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HOME > Product search results > Code No. M058-3 Anti-Caspase-8 (Human) mAb

Code No. M058-3

Anti-Caspase-8 (Human) mAb

Price

¥48,000

Availability (in Japan)

10 or more

(In Japan at 00:05,
Jan 18, 2020 in JST)

Size

100 µg/100 µL

Data
  • Western Blotting

  • Western Blotting

  • Immunoprecipitation

Clonality Monoclonal Clone 5D3
Isotype (Immunized Animal) Mouse IgG2bκ
Applications
WB
1 µg/mL  
IP
1 µg/200 µL of cell extract from 2.5 x 10 6 cells  
Immunogen (Antigen) Recombinant Human Caspase-8 (C-terminal 180-480 a.a.)
Reactivity [Gene ID]

Human[841], Mouse(-), Rat(-)

Storage buffer PBS/50% glycerol, pH 7.2
Storage temp. -20°C Conjugate Unlabeled Manufacturer MBL
Alternative names CASP8,CAP4, MACH, MCH5, FLICE, ALPS2B, Casp-8
Background Caspase-8 (FLICE/MACH/Mch5) is a member of the ICE (interleukin-1 converting enzyme)/CED-3 family cysteine protease. It is the most upstream protease that receives the activation signal from the Fas (APO1/CD95) and TNFR1 (Tumor Necrosis Factor Receptor 1) to initiate the apoptotic protease cascade that leads to activation of ICE/CED-3 family proteases. Caspase-8 has high homologous region to the ICE/CED-3 family in C-terminal and two death effecter domains (DED) in N-terminal. Binding of caspase-8 to FADD (MORT1) through association of their DED, and consequent activation of the caspases by their proteolytic cleavage, are thought to be critical steps in the initiation of Fas- and TNFR1-induced apoptosis. Recently the inhibitor of Fas- and TNFR1-induced apoptosis is identified, called I-FLICE (FLIP/Casper/FLAME/CASH). I-FLICE has high homology to caspase-8 and it contains two DED, which interacts with caspase-8 and FADD, and potently inhibits Fas- and TNFR1-induced apoptosis.
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Citations
  1. Tsujii H et al. Screening of cell death genes with a mammalian genome-wide RNAi library. J Biochem. 148, 157-70 (2010)(PMID:20421362)

Western Blotting

  1. Tsuruma K et al. Glucocorticoid modulatory element-binding protein 1 binds to initiator procaspases and inhibits ischemia-induced apoptosis and neuronal injury. J Biol Chem. 281, 11397-404 (2006)(PMID:16497673)
  2. O'Reilly LA et al. Modifications and intracellular trafficking of FADD/MORT1 and caspase-8 after stimulation of T lymphocytes. Cell Death Differ. 11, 724-36 (2004)(PMID:15017386)
  3. Huang CR et al. Cisplatin augments FAS-mediated apoptosis through lipid rafts. Anticancer Res. 30, 2065-71 (2010)(PMID:20651352)
  4. Martin S et al. Cyclooxygenase-2 inhibition sensitizes human colon carcinoma cells to TRAIL-induced apoptosis through clustering of DR5 and concentrating death-inducing signaling complex components into ceramide-enriched caveolae. Cancer Res. 65, 11447-58 (2005)(PMID:16357153)
  5. Phillips DC et al. Sphingosine-induced apoptosis in rhabdomyosarcoma cell lines is dependent on pre-mitochondrial Bax activation and post-mitochondrial caspases. Cancer Res. 67, 756-64 (2007)(PMID:17234787)
Product category
Research area
Apoptosis
Brands
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  • The availability is based on the information in Japan at 00:05, Jan 18, 2020 in JST.
  • The special price is shown in red color.
  • Please note that products cannot be ordered from this website. To purchase the items listed in this website, please contact us or local distributers.
  • Abbreviations for applications:
    WB: Western Blotting, IH: Immunohistochemistry, IC: Immunocytochemistry, IP: Immunoprecipitation
    FCM: Flow Cytometry, NT: Neutralization, IF: Immunofluorescence, RIP: RNP Immunoprecipitation
    ChIP: Chromatin Immunoprecipitation, CoIP: Co-Immunoprecipitation
    DB: Dot Blotting, NB: Northern Blotting, RNA FISH: RNA Fluorescence in situ hybridization
  • For applications and reactivity:
    *: The use is reported in a research article (Not tested by MBL). Please check the data sheet for detailed information.
    **: The use is reported from the licenser (Under evaluation or not tested by MBL).
  • For storage temparature: RT: room temparature
  • Please note that products in this website might be changed or discontinued without notification in advance for quality improvement.