Product Details
Alternative Name: | MORT1, Fas (TNFRSF6)-associated via death domain |
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Clone: | 1F7 |
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Host: | Mouse |
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Isotype: | IgG1 |
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Immunogen: | Recombinant human FADD. |
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UniProt ID: | Q13158 |
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Species reactivity: | Human, Mouse
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Applications: | WB
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Recommended Dilutions/Conditions: | Western Blot (1µg/ml, ECL) Suggested dilutions/conditions may not be available for all applications. Optimal conditions must be determined individually for each application. |
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Application Notes: | Detects a band of ~28kDa by Western blot. |
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Purity Detail: | Protein A affinity purified. |
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Formulation: | Liquid. In PBS, pH 7.2, with 50% glycerol. |
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Shipping: | Blue Ice |
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Long Term Storage: | -20°C |
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Scientific Background: | Fas-associating death domain containing protein (FADD)/MORT1 serves as a signal transducer of Fas-induced apoptosis. Through its amino-terminal death effector domain (DED), FADD binds to cytosolic proteins such as TRADD, a cytosolic death domaincontaining protein that asssociates with the cytosolic portion of TNF receptor, or MACH/FLICE/caspase-8, a protease with sequence homology to ICE-CED-3 protease family, in order to transduce the death signal. |
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Regulatory Status: | RUO - Research Use Only |
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Western blot probed with FADD mAb (1F7). Lane 1 FADD (recombinant) and cell lysates Jurkat (lane 2), Raji (lane 3), HeLa (lane 4), ZR75-1 (lane 5), A431 (lane 6), and HUC-Fm (lane 7).
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Product Literature References
Upregulation of RIPK1 implicates in HEK 293T cell death upon transient transfection of A53T-α-synuclein: F. Meshkini, et al.; Int. J. Biol. Macromol.
230, 123216 (2023),
Abstract;
Tankyrase-mediated ADP-ribosylation is a regulator of TNF-induced death: L. Liu, et al.; Sci. Adv.
8, eabh2332 (2022),
Abstract;
Antioxidant and food additive BHA prevents TNF cytotoxicity by acting as a direct RIPK1 inhibitor: T. Delanghe, et al.; Cell Death Dis.
12, 699 (2021),
Abstract;
RIPK1 dephosphorylation and kinase activation by PPP1R3G/PP1γ promote apoptosis and necroptosis: J. Du, et al.; Nat. Commun.
12, 7067 (2021),
Abstract;
Autophosphorylation at serine 166 regulates RIP kinase 1-mediated cell death and inflammation: L. Laurien, et al.; Nat. Commun.
11, 1747 (2020),
Abstract;
Full Text
Tristetraprolin regulates necroptosis during tonic Toll-like receptor 4 (TLR4) signaling in murine macrophages: A. Ariana, et al.; J. Biol. Chem.
295, 4661 (2020),
Abstract;
Full Text
Serine 25 phosphorylation inhibits RIPK1 kinase-dependent cell death in models of infection and inflammation: Y. Dondelinger, et al.; Nat. Commun.
10, 1729 (2019),
Abstract;
Full Text
N-glycosylation of mouse TRAIL-R restrains TRAIL-induced apoptosis: Y. Estornes, et al.; Cell Death Dis.
9, 494 (2018),
Abstract;
Full Text
MK2 phosphorylation of RIPK1 regulates TNF-mediated cell death: Y. Dondelinger, et al.; Nat. Cell Biol.
19, 1237 (2017),
Abstract;
The linear ubiquitin chain assembly complex regulates TRAIL-induced gene activation and cell death: E. Lafont, et al.; EMBO J.
36, 1147 (2017),
Abstract;
Full Text
When PERK inhibitors turn out to be new potent RIPK1 inhibitors: critical issues on the specificity and use of GSK2606414 and GSK2656157: D. Rojas-Rivera, et al.; Cell Death Differ.
24, 1100 (2017),
Abstract;
Full Text
SPATA2 promotes CYLD activity and regulates TNF-induced NF-κB signaling and cell death: L. Schlicher, et al.; EMBO Rep.
17, 1485 (2016),
Abstract;
Full Text
γ-Secretase Activity Is Required for Regulated Intramembrane Proteolysis of Tumor Necrosis Factor (TNF) Receptor 1 and TNF-mediated Pro-apoptotic Signaling: J. Chhibber-Goel, et al.; J. Biol. Chem.
291, 5971 (2016),
Abstract;
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CYLD and the NEMO Zinc Finger Regulate Tumor Necrosis Factor Signaling and Early Embryogenesis: Y. Zhao, et al.; J. Biol. Chem.
90, 22076 (2015),
Application(s): Western Blot,
Abstract;
In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-κB, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-κB is required to prevent it: D.M. Moujalled, et al.; Cell Death Dis.
19, 808 (2012),
Abstract;
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