Anti-DELE antibody - N-terminal
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(2 Publications)
Rabbit Polyclonal DELE antibody. N-terminal. Suitable for WB, IHC-P and reacts with Rat, Human samples. Cited in 2 publications. Immunogen corresponding to Synthetic Peptide within Human DELE1.
View Alternative Names
DELE, KIAA0141, DELE1, DAP3-binding cell death enhancer 1, Death ligand signal enhancer, DELE1(L)
- IHC-P
Supplier Data
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-DELE antibody - N-terminal (AB189958)
Immunofluorescence analysis of human brain labeling DELE with ab189958 at 20 μg/ml.
- IHC-P
Supplier Data
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-DELE antibody - N-terminal (AB189958)
Immunohistochemical analysis of formalin-fixed, paraffin-embedded human brain cortex labeling DELE with ab189958 at 5 μg/ml.
- WB
Supplier Data
Western blot - Anti-DELE antibody - N-terminal (AB189958)
All lanes:
Western blot - Anti-DELE antibody - N-terminal (ab189958) at 1 µg/mL
Lane 1:
Rat brain tissue lysate
Lane 2:
Rat brain tissue lysate with Blocking peptide
Predicted band size: 56 kDa
false
Reactivity data
Properties and storage information
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Shipped at conditions
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Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
DELE enhances caspase activation in response to apoptotic stimuli facilitating cell death processes. It functions as part of a complex that includes DAP3 and other apoptotic proteins helping to amplify apoptotic signals that lead to mitochondria-mediated apoptosis. By doing so DELE contributes to the maintenance of cellular homeostasis by eliminating damaged or unwanted cells therefore participating in normal cellular turnover and response to stress signals.
Pathways
The protein is an important player in the intrinsic apoptotic pathway which is activated by mitochondrial signals. It closely interacts with proteins such as BAX and BAK which are known to promote mitochondrial dysfunction leading to cytochrome c release and caspase activation. DELE is also linked with pathways involving TNF-alpha a cytokine that can initiate apoptosis through extrinsic and intrinsic pathways reflecting its involvement in cellular responses to stress and damage.
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Target data
Publications (2)
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Nature 579:427-432 PubMed32132707
2020
Applications
Unspecified application
Species
Unspecified reactive species
Technology in cancer research & treatment 18:1533033819874783 PubMed31526099
2019
Applications
Unspecified application
Species
Unspecified reactive species
Product promise
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