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ANXA1 — EPHB2

Text-mined interactions from Literome

Harada et al., Nat Cell Biol 2001 : Our results indicate that sustained activation of ERK is necessary and sufficient for strong induction of p35
Chen et al., Cancer Res 2004 : Additionally, Cdk5/p35 phosphorylates MEK1 and inhibits its ability to phosphorylate its downstream target Erk2
Hayhoe et al., Blood 2006 : ANXA1 and Ac2-26 acted as genuine agonists ; Ac2-26 binding led to ERK activation in both FPR- and FPRL-1/ALX transfected cells, while ANXA1 caused ERK activation only in cells transfected with FPRL-1/ALX
Yang et al., J Immunol 2009 : GC-induced GILZ expression and GC inhibition of NF-kappaB activation were restored by expression of ANXA1 in ANXA1 ( -/- ) cells, and GILZ overexpression in ANXA1 ( -/- ) macrophages reduced ERK MAPK phosphorylation and restored sensitivity of cytokine expression and NF-kappaB activation to GC
Reuter et al., PloS one 2012 (Inflammation...) : These differences in epithelial restitution were TGF-ß independent but Dex inhibited the EGF/ERK1/2/MAPK-pathway important for intestinal epithelial wound healing by induction of MKP-1 and Annexin-1 which was not affected by CpdA or ZK216348
Jia et al., J Cell Physiol 2013 (MAP Kinase Signaling System...) : AnxA1 regulation of ERK and NF-?B activation was associated with effects on proliferation
Yang et al., J Immunol 2013 (Arthritis, Experimental...) : Similarly, experiments using AnxA1 ( -/- ) OT-II CD4 ( + ) T cells demonstrated that the absence of AnxA1 in T cells was sufficient to induce increased Ag-specific CD4 ( + ) T cell proliferation in vivo, augment T cell production of IFN-?, IL-17, TNF, and IL-6, and increase Akt, ERK , and p38 activation