The progesterone receptor in human term amniochorion and placenta is isoform C.

The mechanism that initiates human parturition has been proposed to be functional progesterone withdrawal whereby the 116-kDa B-isoform of the progesterone receptor (PR-B) switches in favor of the 94-kDa A-isoform (PR-A) in reproductive tissues. Recently other PR isoforms, PR-S, PR-C, and PR-M generated from the same gene have been identified and partially characterized. Using immunohistochemical, Western blotting, and RT-PCR techniques, evidence is provided that the major PR isoform present in human term fetal membranes (amnion and chorion) and syncytiotrophoblast of the placenta is neither of the classical nuclear PR-B or PR-A isoforms but is the N terminally truncated 60-kDa PR-C isoform. Evidence is also provided that the PR-C isoform resides in the cytoplasm of the expressing cell types. Data are also presented to show that PR-B, PR-A, and PR-S isoforms are essentially absent from the amnion and chorion, whereas PR isoforms A, B, C, and S are all present in the decidua, with PR-A being the major isoform. The syncytiotrophoblast of the placenta contains the cytoplasmic PR-C isoform but not PR-A, PR-B, or PR-S. The major PR isoform in the amnion, chorion, and placenta is PR-C, suggesting that the cytoplasmic PR-C isoform has a specific role in extraembryonic tissues and may be involved in the regulation of human parturition

Computational Studies Explain the Importance of Two Different Substituents on the Chelating Bis(amido) Ligand for Transfer Hydrogenation by Bifunctional Cp*Rh(III) Catalysts

A computational approach (DFT-B3PW91) is used to address previous experimental studies (<i>Chem. Commun.</i> <b>2009</b>, 6801) that showed that transfer hydrogenation of a cyclic imine by Et₃N·HCO₂H in dichloromethane catalyzed by 16-electron bifunctional Cp*Rh^III­(XNC₆H₄NX′) is faster when XNC₆H₄NX′ = TsNC₆H₄NH than when XNC₆H₄NX′ = HNC₆H₄NH or TsNC₆H₄NTs (Cp* = η⁵-C₅Me₅, Ts = toluenesulfonyl). The computational study also considers the role of the formate complex observed experimentally at low temperature. Using a model of the experimental complex in which Cp* is replaced by Cp and Ts by benzenesulfonyl (Bs), the calculations for the systems in gas phase reveal that dehydrogenation of formic acid generates CpRh^IIIH­(XNC₆H₄NX′H) via an outer-sphere mechanism. The 16-electron Rh complex + formic acid are shown to be at equilibrium with the formate complex, but the latter lies outside the pathway for dehydrogenation. The calculations reproduce the experimental observation that the transfer hydrogenation reaction is fastest for the nonsymmetrically substituted complex CpRh^III­(XNC₆H₄NX′) (X = Bs and X′ = H). The effect of the linker between the two N atoms on the pathway is also considered. The Gibbs energy barrier for dehydrogenation of formic acid is calculated to be much lower for CpRh^III­(XNCHPhCHPhNX′) than for CpRh^III­(XNC₆H₄NX′) for all combinations of X and X′. The energy barrier for hydrogenation of the imine by the rhodium hydride complex is much higher than the barrier for hydride transfer to the corresponding iminium ion, in agreement with mechanisms proposed for related systems on the basis of experimental data. Interpretation of the results by MO and NBO analyses shows that the most reactive catalyst for dehydrogenation of formic acid contains a localized Rh–NH π-bond that is associated with the shortest Rh–N distance in the corresponding 16-electron complex. The asymmetric complex CpRh^III(BsNC₆H₄NH) is shown to generate a good bifunctional catalyst for transfer hydrogenation because it combines an electrophilic metal center and a nucleophilic NH group

Computational Studies Explain the Importance of Two Different Substituents on the Chelating Bis(amido) Ligand for Transfer Hydrogenation by Bifunctional Cp*Rh(III) Catalysts

A computational approach (DFT-B3PW91) is used to address previous experimental studies (<i>Chem. Commun.</i> <b>2009</b>, 6801) that showed that transfer hydrogenation of a cyclic imine by Et₃N·HCO₂H in dichloromethane catalyzed by 16-electron bifunctional Cp*Rh^III­(XNC₆H₄NX′) is faster when XNC₆H₄NX′ = TsNC₆H₄NH than when XNC₆H₄NX′ = HNC₆H₄NH or TsNC₆H₄NTs (Cp* = η⁵-C₅Me₅, Ts = toluenesulfonyl). The computational study also considers the role of the formate complex observed experimentally at low temperature. Using a model of the experimental complex in which Cp* is replaced by Cp and Ts by benzenesulfonyl (Bs), the calculations for the systems in gas phase reveal that dehydrogenation of formic acid generates CpRh^IIIH­(XNC₆H₄NX′H) via an outer-sphere mechanism. The 16-electron Rh complex + formic acid are shown to be at equilibrium with the formate complex, but the latter lies outside the pathway for dehydrogenation. The calculations reproduce the experimental observation that the transfer hydrogenation reaction is fastest for the nonsymmetrically substituted complex CpRh^III­(XNC₆H₄NX′) (X = Bs and X′ = H). The effect of the linker between the two N atoms on the pathway is also considered. The Gibbs energy barrier for dehydrogenation of formic acid is calculated to be much lower for CpRh^III­(XNCHPhCHPhNX′) than for CpRh^III­(XNC₆H₄NX′) for all combinations of X and X′. The energy barrier for hydrogenation of the imine by the rhodium hydride complex is much higher than the barrier for hydride transfer to the corresponding iminium ion, in agreement with mechanisms proposed for related systems on the basis of experimental data. Interpretation of the results by MO and NBO analyses shows that the most reactive catalyst for dehydrogenation of formic acid contains a localized Rh–NH π-bond that is associated with the shortest Rh–N distance in the corresponding 16-electron complex. The asymmetric complex CpRh^III(BsNC₆H₄NH) is shown to generate a good bifunctional catalyst for transfer hydrogenation because it combines an electrophilic metal center and a nucleophilic NH group