Defective MyD88 does not bind MAL(TIRAP):TLR2/4

Stable Identifier
Reaction [transition]
Homo sapiens
Related Species
Chlamydia trachomatis, Neisseria meningitidis serogroup B
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The sorting MyD88 adaprtor-like (MAL or TIRAP) normally recruits MyD88 to activated TLR2 and TLR4 receptor complexes (Horng T et al. 2002; Verstak B et al. 2009). MyD88 interacts with MAL (TIRAP) via their TIR domains and activates a downstream signaling pathway mediated by TLR2 and TLR4 (Ohnishi H et al. 2009). A GST pull-down assay showed that defective MyD88 R196C variant loses its ability to bind to MAL (Yamamoto T et al. 2014).

Literature References
PubMed ID Title Journal Year
24316379 Functional assessment of the mutational effects of human IRAK4 and MyD88 genes

Kondo, N, Shirakawa, M, Ohnishi, H, Tochio, H, Kato, Z, Tsutsumi, N, Kubota, K, Yamamoto, T

Mol. Immunol. 2014
19506249 Structural basis for the multiple interactions of the MyD88 TIR domain in TLR4 signaling

Kondo, N, Shirakawa, M, Hiroaki, H, Ohnishi, H, Tochio, H, Kato, Z, Orii, KE, Kimura, T, Li, A

Proc. Natl. Acad. Sci. U.S.A. 2009
Normal reaction
Functional status

Loss of function of MyD88 R196C [cytosol]

Name Identifier Synonyms
primary immunodeficiency disease DOID:612 immune deficiency disorder, immunodeficiency syndrome, hypoimmunity
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