Ask about this productRelated genes to: PSG9 Blocking Peptide
- Gene:
- PSG9 NIH gene
- Name:
- pregnancy specific beta-1-glycoprotein 9
- Previous symbol:
- PSG11
- Synonyms:
- PSGII
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: PSG9 Blocking Peptide
Related articles to: PSG9 Blocking Peptide
- Understanding the causes of the exceptional rate of evolution of the mammalian placenta is likely to aid the understanding of placental development and the etiology of the human-specific pregnancy disorder pre-eclampsia (PE). As retroelements are often lineage-specific and known to be co-opted for placental function, here we consider the binding of the transcription factors GATA3 and DLX5 to retroelements. These factors are dysregulated in pre-eclampsia, as are their downstream consequences. - Source: PubMed
Publication date: 2026/03/09
Singh ManvendraQu YuliangPande AmitZadora JuliannaHerse FlorianGauster MartinKong XuhuiZheng RongyanAnwar RabiaStevanovic KatarinaDechend RalfCohen MarieMolvarec AttilaWang JichangKonkel Miriam KZhang BinFeschotte CedricDveksler GabrielaBlois Sandra MHurst Laurence DIzsvák Zsuzsanna - Miscarriages affect 50-70% of all gestations and 15-20% of clinically recognized pregnancies. Recurrent pregnancy loss (RPL) occurs in 1-5% of clinical pregnancies and has an enormous demographic impact. However, the etiologies and molecular pathways of RPL are scarcely understood, and therefore, reliable diagnostic and preventive methods are not yet available. Here, we aimed to discover novel biomarkers for RPL using next-generation proteomics technology to help develop early and effective diagnostic tools. - Source: PubMed
Publication date: 2025/08/28
Tóth EszterPosta MátéGyörffy DánielOravecz OrsolyaFarkas EmeseBalogh AndreaEscher ClaudiaBober MagdalenaSzilágyi AndrásHupuczi PetronellaVeress LajosTörök OlgaNagy SándorRinner OliverErez OfferPapp ZoltánÁcs NándorThan Nándor Gábor - From fertilisation to delivery, calcium must be transported into and within the foetoplacental unit for intracellular signalling. This requires very rapid, precisely located Ca transfers. In addition, from around the eighth week of gestation, increasing amounts of calcium must be routed directly from maternal blood to the foetus for bone mineralisation through a flow-through system, which does not impact the intracellular Ca concentration. These different processes are mediated by numerous membrane-sited Ca channels, transporters, and exchangers. Understanding the mechanisms is essential to direct interventions to optimise foetal development and postnatal bone health and to protect the mother and foetus from pre-eclampsia. Ethical issues limit the availability of human foetal tissue for study. Our insight into the processes of placental Ca handling is advancing rapidly, enabled by developing genetic, analytical, and computer technology. Because of their diverse sources, the reports of new findings are scattered. This review aims to pull the data together and to highlight areas of uncertainty. Areas needing clarification include trafficking, membrane expression, and recycling of channels and transporters in the placental microvilli; placental metabolism of vitamin D in gestational diabetes and pre-eclampsia; and the vascular effects of increased endothelial Orai expression by pregnancy-specific beta-1-glycoproteins PSG1 and PSG9. - Source: PubMed
Publication date: 2025/01/04
Walker Valerie - Differentiating between a normal intrauterine pregnancy (IUP) and abnormal conditions including early pregnancy loss (EPL) or ectopic pregnancy (EP) is a major clinical challenge in early pregnancy. Currently, serial β-human chorionic gonadotropin (β-hCG) and progesterone are the most commonly used plasma biomarkers for evaluating pregnancy prognosis when ultrasound is inconclusive. However, neither biomarker can predict an EP with sufficient and reproducible accuracy. Hence, identification of new plasma biomarkers that can accurately diagnose EP would have great clinical value. - Source: PubMed
Publication date: 2023/09/15
Beer Lynn AYin XiangfanDing JianyiSenapati SuneetaSammel Mary DBarnhart Kurt TLiu QinSpeicher David WGoldman Aaron R - We explored changes in pregnancy-specific glycoprotein 9 (PSG9) levels in the serum of patients with preeclampsia and the effects and underlying mechanisms of PSG9 effects on calcium (Ca) homeostasis and nitric oxide (NO) release in human umbilical vein endothelial cells (HUVECs). Western blotting was used to detect protein expression levels, and an NO fluorescence probe was used to examine NO production. Intracellular Ca concentrations were measured using a Ca-sensitive fluorescent dye under a fluorescence microscope. Compared with those in healthy pregnant women, serum PSG9 levels were significantly decreased in patients with preeclampsia. PSG9 (0.1 μg/mL) treatment of HUVECs significantly enhanced the expression levels of store-operated calcium entry (SOCE) channel proteins Orai1 and Orai2, but not Orai3, and of endothelial nitric oxide synthase (eNOS) and NO production. Pretreatment with an inhibitor of SOCE (BTP2) abolished PSG9-enhanced Orai1, Orai2, and eNOS expression levels and NO production in HUVECs. The mechanisms underlying SOCE that were PSG9 enhanced in HUVECs appear to involve the Ca/eNOS/NO signaling pathway. These findings suggest that serum PSG9 levels may be a potential biomarker for monitoring the occurrence or development of preeclampsia in pregnancy and that PSG9 may be a potential therapeutic target for the treatment of preeclampsia. - Source: PubMed
Publication date: 2023/03/16
Qin YingMeng QinggangWang QunhuaWu MingzhuFang YanTu ChengchengHu XinyangShen BingChen HongboXu Xiaohong