Title : Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the α2A adrenergic receptor.

Pub. Date : 2012 Mar 30

PMID : 22405824






5 Functional Relationships(s)
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1 Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the alpha2A adrenergic receptor. Desipramine mitogen-activated protein kinase 3 Homo sapiens
2 DMI acted as a signaling potentiator, selectively enhancing NE-induced alpha(2A)AR-mediated ERK1/2 MAPK signaling. Desipramine mitogen-activated protein kinase 3 Homo sapiens
3 DMI acted as a signaling potentiator, selectively enhancing NE-induced alpha(2A)AR-mediated ERK1/2 MAPK signaling. Desipramine mitogen-activated protein kinase 3 Homo sapiens
4 DMI in a physiologically relevant ratio with NE effectively turned on ERK1/2 signaling that is lacking in response to physiological NE alone. Desipramine mitogen-activated protein kinase 3 Homo sapiens
5 Further, the DMI-induced ERK1/2 potentiation relied on heterotrimeric G(i/o) proteins and was arrestin-independent. Desipramine mitogen-activated protein kinase 3 Homo sapiens