GCM1 antibody - N-terminal region (P100836_P050)
- Known as:
- GCM1 (anti-) - N-terminal region (P100836_P050)
- Catalog number:
- p100836_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GCM1 antibody - N-terminal region (P100836_P050)
Related genes to: GCM1 antibody - N-terminal region (P100836_P050)
- Gene:
- GCM1 NIH gene
- Name:
- glial cells missing transcription factor 1
- Previous symbol:
- GCMA
- Synonyms:
- hGCMa
- Chromosome:
- 6p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-02
- Date modifiied:
- 2018-11-09
Related products to: GCM1 antibody - N-terminal region (P100836_P050)
Related articles to: GCM1 antibody - N-terminal region (P100836_P050)
- During gestation, the human fetus is dependent on the placenta for oxygen and nutrient exchange, waste removal, and immunological protection. Glial Cells Missing Transcription Factor 1 (GCM1) is critical to placental development, particularly during syncytialization. This study aims to characterize GCM1 regulation of gene expression using a GCM1 knockdown in placental syncytiotrophoblasts. - Source: PubMed
Publication date: 2026/05/26
Rajput AnikaFirsick Evan JAhuna KyliaLapehn SamanthaKadam LeenaMyatt LesliePaquette Alison G - Trophoblast cell fusion is a vital developmental process that enables the formation of the multinucleated syncytiotrophoblast (STB), which plays a central role in placental function and maternal-fetal exchange. Fusion defects in this lineage are closely associated with pregnancy complications such as preeclampsia (PE) and fetal growth restriction (FGR). Although the fusion of trophoblasts is a highly coordinated event, it involves multiple interdependent steps, including transcriptional programming, membrane remodeling, cytoskeletal rearrangement, metabolic adaptation, and immune regulation. Recent studies have uncovered critical molecular mediators at each of these levels. Transcription factors such as Glial cells missing transcription factor 1(GCM1), Krüppel-like factor 6(KLF6), and Transcription factor EB(TFEB) govern differentiation timing; fusion proteins, including Syncytin-1/2 and Mfn2, facilitate membrane merger; polarity regulators and actin-associated proteins like Par6 and CNN3 organize cytoskeletal architecture; metabolic reprogramming, particularly a shift from oxidative phosphorylation to glycolysis, supplies energy and biosynthetic precursors; and immune modulators such as pregnancy-induced factor 1 and Interleukin-10(IL-10) ensure a permissive environment for fusion at the maternal-fetal interface. Epigenetic mechanisms, including DNA methylation and histone modifications, further fine-tune the expression of fusion-related genes. Alongside mechanistic discoveries, a wide range of experimental models has been developed to investigate trophoblast fusion in vitro. These include traditional monolayer cell lines (e.g., BeWo), primary human trophoblasts, placental explants, trophoblast stem cells, and trophoblast organoids. Each model system provides distinct advantages in recapitulating aspects of syncytialization and placental physiology. Moreover, the integration of multi-omics technologies-such as single-cell and spatial transcriptomics, proteomics, metabolomics, and epigenomics-has expanded our understanding of the spatiotemporal dynamics and molecular complexity underlying trophoblast fusion. Despite these advances, several key challenges remain unresolved, including the lack of models that fully recapitulate the structural and functional features of the human maternal-fetal interface and the limited understanding of posttranslational and spatiotemporal regulatory mechanisms. Addressing these gaps will be essential for translating basic insights into diagnostic and therapeutic innovations for placental diseases. - Source: PubMed
Xiong YanDing Yu-Bin - Polycystic ovary syndrome (PCOS) is a common endocrine disorder that contributes to pregnancy complications like Intra Uterine Growth Restriction (IUGR), leading to compromised foetal outcome. Although maternal metabolic and hormonal imbalances are well-established in PCOS, the specific molecular alterations within the placenta and its outcome remains poorly explored. This study aimed to characterize key molecular signaling alterations in PCOS placentae with respect to steroid hormone receptors, trophoblast lineage specification, along with their structural alterations. To understand the above alterations, PCOS rodent mothers were developed using letrozole treatment for 21days daily orally, following which induction of pregnancy and those pregnant animals were sacrificed at GD18. Tissues were subjected to expression levels of steroidal and placental cell markers using transcriptomic and protein expression, along with morphometric and histological analysis, correlated with hormone profile. Histological analysis of GD 18 PCOS placenta exhibited a reduction in labyrinth zone, with an increased AR expression, along with downregulation of PR, ER ɑ and ER β, indicating an altered steroidal status. Moreover, dysregulation of genes such as Phlda2, Tpbpa, Pcdh12, Prl3b1, CDX2, GCM1, and GATA2 along with reduced expression of SynA, Syn B were observed suggesting an impaired trophoblast differentiation, vascular development, and immune tolerance. Additionally, elevated expressions of Flt4, H2K and IFN gamma suggested compensatory mechanisms attempting to offset placental dysfunction. This study clearly indicates maternal PCOS pathophysiology effects placental development by altering the morphology, along with abnormal hormonal homeostasis, contributing to impaired differentiation. These findings underscore the importance of targeting placental pathways in the management of PCOS-related pregnancy outcomes. - Source: PubMed
Publication date: 2026/05/21
Mahapatra AnanyaPillai GautamiRana RemiShah ZeelNampoothiri Laxmipriya - Cattle have a synepitheliochorial type of placenta characterized by placental cotyledons and maternal endometrial caruncles forming placentomes that are essential for fetal development to term. As the elongated conceptus begins implantation, binucleated trophoblast giant cells (TGC) begin to appear in the chorion. The TGC are hypothesized to arise from progenitor UNC through endoreplication and express unique placenta-specific genes, including placental lactogen (CSH2), pregnancy-associated glycoproteins (PAGs), and prolactin like proteins (PRPs). Despite their essential role in placental cotyledon development and placental function, the cellular and molecular mechanisms regulating trophoblast differentiation in the bovine placenta remain undefined. Here, a differentiation protocol was developed that enabled bovine trophoblast stem cells (TSCs) to generate TGC. The morphologically distinct TGCs were binucleated with a cytoplasm containing abundant secretory granules. Expression of TGC marker genes (CSH2, PAGs, PRPs) was increased in differentiated TSCs. Single-cell transcriptome analysis revealed distinct developmental programs underlying TGC lineage specification. To interrogate regulatory mechanisms governing TGC differentiation, bovine TSCs were engineered to enable inducible GCM1 (glial cells missing 1) expression. Induction of GCM1 during TSC differentiation increased TGC number and TGC-specific gene expression. This robust and tractable in vitro TSC differentiation system is useful to explore trophoblast differentiation and provide fundamental insights into the cellular and molecular mechanisms regulating placenta development in cattle. - Source: PubMed
Publication date: 2026/03/11
Abdelhady Abdallah WWinuthayanon SarayutOrtega M SofiaKelleher Andrew MSpencer Thomas E - The glial cells missing (GCM) genes were first discovered in Drosophila and encode transcription factors important for gliogenesis. In placental mammals, GCM1 regulates several genes that are important for early placenta development, while its paralogue GCM2 is important for parathyroid gland development. The egg-laying monotremes, which represent the most diverged extant mammalian lineage, undergo a short period of intrauterine development and form a simple placenta. To gain more insight into the evolution of GCM genes, we analysed the sequence, expression and genomic localization of GCM1 and GCM2 genes in the platypus and echidna. We found that the chromosomal localization of GCM1 changed after the divergence of therian mammals, coinciding with the evolution of a complex placenta. Expression analysis revealed the presence of GCM transcripts in male and female monotreme gonads, as well as expression of GCM1 in the female reproductive tract. GCM-binding sites in target genes associated with placental development in therian mammals were also present in the monotremes and the chicken. Together, this suggests that the role of GCM1 in reproduction emerged early in mammalian evolution. - Source: PubMed
Wilson IsabellaHamdan Diana Demiyah Mohdvan der Ploeg RachelPerry TahliaGrützner Frank