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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
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug
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N humans, RXFP1 receptors are localized to the nipple, epithelial cells (Kohsaka et al., 1998), and stromal tissue (Ivell et al., 2003). Although relaxin has many well defined roles in reproduction in many species, in humans these effects are often absent or ill defined. Relaxin is produced in the human ovary during the luteal phase of the menstrual cycle and secreted into the circulation (Eddie e
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug
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Ls (Bathgate et al., 2006c), and these effects are impaired in both relaxin-deficient rats (Burger and Sherwood, 1998) and relaxin knockout mice (Zhao et al., 1999; Bathgate et al., 2006c). In humans, although relaxin levels increase during cervical ripening, this still occurs after embryo transfer where circulating relaxin levels are undetectable (Eddie et al., 1990a). In clinical trials, althoug