Caspase 3 Antibody - #AF6311

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Product: Caspase 3 Antibody
Catalog: AF6311
Description: Rabbit polyclonal antibody to Caspase 3
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat, Bovine
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 37kDa; 32kD(Calculated).
Uniprot: P42574
RRID: AB_2835170

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 100ul $280 In stock
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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 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.

Reactivity:
Human,Mouse,Rat,Bovine
Prediction:
Pig(86%), Horse(86%), Sheep(100%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
Caspase 3 Antibody detects endogenous levels of total Caspase 3.
RRID:
AB_2835170
Cite Format: Affinity Biosciences Cat# AF6311, RRID:AB_2835170.
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

A830040C14Rik; Apopain; CASP-3; CASP3; CASP3_HUMAN; Casp3a; Caspase 3; Caspase 3, apoptosis-related cysteine peptidase; Caspase 3, apoptosis-related cysteine protease; Caspase 3, apoptosis-related cysteine protease a; Caspase-3 subunit p12; CC3; CPP-32; CPP32; CPP32B; Cysteine protease CPP32; EC 3.4.22.56; LICE; mldy; OTTHUMP00000165052; OTTHUMP00000165053; OTTHUMP00000165054; PARP cleavage protease; Procaspase3; protein Yama; SCA 1; SCA-1; SREBP cleavage activity 1; Yama;

Immunogens

Immunogen:
Uniprot:

P42574(CASP3_HUMAN) >>Visit HPA database.

Gene(ID):
CASP3(836)
Expression:
P42574 CASP3_HUMAN:

Highly expressed in lung, spleen, heart, liver and kidney. Moderate levels in brain and skeletal muscle, and low in testis. Also found in many cell lines, highest expression in cells of the immune system.

Description:
This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce 2 subunits, large and small, that dimerize to form the active enzyme.
Sequence:
MENTENSVDSKSIKNLEPKIIHGSESMDSGISLDNSYKMDYPEMGLCIIINNKNFHKSTGMTSRSGTDVDAANLRETFRNLKYEVRNKNDLTREEIVELMRDVSKEDHSKRSSFVCVLLSHGEEGIIFGTNGPVDLKKITNFFRGDRCRSLTGKPKLFIIQACRGTELDCGIETDSGVDDDMACHKIPVEADFLYAYSTAPGYYSWRNSKDGSWFIQSLCAMLKQYADKLEFMHILTRVNRKVATEFESFSFDATFHAKKQIPCIVSMLTKELYFYH

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Pig
86
Horse
86
Chicken
75
Xenopus
63
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P42574 As Substrate

Site PTM Type Enzyme
M1 Acetylation
T4 Phosphorylation
S7 Phosphorylation
S10 Phosphorylation
K11 Acetylation
K11 Ubiquitination
S12 Phosphorylation
K14 Ubiquitination
K19 Ubiquitination
S24 Phosphorylation
S26 Phosphorylation
S29 Phosphorylation
Y41 Phosphorylation
K57 Ubiquitination
S65 Phosphorylation
T67 Phosphorylation
K82 Acetylation
K82 Ubiquitination
K88 Ubiquitination
K105 Ubiquitination
K138 Ubiquitination
S150 Phosphorylation Q16539 (MAPK14)
T152 Phosphorylation
C163 S-Nitrosylation
T174 Phosphorylation
S176 Phosphorylation
K210 Ubiquitination
K229 Ubiquitination
S249 Phosphorylation
K260 Ubiquitination
T270 Phosphorylation

Research Backgrounds

Function:

Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a '216-Asp-|-Gly-217' bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage.

PTMs:

Cleavage by granzyme B, caspase-6, caspase-8 and caspase-10 generates the two active subunits. Additional processing of the propeptides is likely due to the autocatalytic activity of the activated protease. Active heterodimers between the small subunit of caspase-7 protease and the large subunit of caspase-3 also occur and vice versa.

S-nitrosylated on its catalytic site cysteine in unstimulated human cell lines and denitrosylated upon activation of the Fas apoptotic pathway, associated with an increase in intracellular caspase activity. Fas therefore activates caspase-3 not only by inducing the cleavage of the caspase zymogen to its active subunits, but also by stimulating the denitrosylation of its active site thiol.

Subcellular Location:

Cytoplasm.

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

Highly expressed in lung, spleen, heart, liver and kidney. Moderate levels in brain and skeletal muscle, and low in testis. Also found in many cell lines, highest expression in cells of the immune system.

Subunit Structure:

Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 17 kDa (p17) and a 12 kDa (p12) subunit. Interacts with BIRC6/bruce.

Family&Domains:

Belongs to the peptidase C14A family.

Research Fields

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

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

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Parkinson's disease.

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

· Human Diseases > Neurodegenerative diseases > Huntington's disease.

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Cardiovascular diseases > Viral myocarditis.

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Serotonergic synapse.

References

1). Iron Oxide Nanoparticles Engineered Macrophage-Derived Exosomes for Targeted Pathological Angiogenesis Therapy. ACS nano, 2024 (PubMed: 38412252) [IF=17.1]
2). Upregulation of BCL-2 by acridone derivative through gene promoter i-motif for alleviating liver damage of NAFLD/NASH. NUCLEIC ACIDS RESEARCH, 2020 (PubMed: 32710621) [IF=14.9]

Application: WB    Species: human    Sample: HepG2

Figure 4. Effect of A22 on anti-apoptosis in 0.5 mM palmitic acid oil (PA) induced cell model. (A) Effect of A22 on cell viability for anti-apoptotic protective effect. (B) Effect of A22 on transcription of BCL-2 and BAX with measurement of mRNA levels. (C) Effect of A22 on protein expressions related with apoptosis (left), which were quantitatively analyzed (right). All the experiments were repeated for three times.
3). Antitumor activity of aumolertinib, a third-generation EGFR tyrosine kinase inhibitor, in non-small-cell lung cancer harboring uncommon EGFR mutations. Acta Pharmaceutica Sinica B, 2023 (PubMed: 37425047) [IF=14.5]

Application: WB    Species: Mouse    Sample: tumor tissue

Figure 6 Antitumor activity of aumolertinib in the PDX model harboring EGFR H773-V774insNPH mutation. Tumor volume (A), tumor weight (B), average body weights of mice at treatment start (Day 0) and study end (Day 26) (C), and the photograph of tumors (D) in a PDX LU0387 (EGFR H773_N774insNPH) NSCLC tumor model in mice over 26-day treatment with aumolertinib. The vehicle was used as the control. (E, F) Expression of pEGFR, EGFR, pAKT, AKT, pERK, ERK, PCNA, cleaved PARP, PARP, cleaved caspase-3, and caspase-3 in tumor tissue after administration of EGFR-TKIs. Tumors were obtained and lysed at 6 h after the last treatment. Data are presented as the ratio relative to the vehicle group. The data of (A), (B), (C), and (F) are presented as the mean ± SEM (n = 6/group) and compared with the vehicle (∗P < 0.05; ∗∗P < 0.01). PDX, patient-derived xenografts; EGFR, epidermal growth factor receptor; TKIs, tyrosine kinase inhibitors; NPH, H773-V774insNPH.
4). 2,3′,4,4′,5-Pentachlorobiphenyl induces mitochondria-dependent apoptosis mediated by AhR/Cyp1a1 in mouse germ cells. Journal of Hazardous Materials, 2023 (PubMed: 37055962) [IF=13.6]
5). Precise editing of FGFR3-TACC3 fusion genes with CRISPR-Cas13a in glioblastoma. Molecular Therapy, 2021 (PubMed: 34274537) [IF=12.4]
6). Heat shock protein 22 modulates NRF1/TFAM-dependent mitochondrial biogenesis and DRP1-sparked mitochondrial apoptosis through AMPK-PGC1α signaling pathway to alleviate the early brain injury of subarachnoid hemorrhage in rats. Redox Biology, 2021 (PubMed: 33472123) [IF=11.4]

Application: WB    Species: rat    Sample: brain

Fig. 6. Hsp22 regulates PGC1α via AMPK signaling pathway in rats after SAH Beam balance scores, Modified Garcia scores and Brainwater content in various groups. n = 6 per group. (B) Representative photomicrographs of TUNEL staining and quantitative analyses in the indicated groups. n = 4 per group. Scale bar = 100 μm. (C) Typical photomicrographs showing double immunofluorescence staining of PGC1α (green) and NeuN (red) in diverse experimental groups. n = 4 per group. Scale bar = 50 μm. (D) Western blot images and quantitative analyses of p-AMPK/AMPK, PGC1α, Drp1, Nrf1, TFAM, UCP2, Cleaved caspase-3/Caspase-3, Bcl2, Bax, Cytosolic and mitochondrial cytochrome c. n = 6 per group. Bars represent mean ± SD. **P < 0.01, *P < 0.05 vs. Sham group. ##P < 0.01, #P < 0.05 vs. SAH + Vehicle group. &&P < 0.01, &P < 0.05 vs. SAH + hsp22+scramble siRNA. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
7). Widening the Lens on Prothioconazole and Its Metabolite Prothioconazole-Desthio: Aryl Hydrocarbon Receptor-Mediated Reproductive Disorders through in Vivo, in Vitro, and in Silico Studies. ENVIRONMENTAL SCIENCE & TECHNOLOGY, 2022 (PubMed: 36332113) [IF=11.4]
8). Oxygen vacancy-engineered cerium oxide mediated by copper-platinum exhibit enhanced SOD/CAT-mimicking activities to regulate the microenvironment for osteoarthritis therapy. Journal of nanobiotechnology, 2024 (PubMed: 39155382) [IF=10.2]

Application: IF/ICC    Species: Rat    Sample:

Fig. 5. ROS scavenging, mitochondrial protection, and apoptosis inhibition by PtCuOX/CeO2-X nanozymes in vitro. a Chondrocyte staining with various ROS assay kits and b corresponding quantification to assess the scavenging capacity of ROS, ·O2−, ·OH, and NO, respectively. c Chondrocyte staining with mitochondrial membrane potential probe (JC-1) and d corresponding quantification to assess the membrane potential. e Chondrocyte staining with MitoSOX probe and f corresponding quantification to assess the level of endogenous ROS. g Chondrocyte staining with Fluo-4 AM probe and h corresponding quantification to assess the disturbance of Ca2+ efflux. i) ATP assay kit to assess ATP levels in chondrocytes after different treatments. j 7-AAD/Annexin V-APC apoptosis kit to assess apoptosis in chondrocytes after different treatments. k Western blotting and l quantitative analysis to assess Bax, Caspase-3, and Bcl-2 protein levels. Concentration: 50 μg/mL; NIR parameters: 808 nm, 1.0 W/cm2, 5 min. Data are expressed as mean ± SD (n = 3). * and # for P 
9). AKAP8L enhances the stemness and chemoresistance of gastric cancer cells by stabilizing SCD1 mRNA. Cell Death & Disease, 2022 (PubMed: 36522343) [IF=9.0]
10). CircGCN1L1 promotes synoviocyte proliferation and chondrocyte apoptosis by targeting miR-330-3p and TNF-α in TMJ osteoarthritis. Cell Death & Disease, 2020 (PubMed: 32332704) [IF=9.0]

Application: WB    Species: human    Sample: synovial cells

Fig. 5 MiR-330-3p mediates the function of circGCN1L1 in human TMJ synoviocyte. a The synovial cells from the control patient were transiently transfected with miR-330-3p mimics, miR-330-3p mimic NC, miR-330-3p inhibitor, or miR-330-3p inhibitor NC, respectively. Forty-eight hours later, the levels of MMP13, MMP3, COL2A1, and ADAMTS4 were detected using WB. N = 4 (four independent experiments). b CircGCNL1 with/ without miR-330-3p mimics was transfected into co-cultured synoviocytes. After 2 days of co-culture, proteins were extracted from chondrocytes in the lower chamber, and WB was performed to detect the levels of MMP13, MMP3, COL2A1, ADAMTS4, TNF-α, p65, Bcl-2, Bax, caspase-3, and cleaved caspase-3. N = 4 (four independent experiments). Data are presented as mean ± S.D. One-way ANOVA with Bonferroni test was performed. WB western blotting, NC normal control, MMP matrix metalloproteinase, TNF tumor necrosis factor, Bcl-2 B-cell lymphoma-2, Bax BCL2-associated X, COL2A1 collagen type II alpha 1.

Application: WB    Species: human    Sample: human TMJ synoviocyte

Fig. 5 |MiR-330-3p mediates the function of circGCN1L1 in human TMJ synoviocyte..b CircGCNL1 with/without miR-330-3p mimics was transfected into co-cultured synoviocytes. After 2 days of co-culture, proteins were extracted from chondrocytes in the lower chamber, and WB was performed to detect the levels of MMP13, MMP3, COL2A1, ADAMTS4, TNF-α, p65, Bcl-2, Bax, caspase-3, and cleaved caspase-3. N = 4 (four independent experiments). Data are presented as mean ± S.D. One-way ANOVA with Bonferroni test was performed. WB western blotting, NC normal control, MMP matrix metalloproteinase, TNF tumor necrosis factor, Bcl-2 B-cell lymphoma-2, Bax BCL2-associated X,COL2A1 collagen type II alpha 1.
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