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Of RXFP1 in the SFO and OVLT that are activated by relaxin to cause a reduction in plasma osmolality (Sunn et al., 2002). This effect in ratsis associated with increased serum relaxin levels during the second half of pregnancy (Sherwood et al., 1980; Lindheimer et al., 1989) and is absent in pregnant rats that have undergone ovariectomy or treatment with relaxin antibodies (Novak et al., 2001). Si
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Of RXFP1 in the SFO and OVLT that are activated by relaxin to cause a reduction in plasma osmolality (Sunn et al., 2002). This effect in ratsis associated with increased serum relaxin levels during the second half of pregnancy (Sherwood et al., 1980; Lindheimer et al., 1989) and is absent in pregnant rats that have undergone ovariectomy or treatment with relaxin antibodies (Novak et al., 2001). Si
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Rences may relate to different colocalization of receptors and G proteins in particular cell types. More recent studies used BRET to investigate ligand-induced interactions between RXFP3-RLuc8 and G proteins (Gg2-Venus) in live cells. Similar to previous studies, treatment of CHO-RXFP3-RLuc8 cells with human relaxin-3 caused activation of Gai2, GaoA, and GaoB, but also revealed an interaction betw
1
Rences may relate to different colocalization of receptors and G proteins in particular cell types. More recent studies used BRET to investigate ligand-induced interactions between RXFP3-RLuc8 and G proteins (Gg2-Venus) in live cells. Similar to previous studies, treatment of CHO-RXFP3-RLuc8 cells with human relaxin-3 caused activation of Gai2, GaoA, and GaoB, but also revealed an interaction betw
1
Rences may relate to different colocalization of receptors and G proteins in particular cell types. More recent studies used BRET to investigate ligand-induced interactions between RXFP3-RLuc8 and G proteins (Gg2-Venus) in live cells. Similar to previous studies, treatment of CHO-RXFP3-RLuc8 cells with human relaxin-3 caused activation of Gai2, GaoA, and GaoB, but also revealed an interaction betw
1
Pressing dominant negative (V53D) versus wild-type (WT) b-arrestin-1. There was no inhibitory effect of the dominant negative b-arrestin-1 on ERK1/2 activation, suggesting that, unlike several other GPCRs (Cottrell et al., 2009; Luttrell and Gesty-Palmer, 2010), the RXFP3/b-arrestin-1 interaction contributes little to ERK1/2 signaling (Kocan et al., 2014). Previous studies demonstrated internaliza
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Pressing dominant negative (V53D) versus wild-type (WT) b-arrestin-1. There was no inhibitory effect of the dominant negative b-arrestin-1 on ERK1/2 activation, suggesting that, unlike several other GPCRs (Cottrell et al., 2009; Luttrell and Gesty-Palmer, 2010), the RXFP3/b-arrestin-1 interaction contributes little to ERK1/2 signaling (Kocan et al., 2014). Previous studies demonstrated internaliza
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S of relaxin family peptides and their receptors have been extensively reviewed (Ivell and Anand-Ivell, 2009; Smith et al., 2011; Bathgate et al., 2013a). In particular, the role of relaxin in female and male reproductive physiology have been well studied (Sherwood, 1994, 2004; Bathgate et al., 2013a, 2006c). For this reason, only brief overviews will be given here. A. Relaxin and Relaxin Family P