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EIF2AK2 — NFKBIA
Pathways - manually collected, often from reviews:
-
KEGG Hepatitis C:
EIF2AK1/EIF2AK2/EIF2AK3/EIF2AK4
→
NFKBIA
(protein-protein, activation)
-
KEGG Influenza A:
EIF2AK1/EIF2AK2/EIF2AK3/EIF2AK4
→
NFKBIA/NFKBIB
(protein-protein, activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Hprd Interaction:
EIF2AK2
—
NFKBIA
(in vitro)
Gil et al., Oncogene 2000, Chen et al., Cell 1996, Schouten et al., EMBO J 1997*, Zandi et al., Science 1998
-
IRef Hprd Interaction:
EIF2AK2
—
NFKBIA
(in vivo)
Gil et al., Oncogene 2000, Chen et al., Cell 1996, Schouten et al., EMBO J 1997*, Zandi et al., Science 1998
Text-mined interactions from Literome
Ishii et al., Oncogene 2001
(Cell Transformation, Neoplastic) :
These data strongly support an indirect
role of
PKR in
I kappa B alpha phosphorylation by modulating IKK activity through pathways that do not utilize the enzymatic and dsRNA binding properties of PKR
Morimoto et al., Mol Cell Biochem 2005
(Osteosarcoma) :
Our results suggest that okadaic acid induced tyrosine phosphorylation of
IkappaBalpha was
mediated by
PKR kinase activity, thus indicating the involvement of this kinase in the control mechanism governing the activation of NF-kappaB