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EDN1 — SLC2A4

Text-mined interactions from Literome

Ishibashi et al., J Clin Invest 2001 : We recently reported that insulin and endothelin-1 (ET-1) can stimulate GLUT4 translocation via the heterotrimeric G protein G alpha q/11 and through PI3-kinase -- mediated pathways in 3T3-L1 adipocytes
Bose et al., Mol Cell Biol 2001 : Remarkably, expression of a dominant inhibitory form of the actin-regulatory GTPase ARF6 [ ARF6 ( T27N ) ] in cultured adipocytes selectively inhibited both F-actin formation and GLUT4 translocation in response to endothelin 1 but not insulin
Lawrence et al., Mol Cell Biol 2001 : However, the same ARF6 inhibitory mutant blocked the stimulation of hexose uptake and GLUT4 translocation in response to either endothelin 1 or an activated form of Galphaq, Galphaq ( Q209L )
Rachdaoui et al., Am J Physiol Endocrinol Metab 2003 : Activation of proline-rich tyrosine kinase 2 (PYK2), a downstream target of Galphaq/11 that is required for endothelin-1 stimulated GLUT4 translocation in 3T3-L1 adipocytes, was also suppressed after chronic ethanol feeding
Rachdaoui et al., Am J Physiol Endocrinol Metab 2003 : Here, we report that exposure of 3T3-L1 adipocytes to TNF-alpha for 48 h dose-dependently decreased endothelin-1 stimulated glucose uptake and translocation of GLUT4 to the plasma membrane ... Taken together, these results suggest that TNF-alpha induced desensitization of endothelin-1 stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes is due, at least in part, to a decreased expression of Galphaq/11, leading to a suppression in tyrosine phosphorylation of PYK2
Strawbridge et al., J Cell Biochem 2006 : Endothelin-1 (ET-1) disrupts insulin regulated glucose transporter GLUT4 trafficking