MyD88 Antibody

MyD88 Antibody

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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2025年08月14日
  • W
  • Rabbit
  • H,Mk
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    • 详细信息
    • 技术资料
    • 抗体英文名

      MyD88 Antibody

    • 抗原

      synthetic peptide corresponding to residues surrounding lysine 119 of human MyD88

    • 应用范围

      W

    • 宿主

      Rabbit

    • 适应物种

      H,Mk

    • 供应商

      CST

    • 保质期

      详见说明书

    • 库存

      大量

    • 级别

      详见MSDS文件

    • 是否单克隆

      2

    • 保存条件

      -20°c

    • 规格

      100 ul (10 western blots)/carrier free & custom formulation / quantity

    规格:产品价格:¥请询价
    规格:100 ul (10 western blots)产品价格:¥请询价
    规格:carrier free & custom formulation / quantity产品价格:¥请询价

    pathway more info application references datasheet PDF MSDS PDF protocols

    Applications Key:  W=Western Blotting
    Reactivity Key:  H=Human  Mk=Monkey
    Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

    Applications Reactivity Sensitivity MW (kDa) Source
    W H Mk Endogenous 33 Rabbit
    Protocols
    Specificity / Sensitivity

    MyD88 Antibody detects endogenous levels of total MyD88 protein.

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding lysine 119 of human MyD88. Antibodies were purified by protein A and peptide affinity chromatography.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from HeLa cells, either mock transfected or transfected with MyD88, using MyD88 Antibody.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from Jurkat, K562 and Raji cells, using MyD88 Antibody.

    Background

    Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila , play a pivotal role in innate immune responses (1-3). TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon), and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity by sequestering it in the cytoplasm.

    MyD88 was originally isolated as a myeloid differentiation primary response gene that is rapidly induced upon IL-6 stimulated differentiation of M1 myeloleukemic cells into macrophages (4-6). It contains an amino-terminal death domain separated from a carboxyl-terminal TIR domain and functions as an adaptor in TLR/IL-1 receptor signaling (7). The death domain of MyD88 mediates interactions with the IRAK complex triggering a signaling cascade that includes the activation of NF-κB (8,9).

    1. Akira, S. (2003) J Biol Chem 278, 38105-8.
    2. Beutler, B. (2004) Nature 430, 257-63.
    3. Dunne, A. and O'Neill, L.A. (2003) Sci STKE 2003, re3.
    4. Harroch, S. et al. (1995) Nucleic Acids Res. 23, 3539-46.
    5. Hardiman, G. et al. (1996) Oncogene 13, 2467-75.
    6. Bonnert, T.P. et al. (1997) FEBS Lett. 402, 81-4.
    7. Medzhitov, R. et al. (1998) Mol. Cell 2, 253-8.
    8. Wesche, H. et al. (1997) Immunity 7, 837-47.
    9. Muzio, M. et al. (1997) Science 278, 1612-1615.
    Application References

    Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know !

    Companion Products

    For Research Use Only. Not For Use In Diagnostic Procedures.

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