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EPHB2 — UBC

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: UBC — EPHB2 (physical association, affinity chromatography technology) Lee et al., J Biol Chem 2011
• IRef Biogrid Interaction: UBC — EPHB2 (physical association, affinity chromatography technology) Povlsen et al., Nat Cell Biol 2012
• IRef Biogrid Interaction: UBC — EPHB2 (physical association, affinity chromatography technology) Litterst et al., J Biol Chem 2007*
• IRef Biogrid Interaction: UBC — EPHB2 (physical association, affinity chromatography technology) Danielsen et al., Mol Cell Proteomics 2011

Text-mined interactions from Literome

Woo et al., Circ Res 2008 (Diabetes Mellitus...) : ERK5 transcriptional activity, but not kinase activity, was inhibited by expression of Ubc9 ( SUMO E2 conjugase ) or PIAS1 ( E3 ligase ), suggesting the involvement of ERK5 SUMOylation on its transcriptional activity
Shishido et al., Circ Res 2008 (Diabetes Mellitus, Experimental...) : In the current study, we investigated the role of ERK5-SUMOylation in ERK5 transcriptional activity as well as on DM-mediated exacerbation of LV dysfunction and apoptosis after MI. ERK5 wild-type transcriptional activity was inhibited by Ubc9 ( SUMO E2 conjugase ) or PIAS1 ( E3 ligase ), but not in the ERK5-SUMOylation-site defective mutant ( K6R/K22R ) ... H2O2 and high glucose, 2 well-known mediators of diabetes, induced ERK5-SUMOylation , and the K6R/K22R mutant, dominant negative form of Ubc9 , and siRNA-PIAS1 reversed H2O2 mediated reduction of ERK5 transcriptional activity in cardiomyocytes, indicating the presence of SUMOylation dependent ERK5 transcriptional repression