Gene interactions and pathways from curated databases and text-mining

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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