protein
| associating with IL1R1, IL1R2, IL1RAP, IL18R1, IL18RAP, IRAK1, IRAK2 |
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binding LBP, Toll-like receptors (TLR2, TLR4, TIRAP) |
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IL1, IL18 |
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interaction with PTK2B, increased in macrophages, stimulated by LPS,and requiring the death domain of MYD88 |
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interacting with FREM1 (potentiates MYD88 recruitment to control Ras-dependent amplification of NF-kappaB) |
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interaction with PRKD1 (PRKD1 is essential for MYD88-dependent proinflammatory immune responses) |
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interacting with LRRFIP2 and LRRFIP1, and both are positive regulators of NF-kappaB activity |
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triggers immunoglobulin class switching by activating B cells through the adaptor MYD88 |
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TLR4 requires myeloid differentiation (LY96), and both TLR2 and TLR4 signal need myeloid differentiation factor (MYD88) |
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LRRFIP2 binds to MYD88 through its serine-rich domain (phosphorylation at serine 202 was found to regulate the dynamics of the LRRFIP2-MYD88 interaction, which in turn modulated the strength and duration of TLR4 signaling) |
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DEFB103B affects the activity of pro-inflammatory pathways associated with MYD88 and TICAM1 |
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CD180 stimulation induces intrinsic B cell proliferation and differentiation, causing rapid increases in IgG, and integrates MyD88-dependent TLR signals to regulate proliferation, cytokine production, and differentiation |
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TBC1D23 likely acts downstream of the TLR-signaling adaptors MYD88 and TICAM2 and upstream of the transcription factor XBP1 |
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DOCK8 functions as an adaptor in a TLR9-MYD88 signaling pathway in B cells |
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TICAM2 serves as the sorting adaptor for MYD88 in IL18 signaling, which then facilitates the signal transduction |
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CYTH2 binds directly to the adaptor protein MYD88, and likely MYD88-CYTH2-ARF6 is a proximal IL1B signalling pathway distinct from that mediated by NFKB1 |
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IL10 activates TLR4 and requires MYD88 for cardiomyocyte survival |
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adaptor, linking TLR and IL1R1 to downstream signaling pathways in the innate immune system |
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MYD88-dependent IL23R expression contributes to IL17A production |
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MYD88 plays a critical role in integrating IL1A and IL23A signaling for Th17 cell proliferation and expansion |
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TIRAP and MYD88 are adaptor proteins for Toll-like receptors-2 and -4 (TLR2/4) which are engaged in transducing the signal to downstream molecules |
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ATG5, a key regulatory protein of autophagy, inhibits the formation of MYD88 condensed structures |
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mRNA splicing regulator EFTUD2, controls the alternate splicing of the MYD88 innate immunity signaling adaptor to modulate the extent of the innate immune response |
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PPP1CC is a positive regulator of MYD88-dependent proinflammatory innate immune activation |
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IRAK4 is recruited to the membrane-proximal adaptor MYD88 through death domain (DD) interactions, forming the oligomeric Myddosome and mediating NFKB1 activation |
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TICAM2 is required for the TLR2-dependent movement of MYD88 to endosomes following ligand engagement |
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TIRAP plays the crucial role of activating the MYD88-dependent pathway, which in turn controls the immune response (innate and adaptive) to Helicobacter pylori |
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METTL3 positively regulates expression of MYD88, a critical upstream regulator of NFKB1 signaling, by facilitating m6A methylation modification to MYD88-RNA |