Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112575 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
2020-11-25 | GSE162118 | GEO
Project description:Biological significance of LEF1 in endometrial receptivity
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Project description:Biological significance of LEF1 in endometrial receptivity
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Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
2020-12-03 | GSE162543 | GEO
Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
2022-02-18 | GSE196754 | GEO
Project description: Not available
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Endometrial receptivity is imperative to achieving pregnancy in humans. A disruption in the development of endometrial receptivity is responsible for recurrent implantation failures (RIF) of endometrial origin. To further understand the molecular mechanisms behind the endometrial receptivity process, we used the 8-plex isobaric tag for relative and absolute quantitation (iTRAQ) method to compare and quantify the proteomes from endometrial biopsies of three different endometrial statuses (fertile women, IUD carriers and RIF patients). Overall, iTRAQ allowed to identify 1,889 non-redundant proteins. Of these, 188 were differentially expressed proteins (DEP) (p-value < 0.05) among the three endometrial groups. Pairwise comparisons revealed 133 significant DEP in fertile vs. IUD carriers and 158 DEP in RIF vs. IUD carriers. However, no DEP were identified between fertile and RIF patients. Western blot validation of three DEP involved in endometrial receptivity (Plastin 2, Lactotrasferrin, and Lysozyme) confirmed our iTRAQ results. Moreover, functional KEGG enrichment revealed that complement and coagulation cascades and peroxisome were the two most significant pathways for the RIF vs. IUD comparison and ribosome and spliceosome for the fertile vs. IUD comparison, as possible important pathways involved in the endometrial receptivity acquisition. Our findings confirm that an IUD introduces numerous changes in the endometrial protein profile when compared to fertile and RIF endometria, revealing some key proteins involved in endometrial receptivity. The lack of DEP between fertile and RIF patient endometria suggest either that idiopathic RIF may not have an endometrial origin, with other as-yet-unknown factors involved.
2019-11-06 | PXD011094 | Pride
Project description:Endometrial receptivity is defined as the functional, morphological, and molecular changes of the endometrium occurring during a limited time period in the menstrual cycle called the ‘window of implantation’. The endometrial luminal epithelial cells are critical in producing this receptivity as their adhesive capacity enables embryo implantation; however, how this occurs is poorly understood. Recently, using endometrial epithelial organoids, we identified that Myosin Heavy Chain 10 (MYH10) was abnormally downregulated in infertile endometrial epithelial cells during the window of implantation, suggesting a role in receptivity. MYH10 regulates processes important in endometrial receptivity including cell polarity, adhesion, and migration; however, whether it regulates endometrial receptivity has yet to be researched. We aimed to investigate whether MYH10 regulates endometrial epithelial cell adhesive capacity. MYH10 localised to all major cellular compartments within endometrial tissue. However, immunostaining intensity was higher in luminal epithelial cells during the window of implantation compared to the proliferative phase in fertile endometrium. Conversely, this increased expression was not maintained in infertile endometrium during the window of implantation. siRNA knockdown of MYH10 in the receptive Ishikawa cell line significantly decreased cell adhesion to human cytotrophoblast-progenitor spheroids. MYH10 knockdown in Ishikawa cells also increased PGR, FOXO1, and GPX3 expression, while decreasing PDLIM2 expression. Proteomics analysis following MYH10 knockdown altered the production of 57 proteins with functions critical in endometrial receptivity including tight junction regulators. These results demonstrate that MYH10 alters endometrial epithelial cell adhesive capacity primarily via regulation of the actin cytoskeleton, implying an important role in implantation.
2026-05-05 | PXD062326 | Pride
Project description: Not available
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