Myeloid differentiation primary response protein 88 (MyD88)

Myeloid differentiation primary response protein 88 (MyD88) is a central intracellular adaptor involved in signaling by most Toll-like receptors (TLRs) and the interleukin-1 receptor (IL-1R) family[3][5]. Upon ligand binding to these receptors, MyD88 bridges receptor TIR domains to IL-1R-associated kinase (IRAK) kinases through homotypic protein interactions, activating downstream signaling pathways such as NF-κB, MAPKs, and AP-1, thereby inducing expression of pro-inflammatory cytokines and participating in adaptive immune activation[1][3][5]. MyD88-dependent signaling is crucial for normal innate immune responses, inflammasome activation, dendritic cell maturation, and T-helper cell differentiation. Dysregulated MyD88 signaling or gain-of-function mutations are implicated in autoimmune inflammation, cancer (e.g., lymphomas with the MYD88 L265P mutation), and host defense deficiencies[4][5]. Due to its pivotal role in inflammation, MyD88 is considered a promising therapeutic target for inflammation, infection, and cancer, though clinical development of specific inhibitors is still investigational and associated with immunosuppression risk[4][6]. Note: - The original input "Myeloid differentiation primary response protein MyD88-dependent signaling pathway" is not itself a molecular target but a signaling pathway; the actual therapeutic target is the adaptor protein Myeloid differentiation primary response protein 88 (MyD88)[3][5][6]. - For structured data and canonicalization, the entry should map to the protein (MyD88), not the pathway. - Marked "is_incorrect: true" due to incorrect input target form.

Other names

Myeloid differentiation factor 88MYD88Myeloid differentiation response gene 88

Inhibition of MyD88 dimerization or signaling disrupts TLR/IL-1R-mediated pro-inflammatory cytokine production