| First Author | Bodmann EL | Year | 2017 |
| Journal | FASEB J | Volume | 31 |
| Issue | 8 | Pages | 3663-3676 |
| PubMed ID | 28465324 | Mgi Jnum | J:247642 |
| Mgi Id | MGI:5926964 | Doi | 10.1096/fj.201700026R |
| Citation | Bodmann EL, et al. (2017) Potentiation of receptor responses induced by prolonged binding of Galpha13 and leukemia-associated RhoGEF. FASEB J 31(8):3663-3676 |
| abstractText | Diverse cellular functions are controlled by RhoA-GTPases, which are activated by trimeric G proteins via RhoGEFs, among others. In this study, we focused on the signaling from GPCRs to RhoA via Galpha13 and leukemia-associated RhoGEF (LARG). The activation of Galpha13 was elucidated in living cells with high temporal and spatial resolution by means of FRET. The inactivation after agonist withdrawal occurred in the same range (t1/2 = 25.3 +/- 2.2 s; mean +/- sem; n = 22) as described for other Galpha proteins. The interaction of Galpha13 and LARG and the thereby-induced LARG translocation to the plasma membrane were at least 1 order of magnitude more stable after agonist withdrawal, exceeding Galpha13 deactivation in the absence of LARG several fold. Consequently, we observed an almost 100-fold higher agonist sensitivity of the Galpha13 LARG interaction compared to the Galpha13 activation in the absence of LARG.-Bodmann, E.-L., Krett, A.-L., Bunemann, M. Potentiation of receptor responses induced by prolonged binding of Galpha13 and leukemia-associated RhoGEF. |
