Cleaved-Caspase 4 (Gln81) Antibody - #AF5373

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Product: Cleaved-Caspase 4 (Gln81) Antibody
Catalog: AF5373
Description: Rabbit polyclonal antibody to Cleaved-Caspase 4 (Gln81)
Application: WB IHC
Cited expt.: WB
Reactivity: Human
Mol.Wt.: 43kDa; 43kD(Calculated).
Uniprot: P49662
RRID: AB_2837858

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*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.

Reactivity:
Human
Clonality:
Polyclonal
Specificity:
Cleaved-Caspase4 (Gln81) Antibody detects endogenous levels of fragment of activated Caspase4 resulting from cleavage adjacent to Gln81.
RRID:
AB_2837858
Cite Format: Affinity Biosciences Cat# AF5373, RRID:AB_2837858.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

Apoptotic cysteine protease Mih1/TX; CASP-4; CASP4; CASP4_HUMAN; Caspase 4 apoptosis related cysteine peptidase; Caspase-4 subunit 2; Caspase4; ICE(rel)-II; ICE(rel)II; ICEREL II; ICH2; Mih1/TX; Protease ICH-2; Protease TX; TX;

Immunogens

Immunogen:

A synthesized peptide derived from human CASP4.

Uniprot:

P49662(CASP4_HUMAN) >>Visit HPA database.

Gene(ID):
CASP4(837)
Expression:
P49662 CASP4_HUMAN:

Widely expressed, including in keratinocytes and colonic and small intestinal epithelial cells (at protein level). Not detected in brain.

Description:
Involved in the activation cascade of caspases responsible for apoptosis execution. Cleaves caspase-1.
Sequence:
MAEGNHRKKPLKVLESLGKDFLTGVLDNLVEQNVLNWKEEEKKKYYDAKTEDKVRVMADSMQEKQRMAGQMLLQTFFNIDQISPNKKAHPNMEAGPPESGESTDALKLCPHEEFLRLCKERAEEIYPIKERNNRTRLALIICNTEFDHLPPRNGADFDITGMKELLEGLDYSVDVEENLTARDMESALRAFATRPEHKSSDSTFLVLMSHGILEGICGTVHDEKKPDVLLYDTIFQIFNNRNCLSLKDKPKVIIVQACRGANRGELWVRDSPASLEVASSQSSENLEEDAVYKTHVEKDFIAFCSSTPHNVSWRDSTMGSIFITQLITCFQKYSWCCHLEEVFRKVQQSFETPRAKAQMPTIERLSMTRYFYLFPGN

Research Backgrounds

Function:

Inflammatory caspase. Essential effector of NLRP3 inflammasome-dependent CASP1 activation and IL1B and IL18 secretion in response to non-canonical activators, such as UVB radiation, cholera enterotoxin subunit B and cytosolic LPS. Independently of NLRP3 inflammasome and CASP1, promotes pyroptosis, through GSDMD cleavage and activation, and IL1A, IL18 and HMGB1 release in response to non-canonical inflammasome activators. Plays a crucial role in the restriction of Salmonella typhimurium replication in colonic epithelial cells during infection. In later stages of the infection, LPS from cytosolic Salmonella triggers CASP4 activation, which ultimately results in pyroptosis of infected cells and their extrusion into the gut lumen, as well as in IL18 secretion. Pyroptosis limits bacterial replication, while cytokine secretion promotes the recruitment and activation of immune cells and triggers mucosal inflammation. Involved in LPS-induced IL6 secretion; this activity may not require caspase enzymatic activity. Involved in cell death induced by endoplasmic reticulum stress and by treatment with cytotoxic APP peptides found Alzheimer's patient brains. Activated by direct binding to LPS without the need of an upstream sensor. 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.

PTMs:

In response to activation signals, including endoplasmic reticulum stress or treatment with amyloid-beta A4 protein fragments (such as amyloid-beta protein 40), undergoes autoproteolytic cleavage.

Subcellular Location:

Cytoplasm>Cytosol. Endoplasmic reticulum membrane>Peripheral membrane protein>Cytoplasmic side. Mitochondrion. Inflammasome. Secreted.
Note: Predominantly localizes to the endoplasmic reticulum (ER). Association with the ER membrane requires TMEM214 (PubMed:15123740). Released in the extracellular milieu by keratinocytes following UVB irradiation (PubMed:22246630).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Widely expressed, including in keratinocytes and colonic and small intestinal epithelial cells (at protein level). Not detected in brain.

Family&Domains:

The CARD domain mediates LPS recognition and homooligomerization.

Belongs to the peptidase C14A family.

Research Fields

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

References

1). Inhibition of IL1R1 or CASP4 attenuates spinal cord injury through ameliorating NLRP3 inflammasome-induced pyroptosis. Frontiers in Immunology, 2022 (PubMed: 35990672) [IF=5.7]
2). Ochratoxin A induces cytotoxicity through ROS-mediated endoplasmic reticulum stress pathway in human gastric epithelium cells. TOXICOLOGY, 2022 (PubMed: 36058351) [IF=4.8]
3). Qilian Jiechang Ning Alleviates TNBS-Induced Ulcerative Colitis in Mice and Segatella copri Outer Membrane Vesicle-Triggered Inflammation in Colon Epithelial Cells via the Caspase-1/11-GSDMD Pathways. Journal of innate immunity, 2025 (PubMed: 40367931) [IF=4.7]

Application: WB    Species: Mouse    Sample: Colonic Epithelial Cells

Fig. 2. S. copri OMVs induce inflammation and dysregulation of tight junction protein expression in colonic epithelial cells. a ELISA detection of IL-1β, IL-18, IL-6, and TNF-α expression. b Western blot analysis of protein levels of GSDMD-N, NLRP3, ASC, cleaved Caspase-1, cleaved Caspase-11, ZO-1, and Occludin in cell lysates. The presented blots were derived from the same gels. Colonic epithelial cells were cultured in standard conditions and treated with 1 µg/mL of S. copri OMVs or LPS for 24 h. Statistical differences among groups were assessed using one-way analysis of variance (ANOVA), with comparisons made among the S. copri OMVs or LPS-treated group and the untreated control group. n = 3.
4). Anoikis regulator GLI2 promotes NC cell immunity escape by TGF-β-mediated non-classic hedgehog signaling in colorectal cancer: based on artificial intelligence and big data analysis. Aging, 2023 (PubMed: 38159250) [IF=3.9]

Application: WB    Species: human    Sample:

Figure 9. GLI2 promoted drug tolerance. (A) Expression level of GLI2 after siRNA treatment in colorectal cancer cell (lovo) and gastric cancer by (a) PCR assay and (B) WB. (C) CCK-8 assay. Alive and dead cell staining in (D) colorectal cancer and (E) gastric cancer.
5). Caerin 1.1 and 1.9 peptides induce acute caspase 3/GSDME-mediated pyroptosis in epithelial cancer cells. Scientific reports, 2025 (PubMed: 40251208) [IF=3.8]

Application: WB    Species: human    Sample:

Fig. 4 F1/F3 mediates HeLa cell pyroptosis through the caspase-3/GSDME signalling pathway. (A)-(I): HeLa cells (1.0 × 106) were treated with F1/F3 (10 µg/ml), P3 or left untreated for 1 h, the expression of pyroptosis-related proteins was tested by Western blot. (A) GSDMD. (B) Caspase-1. (C) Caspase-4. (D) Caspase-5. (E) Cleaved caspase-4. (F) GSDMB. (G) Caspase-3. (H) Cleaved caspase-3. (I) Cleaved GSDME-N. (J) LDH release was detected by F1/F3, caspase inhibitor and caspase-3 inhibitor (Ac-DEVD-CHO) combined with F1/F3. These results come from a representative experiment in which two independent experiments were conducted. All data are presented as the mean ± SEM. *P-value 
6). Melatonin alleviates deoxynivalenol-induced apoptosis of human granulosa cells by reducing mutually accentuated FOXO1 and ER stress. Biology of Reproduction, 2021 (PubMed: 33907797) [IF=3.1]

Application: WB    Species: Human    Sample: granulosa cells

Figure 4. Melatonin attenuates DON-induced apoptosis by suppressing ER stress in human granulosa cells. (A) Cells were treated with different concentrations of DON for 24 h. The protein levels of BiP, CHOP, and phosphorylated-eIF2α were assessed by western blot. (B) For the inhibition of ROS production, Mito-TEMPO was added 1 h before DON treatment. Cells were cultured for another 24 h and the levels of BiP, CHOP, and phosphorylated-eIF2α were measured by western blot. (C) Granulosa cells were cultured in medium containing DON with or without melatonin for 24 h. The levels of BiP, CHOP, and phosphorylated-eIF2α were analyzed by western blot. (D) The levels of Cleaved Caspase 4 and Phosphorylated JNK were analyzed by western blot. (E) ER stress inhibitor 4-PBA was added 1 h before DON and melatonin incubation. The cells were cultured for 24 h and cell viability was determined using MTT assay kit. (F) The protein levels of Bax, Bcl-2, and Cleaved Caspase-3 from granulosa cells treated as depicted in Figure 4D were analyzed by western blot. (G) Quantification of Bcl-2 and Bax expression using densitometric analysis. β-actin served as the control for loading. Data are represented as means ± SEM of three independent experiments. ∗P < 0.05, ∗∗P < 0.01.

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