Antibody data
- Antibody Data
- Antigen structure
- References [5]
- Comments [0]
- Validations [0]
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- Product number
- ABIN401364 - Provider product page
- Provider
- antibodies-online
- Product name
- anti-Myeloid Differentiation Primary Response Gene (88) (MYD88) antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide corresponding to a region near the carboxy terminus of human MyD88protein
- Reactivity
- Human, Mouse
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 0.1 mg
- Concentration
- 0.5 mg/ml (by UV absorbance at 280 nm)
- Storage
- Store the antibody at -20°C. Avoid repeated freezing and thawing. Shelf life: one year from despatch.
Submitted references Unresponsiveness of MyD88-deficient mice to endotoxin.
Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.
MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways.
IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling.
The cloning and characterization of human MyD88: a member of an IL-1 receptor related family.
Kawai T, Adachi O, Ogawa T, Takeda K, Akira S
Immunity 1999 Jul;11(1):115-22
Immunity 1999 Jul;11(1):115-22
Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.
Adachi O, Kawai T, Takeda K, Matsumoto M, Tsutsui H, Sakagami M, Nakanishi K, Akira S
Immunity 1998 Jul;9(1):143-50
Immunity 1998 Jul;9(1):143-50
MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways.
Medzhitov R, Preston-Hurlburt P, Kopp E, Stadlen A, Chen C, Ghosh S, Janeway CA Jr
Molecular cell 1998 Aug;2(2):253-8
Molecular cell 1998 Aug;2(2):253-8
IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling.
Muzio M, Ni J, Feng P, Dixit VM
Science (New York, N.Y.) 1997 Nov 28;278(5343):1612-5
Science (New York, N.Y.) 1997 Nov 28;278(5343):1612-5
The cloning and characterization of human MyD88: a member of an IL-1 receptor related family.
Bonnert TP, Garka KE, Parnet P, Sonoda G, Testa JR, Sims JE
FEBS letters 1997 Jan 27;402(1):81-4
FEBS letters 1997 Jan 27;402(1):81-4
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