 by caspase-4 noncanonical inflammasome. Nature. 2023 Dec;624(7991):442-450. [Content Brief]
[8]. Blasche S, et al. The E. coli effector protein NleF is a caspase inhibitor. PLoS One. 2013;8(3):e58937. [Content Brief]
[9]. Kamens J, et al. Identification and characterization of ICH-2, a novel member of the interleukin-1 beta-converting enzyme family of cysteine proteases. J Biol Chem. 1995 Jun 23;270(25):15250-6. [Content Brief]
[10]. Gaggero A, et al. A novel isoform of pro-interleukin-18 expressed in ovarian tumors is resistant to caspase-1 and -4 processing. Oncogene. 2004 Sep 30;23(45):7552-60. [Content Brief]
[11]. Wang Y, et al. Inflammasome Activation Triggers Caspase-1-Mediated Cleavage of cGAS to Regulate Responses to DNA Virus Infection. Immunity. 2017 Mar 21;46(3):393-404. [Content Brief]
[12]. Knodler LA, et al. Noncanonical inflammasome activation of caspase-4/caspase-11 mediates epithelial defenses against enteric bacterial pathogens. Cell Host Microbe. 2014 Aug 13;16(2):249-256. [Content Brief]
[13]. Fisch D, et al. Human GBP1 is a microbe-specific gatekeeper of macrophage apoptosis and pyroptosis. EMBO J. 2019 Jul 1;38(13):e100926. [Content Brief]
[14]. Chu LH, et al. The oxidized phospholipid oxPAPC protects from septic shock by targeting the non-canonical inflammasome in macrophages. Nat Commun. 2018 Mar 8;9(1):996. [Content Brief]
[15]. Kutsch M, et al. Direct binding of polymeric GBP1 to LPS disrupts bacterial cell envelope functions. EMBO J. 2020 Jul 1;39(13):e104926. [Content Brief]
[16]. Santos JC, et al. Human GBP1 binds LPS to initiate assembly of a caspase-4 activating platform on cytosolic bacteria. Nat Commun. 2020 Jun 24;11(1):3276. [Content Brief]
[17]. Sollberger G, et al. Caspase-4 is required for activation of inflammasomes. J Immunol. 2012 Feb 15;188(4):1992-2000. [Content Brief]
[18]. Kajiwara Y, et al. A critical role for human caspase-4 in endotoxin sensitivity. J Immunol. 2014 Jul 1;193(1):335-43. [Content Brief]
[19]. Casson CN, et al. Human caspase-4 mediates noncanonical inflammasome activation against gram-negative bacterial pathogens. Proc Natl Acad Sci U S A. 2015 May 26;112(21):6688-93. [Content Brief]
[20]. Baker PJ, et al. NLRP3 inflammasome activation downstream of cytoplasmic LPS recognition by both caspase-4 and caspase-5. Eur J Immunol. 2015 Oct;45(10):2918-26. [Content Brief]
[21]. Schmid-Burgk JL, et al. Caspase-4 mediates non-canonical activation of the NLRP3 inflammasome in human myeloid cells. Eur J Immunol. 2015 Oct;45(10):2911-7. [Content Brief]
[22]. Viganò E, et al. Human caspase-4 and caspase-5 regulate the one-step non-canonical inflammasome activation in monocytes. Nat Commun. 2015 Oct 28;6:8761. [Content Brief]
[23]. Tian XX, et al. NLRP6-caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation. Int Endod J. 2021 Jun;54(6):916-925. [Content Brief]
[24]. Hitomi J, et al. Involvement of caspase-4 in endoplasmic reticulum stress-induced apoptosis and Abeta-induced cell death. J Cell Biol. 2004 May 10;165(3):347-56. [Content Brief]
[25]. Li C, et al. Transmembrane Protein 214 (TMEM214) mediates endoplasmic reticulum stress-induced caspase 4 enzyme activation and apoptosis. J Biol Chem. 2013 Jun 14;288(24):17908-17. [Content Brief]
[26]. Faucheu C, et al. A novel human protease similar to the interleukin-1 beta converting enzyme induces apoptosis in transfected cells. EMBO J. 1995 May 1;14(9):1914-22. [Content Brief]
[27]. Munday NA, et al. Molecular cloning and pro-apoptotic activity of ICErelII and ICErelIII, members of the ICE/CED-3 family of cysteine proteases. J Biol Chem. 1995 Jun 30;270(26):15870-6. [Content Brief]
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