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IRF5 — MYD88

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: MYD88 → IRF5 (increases, MYD88 Activity)
  Evidence: TABLE V Selected genes up-regulated by IRF-5
• OpenBEL Selventa BEL large corpus: IRF5 → MYD88 (increases, MYD88 Activity) Schoenemeyer et al., J Biol Chem 2005*
  Evidence: We also demonstrate that MyD88, interleukin 1 receptor-associated kinase 1, and tumor necrosis factor receptor-associated factor 6 are required for the activation of IRF5 and IRF7 in the TLR7 signaling pathway.
• OpenBEL Selventa BEL large corpus: IRF5 → MYD88 (directlyIncreases, MYD88 Activity, IRF5 Activity) Takaoka et al., Nature 2005*
  Evidence: We also provide evidence that IRF-5 interacts with and is activated by MyD88 and TRAF6

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: IRF5 — MYD88 (physical association, affinity chromatography technology) Takaoka et al., Nature 2005*
• IRef Biogrid Interaction: IRF5 — MYD88 (direct interaction, fluorescent resonance energy transfer) Takaoka et al., Nature 2005*
• IRef Hprd Interaction: MYD88 — IRF5 (in vivo) Takaoka et al., Nature 2005*

Text-mined interactions from Literome

Takaoka et al., Nature 2005 (Inflammation...) : We also provide evidence that IRF-5 interacts with and is activated by MyD88 and TRAF6, and that TLR activation results in the nuclear translocation of IRF-5 to activate cytokine gene transcription
Schoenemeyer et al., J Biol Chem 2005 : We also demonstrate that MyD88 , interleukin 1 receptor associated kinase 1, and tumor necrosis factor receptor associated factor 6 are required for the activation of IRF5 and IRF7 in the TLR7 signaling pathway
Paun et al., J Biol Chem 2008 (Newcastle Disease) : The murine IRF-5 can be activated by both TBK1 and MyD88 to form homodimers and bind to and activate transcription of type I interferon and inflammatory cytokine genes