CASP8 Knockout A-549 Cell Line

CASP8 Knockout A-549 Cell Line
15% OFF
Cat.No.:

EDC07644

Species:

Human

Cell Name:

A-549

Gene:

CASP8

Gene ID:

841

Size:

1×10⁶cells

CASP8 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. EDC07644
Product Name CASP8 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 CASP8
NCBI Gene ID
841
Gene Synonyms ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5
Summary
This gene encodes 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 composed of a prodomain, a large protease subunit, and a small protease subunit. Activation of caspases requires proteolytic processing at conserved internal aspartic residues to generate a heterodimeric enzyme consisting of the large and small subunits. This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD. This protein was detected in the insoluble fraction of the affected brain region from Huntington disease patients but not in those from normal controls, which implicated the role in neurodegenerative diseases. Many alternatively spliced transcript variants encoding different isoforms have been described, although not all variants have had their full-length sequences determined. [provided by RefSeq, Jul 2008]
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.
LociSTR Info (Sample Cell)
Sample Cell Line: A-549
STR Info (Cell bank)
Cell Line: A-549
Allele1Allele2Allele1Allele2
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.

FAQ

The choice depends on whether you are studying CASP8 in lung cancer context for chemotherapy and TRAIL-targeted therapy research. The Knockout line is the standard tool for asking whether CASP8 is required for these processes in NSCLC context — CASP8 silencing/loss has been characterized in many cancers as an immune evasion and chemotherapy resistance mechanism; CASP8 status influences TRAIL-induced apoptosis. Overexpression is useful for studying CASP8 gain-of-function effects. For lung cancer apoptosis research, the EDITGENE CASP8 Knockout in A-549 is highly relevant. This product complements the parallel CASP8 Knockouts in L-02 (normal hepatocyte) and A-375 (BRAF melanoma) for cross-background validation. Rescue with wild-type or catalytically-dead CASP8 enables structure-function studies. The knockout is valuable for studying death receptor-induced apoptosis in NSCLC, TRAIL-targeted therapy resistance, and apoptosis-necroptosis switching in lung cancer biology.
Primary applications: • NSCLC death receptor signaling: FAS/TRAIL-R-induced apoptosis analysis in NSCLC context. • TRAIL-targeted therapy: in heterologous TRAIL-targeted therapy contexts, characterization of CASP8-dependent TRAIL-induced apoptosis. • Cross-background validation: parallel analysis with CASP8 KOs in L-02 and A-375 (both available) for cross-tissue context studies. • Lung cancer chemotherapy: cisplatin, paclitaxel-induced apoptosis analysis in CASP8-null cells. EDITGENE recommends this NSCLC model for researchers investigating death receptor apoptosis and TRAIL-targeted therapy resistance in lung cancer.
Yes. CASP8 rescue experiments in A-549 are well-suited for lung cancer apoptosis research: • Construct design: same considerations as CASP8/L-02 rescue — preserve DED and protease domains. • Catalytically-dead C360S rescue: enables separation of proteolytic from scaffolding functions in NSCLC context. • Lung cancer mutation rescue: cancer-associated CASP8 mutations enable studies of CASP8 silencing in tumor biology. • Functional readout: rescue should restore TRAIL- and FAS-induced apoptosis in NSCLC context. 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.

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