CASP3 Knockout A-549 Cell Line
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Cat.No.:
EDC07646
Species:
Human
Cell Name:
A-549
Gene:
CASP3
Gene ID:
836
Size:
1×10⁶cells
CASP3 Knockout Cell Line (A549) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDC07646 |
|---|---|
| Product Name | CASP3 Knockout A549 Cell Line |
| Cell Line | A-549 |
| Cellosaurus ID | CVCL_0023 |
| Cell Line Synonyms | A 549, A549, NCI-A549, A549/ATCC, A549 ATCC, A549ATCC, hA549 |
| Gene | CASP3 |
| NCBI Gene ID | |
| Gene Synonyms | CPP32|CPP32B|SCA-1 |
| Summary |
The protein encoded by this gene is a cysteine-aspartic acid protease that plays a central role in the execution-phase of cell apoptosis. The encoded protein cleaves and inactivates poly(ADP-ribose) polymerase while it cleaves and activates sterol regulatory element binding proteins as well as caspases 6, 7, and 9. This protein itself is processed by caspases 8, 9, and 10. It is the predominant caspase involved in the cleavage of amyloid-beta 4A precursor protein, which is associated with neuronal death in Alzheimer's disease. [provided by RefSeq, Aug 2017]
|
| Associated Diseases | Non-Small Cell Lung Carcinoma |
| Morphology | Adherent |
| Passage Ratio | 1/5-1/4 ,2days |
| Complete Culture Medium | F-12K + 10% FBS |
| Freezing Medium | 95% Complete culture medium + 5% DMSO |
| QC | Indels validated by Sanger sequencing; sterility confirmed via microbial testing. |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
| Loci | STR Info (Sample Cell) Sample Cell Line: A-549 | STR Info (Cell bank) Cell Line: A-549 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | Y | X | Y |
| CSF1PO | 10 | 12 | 10 | 12 |
| D2S1338 | 24 | 24 | ||
| D3S1358 | 16 | 16 | ||
| D5S818 | 11 | 11 | ||
| D7S820 | 8 | 11 | 8 | 11 |
| D8S1179 | 13 | 14 | 13 | 14 |
| D13S317 | 11 | 11 | ||
| D16S539 | 11 | 12 | 11 | 12 |
| D18S51 | 14 | 17 | 14 | 17 |
| D19S433 | 13 | 13 | ||
| D21S11 | 29 | 29 | ||
| FGA | 23 | 23 | ||
| Penta D | 9 | 9 | ||
| Penta E | 7 | 11 | 7 | 11 |
| TH01 | 8 | 9.3 | 8 | 9.3 |
| TPOX | 8 | 11 | 8 | 11 |
| vWA | 14 | 14 | ||
| D6S1043 | 11 | 13 | ||
| D12S391 | 18 | 18 | ||
| D2S441 | 10 | 13 | 10 | 13 |
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
Conclusion: The STR identification of this cell is correct.
FAQ
Which is better for studying CASP3 function, CASP3 Knockout A-549 Cell Line or CASP3 overexpression A-549 Cell Line?
The choice depends on whether you are studying CASP3's role as the principal executioner caspase or modeling apoptosis and chemotherapy-induced pyroptosis in lung cancer. The Knockout line is the standard tool for asking whether CASP3 is required for these processes — CASP3 is the principal executioner caspase that cleaves >200 substrates (PARP1, ICAD/DFF45, ROCK1, lamins, GSDME) to execute apoptosis; CASP3 also cleaves GSDME at D270 to drive chemotherapy-induced pyroptosis (the apoptosis-to-pyroptosis switch in GSDME-expressing cells). Overexpression is useful for studying CASP3 gain-of-function effects.
For lung cancer chemotherapy research, the EDITGENE CASP3 Knockout in A-549 is highly relevant — A-549 is an NSCLC cell line, and CASP3 is critical for chemotherapy-induced apoptosis in NSCLC. Rescue with wild-type or catalytically-dead (C163A) CASP3 is the standard specificity control. The knockout is paired with parallel GSDME Knockout in SK-OV-3 (also available) for studying chemotherapy-induced apoptosis-to-pyroptosis switching. The knockout is valuable for studying executioner caspase biology, chemotherapy-induced cell death mechanisms (cisplatin, paclitaxel), and immunogenic cell death pathways.
What are the application scenarios for this model?
Primary applications:
• Apoptosis execution: PARP1, ICAD/DFF45 cleavage and apoptotic morphology analysis in CASP3-null cells.
• Apoptosis-pyroptosis switching: GSDME D270 cleavage analysis given CASP3's role in driving GSDME-mediated chemotherapy-induced pyroptosis (parallel GSDME KO in SK-OV-3 also available).
• Chemotherapy-induced cell death: cisplatin, paclitaxel-induced apoptosis kinetics in CASP3-null NSCLC cells.
• Immunogenic cell death: in heterologous immunotherapy-relevant contexts, characterization of CASP3-dependent immunogenic cell death.
EDITGENE recommends this lung cancer model for researchers investigating apoptosis execution, GSDME-mediated pyroptosis, and chemotherapy mechanism studies.
Is this CASP3 Knockout A-549 Cell Line compatible with overexpression rescue experiments?
Yes. CASP3 rescue experiments are well-established for apoptosis research:
• Construct design: use a codon-modified CASP3 sequence with a small C-terminal tag (FLAG, HA). CASP3 has the canonical caspase prodomain-large subunit-small subunit architecture with catalytic C163 — preserve all elements.
• Catalytically-dead rescue: C163A mutation in the catalytic cysteine abolishes proteolytic activity.
• Constitutively active rescue: prodomain truncation generates revCASP3 with constitutive catalytic activity.
• GSDME-uncleavable rescue: substrate-recognition mutations affecting GSDME D270 cleavage enable separation of apoptotic from pyroptotic functions.
• Functional readout: rescue should restore PARP1 cleavage, apoptotic execution, and GSDME-mediated chemotherapy-induced pyroptosis.
A-549 transduces efficiently with lentivirus and supports stable rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
Related Publications
Polymerase acidic subunit of H9N2 polymerase complex induces cell apoptosis by binding to PDCD 7 in A549 cells.
IF=3.8
Virology journal
BACKGROUND:H9N2 influenza virus, a subtype of influenza A virus, can spread across different species and induce the respiratory infectious disease in humans, leading to a severe public health risk and a huge economic loss to poultry production. Increasing studies have shown that polymerase acidic (PA) subunit of RNA polymerase in ribonucleoproteins complex of H9N2 virus involves in crossing the host species barriers, the replication and airborne transmission of H9N2 virus. METHODS:Here, to further investigate the role of PA subunit during the infection of H9N2 influenza virus, we employed mass spectrometry (MS) to search the potential binding proteins of PA subunit of H9N2 virus. Our MS results showed that programmed cell death protein 7 (PDCD7) is a binding target of PA subunit. Co-immunoprecipitation and pull-down assays further confirmed the interaction between PDCD7 and PA subunit. Overexpression of PA subunit in A549 lung cells greatly increased the levels of PDCD7 in the nuclear and induced cell death assayed by MTT assay. RESULTS:Flow cytometry analysis and Western blot results showed that PA subunit overexpression significantly increased the expression of pro-apoptotic protein, bax and caspase 3, and induced cell apoptosis. However, knockout of PDCD7 effectively attenuated the effects of PA overexpression in cell apoptosis. CONCLUSIONS:In conclusion, the PA subunit of H9N2 virus bind with PDCD7 and regulated cell apoptosis, which provide new insights in the role of PA subunit during H9N2 influenza virus infection.
Required Accessories
Cell Culture Optimization Series
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