CASP8 Knockout HCT 116 Cell Line
Cat.No.:
EDJ-KQ21053
Species:
Human
Cell Name:
HCT 116
Gene:
CASP8
Gene ID:
841
Size:
1×10⁶cells
CASP8 Knockout Cell Line (HCT116) 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. | EDJ-KQ21053 |
|---|---|
| Product Name | CASP8 Knockout HCT 116 Cell Line |
| Cell Line | HCT 116 |
| Cellosaurus ID | CVCL_0291 |
| Cell Line Synonyms | HCT-116, HCT.116, HCT_116, HCT116, HCT116wt, HCT-116/P, HCT-116/parental, CoCL2 |
| Gene | CASP8 |
| NCBI Gene ID | |
| 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 | Colorectal Carcinoma |
| Morphology | Adherent |
| Passage Ratio | 1/5-1/4,2days |
| Complete Culture Medium | mcCoy5A+10%FBS |
| Freezing Medium | 90%FBS/Complete culture medium+10% 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: HCT 116 | STR Info (Cell bank) Cell Line: HCT 116 | ||||||
| Allele1 | Allele2 | Allele3 | Allele4 | Allele1 | Allele2 | Allele3 | Allele4 | |
| Amelogenin | X | X | ||||||
| CSF1PO | 7 | 10 | 7 | 9 | 10 | 11 | ||
| D2S1338 | 16 | 16 | ||||||
| D3S1358 | 12 | 17 | 18 | 19 | 12 | 18 | 19 | |
| D5S818 | 10 | 11 | 10 | 11 | ||||
| D7S820 | 11 | 12 | 11 | 12 | ||||
| D8S1179 | 10 | 12 | 14 | 15 | 10 | 12 | 14 | 15 |
| D13S317 | 10 | 12 | 10 | 12 | ||||
| D16S539 | 11 | 13 | 11 | 12 | 13 | 14 | ||
| D18S51 | 16 | 17 | 16 | 17 | ||||
| D19S433 | 12 | 13 | 12 | |||||
| D21S11 | 29 | 30 | 29 | 30 | ||||
| FGA | 18 | 23 | 18 | 23 | ||||
| Penta D | 9 | 13 | 9 | 13 | ||||
| Penta E | 12 | 13 | 14 | 12 | 13 | 14 | ||
| TH01 | 8 | 9 | 8 | 9 | ||||
| TPOX | 8 | 8 | ||||||
| vWA | 17 | 21 | 22 | 23 | 17 | 21 | 22 | 23 |
| D6S1043 | 13 | |||||||
| D12S391 | 17 | 21 | 22 | |||||
| D2S441 | 11 | 12 | ||||||
* 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.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
Related Publications
MIND bomb 2 prevents RIPK1 kinase activity-dependent and -independent apoptosis through ubiquitylation of cFLIP.
IF=5.1
Communications biology
Mind bomb 2 (MIB2) is an E3 ligase involved in Notch signalling and attenuates TNF-induced apoptosis through ubiquitylation of receptor-interacting protein kinase 1 (RIPK1) and cylindromatosis. Here we show that MIB2 bound and conjugated K48- and K63-linked polyubiquitin chains to a long-form of cellular FLICE-inhibitory protein (cFLIP), a catalytically inactive homologue of caspase 8. Deletion of MIB2 did not impair the TNF-induced complex I formation that mediates NF-κB activation but significantly enhanced formation of cytosolic death-inducing signalling complex II. TNF-induced RIPK1 Ser phosphorylation, a hallmark of RIPK1 death-inducing activity, was enhanced in MIB2 knockout cells, as was RIPK1 kinase activity-dependent and -independent apoptosis. Moreover, RIPK1 kinase activity-independent apoptosis was induced in cells expressing cFLIP mutants lacking MIB2-dependent ubiquitylation. Together, these results suggest that MIB2 suppresses both RIPK1 kinase activity-dependent and -independent apoptosis, through suppression of RIPK1 kinase activity and ubiquitylation of cFLIP, respectively.