PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28713912-7 2017 Moreover, the knockdown of mPRalpha expression impaired the inhibitory effects of progesterone on mPRalpha+ tumor growth and metastasis in vivo. Progesterone 82-94 S100 calcium binding protein A6 (calcyclin) Mus musculus 27-35 31416049-0 2019 Role of mPRalpha (PAQR7) in progesterone-induced Ca2+ decrease in human vascular smooth muscle cells. Progesterone 28-40 S100 calcium binding protein A6 (calcyclin) Mus musculus 8-16 31416049-10 2019 The results suggest that progesterone induces VSMC relaxation by reducing cellular calcium levels through mPRalpha-induced alterations in multiple signaling pathways. Progesterone 25-37 S100 calcium binding protein A6 (calcyclin) Mus musculus 106-114 29428395-0 2018 Progesterone induces relaxation of human umbilical cord vascular smooth muscle cells through mPRalpha (PAQR7). Progesterone 0-12 S100 calcium binding protein A6 (calcyclin) Mus musculus 93-101 29869822-1 2018 The membrane progesterone receptors (mPRalpha, mPRbeta, mPRgamma, mPRdelta and mPRepsilon) are known to mediate rapid nongenomic progesterone functions in different cell types. Progesterone 13-25 S100 calcium binding protein A6 (calcyclin) Mus musculus 37-45 29869822-15 2018 Taken together, these data provide new evidence suggesting that mPRalpha mediates the progesterone inhibitory effect on PRL secretion through both decreases in cAMP levels and activation of TGFbeta1 in the lactotroph population. Progesterone 86-98 S100 calcium binding protein A6 (calcyclin) Mus musculus 64-72 28713912-7 2017 Moreover, the knockdown of mPRalpha expression impaired the inhibitory effects of progesterone on mPRalpha+ tumor growth and metastasis in vivo. Progesterone 82-94 S100 calcium binding protein A6 (calcyclin) Mus musculus 98-106 26804062-1 2016 The steroid hormone progesterone (P), acting via the progesterone receptor (PR) isoforms, PR-A and PR-B, exerts a profound influence on uterine functions during early gestation. Progesterone 20-32 S100 calcium binding protein A6 (calcyclin) Mus musculus 90-94 23467643-5 2013 In additional experiments, we found that mPRalpha functioned as an essential mediator for progesterone (P4)-induced inhibitory effects on cell migration and invasion of A549 cells. Progesterone 90-102 S100 calcium binding protein A6 (calcyclin) Mus musculus 41-49 26275946-10 2015 Finally, by in silico analysis, we identified that mPRalpha, mPRbeta and mPRgamma promoters contain several progesterone and estrogen response elements. Progesterone 108-120 S100 calcium binding protein A6 (calcyclin) Mus musculus 51-59 25639501-10 2015 CONCLUSIONS: This research shows that Treg cells express mPRalpha during pregnancy, which might play an important role in immune modulation by progesterone. Progesterone 143-155 S100 calcium binding protein A6 (calcyclin) Mus musculus 57-65 26075237-6 2015 Our in vitro study demonstrated that mPRalpha was expressed and functioned as an essential mediator for progesterone induced inhibitory effects on cell migration and invasion in BPBC cells. Progesterone 104-116 S100 calcium binding protein A6 (calcyclin) Mus musculus 37-45 24424068-2 2014 Here we show that stable overexpression of human PGRMC1 in nuclear progesterone receptor (PR)-negative breast cancer cell lines causes increased expression of PGRMC1 and membrane progesterone receptor alpha (mPRalpha) on cell membranes that is associated with increased specific [(3)H]progesterone binding. Progesterone 67-79 S100 calcium binding protein A6 (calcyclin) Mus musculus 208-216 23211561-13 2013 The induction of mPRalpha after TBI in microglia, astrocytes and oligodendrocytes, points to a potential role in mediating the modulatory effects of progesterone in inflammation, ion and water homeostasis and myelin repair in the injured brain. Progesterone 149-161 S100 calcium binding protein A6 (calcyclin) Mus musculus 17-25 14667967-4 2003 More recently, selective ablation of the PR-A and PR-B proteins in mice had facilitated examination of the contribution of the individual PR isoforms to the pleiotropic reproductive activities of progesterone. Progesterone 196-208 S100 calcium binding protein A6 (calcyclin) Mus musculus 41-45 17317767-1 2007 In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. Progesterone 55-67 S100 calcium binding protein A6 (calcyclin) Mus musculus 117-120 16873445-9 2006 Transcription studies in +/+ and -/- mouse embryonic fibroblast cells showed a near-complete loss of PR-A activity at mouse mammary tumor virus and synthetic progesterone response element promoters, although partial reductions of ER and PR-B were also observed. Progesterone 158-170 S100 calcium binding protein A6 (calcyclin) Mus musculus 101-105 17003284-6 2006 Exposure of E(2)-treated pituitary cells to 200 nM progesterone for 6 h decreased both PR-A and PR-B levels in rat cells, but had no effect on PR isoform expression in mouse cells even when exposure was extended to 12 h. The low level of PR expression found in LbetaT2 gonadotropes was unaffected by E(2), alone or with progesterone. Progesterone 51-63 S100 calcium binding protein A6 (calcyclin) Mus musculus 87-91 16484336-7 2006 Finally, we also demonstrate that antiprogestin, RU38486, was an effective inhibitor of PR-A-mediated, progesterone-dependent, but not SKF or 8-bromo-cAMP-dependent sexual receptivity. Progesterone 103-115 S100 calcium binding protein A6 (calcyclin) Mus musculus 88-92 15280552-5 2004 Analysis of the reproductive phenotypes of these mice has indicated that PR-A and PR-B mediate mostly distinct but partially overlapping reproductive responses to progesterone. Progesterone 163-175 S100 calcium binding protein A6 (calcyclin) Mus musculus 73-77 15280552-6 2004 While selective ablation of the PR-A protein (PR-A knockout mice, PRAKO mice) shows normal mammary gland response to progesterone but severe uterine hyperplasia and ovarian abnormalities, ablation of PR-B protein (PRBKO mice) does not affect biological responses of the ovary or uterus to progesterone but results in reduced pregnancy-associated mammary gland morphogenesis. Progesterone 117-129 S100 calcium binding protein A6 (calcyclin) Mus musculus 32-36 15280552-6 2004 While selective ablation of the PR-A protein (PR-A knockout mice, PRAKO mice) shows normal mammary gland response to progesterone but severe uterine hyperplasia and ovarian abnormalities, ablation of PR-B protein (PRBKO mice) does not affect biological responses of the ovary or uterus to progesterone but results in reduced pregnancy-associated mammary gland morphogenesis. Progesterone 289-301 S100 calcium binding protein A6 (calcyclin) Mus musculus 32-36 21472196-6 2010 Stimulation of M11 cells with progesterone (P4, 100 nM) resulted in internalisation of mPRalpha from the plasma membrane to the cytoplasm (10 min) and subsequent partial translocation back to the cell surface (20 min). Progesterone 30-42 S100 calcium binding protein A6 (calcyclin) Mus musculus 87-95 19432978-11 2009 RESULTS: Only progesterone, 20alpha-hydroxyprogesterone and 17alpha-hydroxyprogesterone were able to displace binding of 3H-P4 (P < 0.001) to membrane fractions from CHO cells expressing ovine mPR-alpha. Progesterone 14-26 S100 calcium binding protein A6 (calcyclin) Mus musculus 196-205 19432978-14 2009 CONCLUSION: The mPR-alpha specifically binds progestins and its expression was correlated to progesterone secretion during the ovine estrous cycle. Progesterone 93-105 S100 calcium binding protein A6 (calcyclin) Mus musculus 16-25 18722485-3 2008 We first focused our investigations on mPRalpha and gamma by analyzing three parameters 1/ their distribution along the mouse nephron and their subcellular location in native kidney, 2/ the ability of progesterone to stimulate ERK pathway and/or Ca(2+) release from internal stores in native kidney structures and 3/ the cellular localization of mPRalpha and its molecular determinants in heterologous expression system. Progesterone 201-213 S100 calcium binding protein A6 (calcyclin) Mus musculus 39-47 18722485-3 2008 We first focused our investigations on mPRalpha and gamma by analyzing three parameters 1/ their distribution along the mouse nephron and their subcellular location in native kidney, 2/ the ability of progesterone to stimulate ERK pathway and/or Ca(2+) release from internal stores in native kidney structures and 3/ the cellular localization of mPRalpha and its molecular determinants in heterologous expression system. Progesterone 201-213 S100 calcium binding protein A6 (calcyclin) Mus musculus 346-354 18543434-7 2007 Finally, two distinct isoforms of PRs (PR-A and PR-B) are coexpressed in the mammary gland and display extensively overlapping but partially distinct gene regulatory properties in relaying the progesterone signal. Progesterone 193-205 S100 calcium binding protein A6 (calcyclin) Mus musculus 39-43 14667967-5 2003 Analysis of the phenotypic consequences of these mutations on female reproductive function has provided proof of concept that the distinct transcriptional responses to PR-A and PR-B observed in cell-based transactivation assays are reflected in a distinct tissue-selective contribution of the individual isoforms to the reproductive activities of progesterone. Progesterone 347-359 S100 calcium binding protein A6 (calcyclin) Mus musculus 168-172 10976068-1 2000 Progesterone regulates reproductive function through two intracellular receptors, progesterone receptor-A (PR-A) and progesterone receptor-B (PR-B), that arise from a single gene and function as transcriptional regulators of progesterone-responsive genes. Progesterone 82-94 S100 calcium binding protein A6 (calcyclin) Mus musculus 107-111 12017551-2 2002 Physiological effects of progesterone are mediated by interaction of the hormone with specific intracellular progesterone receptors (PRs) that are expressed as two protein isoforms, PR-A and PR-B. Progesterone 25-37 S100 calcium binding protein A6 (calcyclin) Mus musculus 182-186 12017551-6 2002 First, analysis of the structural and functional relationships of each isoform using in vitro systems has generated compelling evidence to support the conclusion that PR-A and PR-B have different transcription activation properties when liganded to progesterone. Progesterone 249-261 S100 calcium binding protein A6 (calcyclin) Mus musculus 167-171 12017551-8 2002 Selective ablation of PR-A and PR-B proteins in mice using these technologies has allowed us to address the spatiotemporal expression and contribution of the individual PR isoforms to the pleiotropic reproductive activities of progesterone. Progesterone 227-239 S100 calcium binding protein A6 (calcyclin) Mus musculus 22-26 12017551-9 2002 Analysis of the phenotypic consequences of these mutations on female reproductive function has provided proof of concept that the distinct transcriptional responses to PR-A and PR-B observed in cell-based transactivation assays are, indeed, reflected in an ability of the individual isoforms to elicit distinct, physiological responses to progesterone. Progesterone 339-351 S100 calcium binding protein A6 (calcyclin) Mus musculus 168-172 12017551-14 2002 Thus, PR-A is both necessary and sufficient to elicit the progesterone-dependent reproductive responses necessary for female fertility, while PR-B is required to elicit normal proliferative responses of the mammary gland to progesterone. Progesterone 58-70 S100 calcium binding protein A6 (calcyclin) Mus musculus 6-10 10976068-3 2000 By selective ablation of PR-A in mice, we show that the PR-B isoform modulates a subset of reproductive functions of progesterone by regulation of a subset of progesterone-responsive target genes. Progesterone 117-129 S100 calcium binding protein A6 (calcyclin) Mus musculus 25-29 10976068-3 2000 By selective ablation of PR-A in mice, we show that the PR-B isoform modulates a subset of reproductive functions of progesterone by regulation of a subset of progesterone-responsive target genes. Progesterone 159-171 S100 calcium binding protein A6 (calcyclin) Mus musculus 25-29 33427050-1 2021 Progesterone acts directly on vascular smooth muscle cells (VSMCs) through activation of membrane progesterone receptor alpha (mPRalpha)-dependent signaling to rapidly decrease cytosolic Ca2+ concentrations and induce muscle relaxation. Progesterone 0-12 S100 calcium binding protein A6 (calcyclin) Mus musculus 127-135 33427050-0 2021 Involvement of sarco/endoplasmic reticulum Ca2+ _ATPase (SERCA) in mPRalpha (PAQR7)- mediated progesterone induction of vascular smooth muscle relaxation. Progesterone 94-106 S100 calcium binding protein A6 (calcyclin) Mus musculus 67-75 33427050-3 2021 The present results show that treatment of cultured human VSMCs with progesterone and the selective mPR agonist, Org OD-02-0 (OD 02-0), but not with the nuclear PR agonist, R5020, increased SERCA protein expression which was blocked by knockdown of mPRalpha with siRNA. Progesterone 69-81 S100 calcium binding protein A6 (calcyclin) Mus musculus 249-257 33427050-8 2021 These results suggest that the rapid effects of progesterone on cytosolic Ca2+ levels and relaxation of VSMCs through mPRalpha involves regulation of the functions of SERCA2 and PLB through Gi, MAP kinase and Akt signaling pathways, and downregulation of RhoA activity. Progesterone 48-60 S100 calcium binding protein A6 (calcyclin) Mus musculus 118-126 32077034-5 2020 It has been reported that human-derived GBM cells express the mPRalpha, mPRbeta, and mPRgamma subtypes, and that progesterone promotes GBM progression in part by mPRalpha specific activation; however, it is still unknown if mPRdelta and mPRepsilon are also expressed in this type of tumor cells. Progesterone 113-125 S100 calcium binding protein A6 (calcyclin) Mus musculus 162-170 32529777-1 2020 BACKGROUND: The aim of this study was to determine whether progesterone could inhibit the growth of lung adenocarcinoma cells via membrane progesterone receptor alpha (mPRalpha) and elucidate its potential mechanism. Progesterone 59-71 S100 calcium binding protein A6 (calcyclin) Mus musculus 168-176 32529777-11 2020 CONCLUSIONS: In summary, the results of our study show that progesterone can inhibit lung adenocarcinoma cell growth via mPRalpha. Progesterone 60-72 S100 calcium binding protein A6 (calcyclin) Mus musculus 121-129 31777985-3 2020 In this study, we identified that the expression of membrane progesterone receptor alpha (mPRalpha) was associated with EGFR mutations in lung adenocarcinoma patients and subsequently affected the efficacy of EGFR-TKIs. Progesterone 61-73 S100 calcium binding protein A6 (calcyclin) Mus musculus 90-98 31777985-4 2020 Progesterone (P4) or its derivative Org OD02-0 (Org), which is mediated by mPRalpha, increases the function of EGFR-TKIs to suppress the proliferation, migration, and invasion of lung adenocarcinoma cells in vitro and in vivo. Progesterone 0-12 S100 calcium binding protein A6 (calcyclin) Mus musculus 75-83