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19?��?0.03 in control to 1.39?��?0.02?mM in PTGCaSR(+/�C) mice [��?=?0.20?mM; p? We also observed a left-shift of the Ca2+ set point in the PTGs from PTGCaSR(+/�C) at 12 versus 3 months of age (Fig. 2B, C), as seen in the control mice, indicating that an age-dependent adaptive response of PTGs to chronic HPT also occurred in these mice. Similarly, increased CaSR expression is likely the underlying mechanism enhancing the sensitivity to extracellular Ca2+ in the glands from aging PTGCaSR(+/�C) mice, and this was demonstrated by Western blotting (Supporting Fig. S2B, S2C). However, the limited ability of 12-month-old PTGCaSR(+/�C) PTGs to increase CaSR expression (due to deletion of one Casr allele) prevented the restoration of Ca2+ set points into the normal range, especially in the females. This inadequate compensation by the PTGs may underlie the more profound HPT of the female PTGCaSR(+/�C) mice. Heterozygous KO of the CaSR in PTGs also impacted the PTHR-max and PTHR-min in a sex- and age-dependent manner (Fig. 2A, C). At 3 months of age, PTHR-max significantly increased by ?60% from 309?��?28?pg/30?min/gland in male control PTGs to 498?��?110?pg/30?min/gland in male PTGCaSR(+/�C) mice (p?90% assessed in PTGCaSR(+/�C) mice of both sexes (male: 1197?��?320?pg/30?min/gland; female: 1282?��?279?pg/30?min/gland) compared to control mice (male: 588?��?158?pg/30?min/gland; female: 733?��?181?pg/30?min/gland) (p?