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AKT1 — MYD88
Text-mined interactions from Literome
Santos-Sierra et al., EMBO J 2009
:
MyD88 is not
essential for PI3K activation and
Akt phosphorylation ; however, cooperates with Mal for PIP ( 3 ) formation and accumulation at the leading edge ... In contrast to TLR2/6, TLR2/1 does not
require Mal or
MyD88 for
Akt phosphorylation
Bauerfeld et al., J Immunol 2012
:
TLR4 mediated
AKT activation is
MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages
Chun et al., Int Immunopharmacol 2012
:
A further study indicated that alantolactone attenuated the phosphorylation of
Akt and
inhibited the expression of
MyD88 and Toll-interleukin 1 receptor domain containing adaptor protein ( TIRAP ), an upstream signaling molecule required for IKK and MAPKs activation
Liang et al., Clin Cancer Res 2013
:
Finally, silencing of
MyD88 inhibited the activation of NF-?B and
AKT in HCC cells, whereas forced expression of MyD88 was able to enhance the activation of NF-?B and p38/extracellular signal regulated kinase without Toll-like receptor/interleukin-1 receptor ( TLR/IL-1R ) signaling