Anti-MyD88 Monoclonal Antibody for WB, ELISA - Q99836

Core Product Specifications and Parameters

Biological Background: MyD88 Function and Localization

• MyD88 is a pivotal adaptor in Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling, promoting NF-kappa-B activation and pro-inflammatory cytokine production through interactions with IRAK1, IRAK2, TRAF6, and IRF7.
  Related references: PMID:15361868, PMID:18292575, PMID:33718825, PMID:19506249, PMID:24316379

• MyD88 activates IRF1, inducing its rapid nuclear translocation to drive IFN-beta, NOS2, and IL12A gene expression, bridging innate and adaptive immunity.

• It mediates IL-18 signaling and enhances IL-8 transcription, contributing to inflammatory responses.
  Related references: PMID:9013863

• During viral infection, MyD88 responds to GU-rich single-stranded RNA via TLR8 and triggers NLRP3 inflammasome-dependent IL-1β secretion, highlighting its role in antiviral defense.
  Related references: PMID:33718825

• Subcellular localization is primarily cytoplasmic, with nuclear translocation observed under certain signaling conditions.

• Post-translational modifications, including phosphorylation and ubiquitination, regulate MyD88 signaling dynamics and protein interactions.

• Ubiquitously expressed, MyD88 maintains gut homeostasis by controlling antimicrobial REG3G lectin expression in intestinal epithelial cells (By similarity).

Experimental Guidance and Technical Tips

• The immunogen corresponds to an N-terminal peptide (aa 50–150) of human MyD88, a region with high conservation; verify cross-reactivity with mouse and rat by sequence alignment.
• For Western blot (WB), detect a band at approximately 33 kDa; due to ubiquitous expression, normalize loading and consider tissue-specific or treatment-dependent changes.
• When performing ELISA, titrate antibody concentrations and include appropriate controls to minimize background; validate in your specific matrix to ensure assay reproducibility.
• MyD88 is a signaling molecule; stimulation of TLR/IL-1R pathways may influence abundance or modification, so standardize cell treatment conditions in your experiments.

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