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Global Transcriptome analyses in PRMT1-depleted CT 27 Juman trophoblast stem cells (human TSCs).

ABSTRACT: The data presented here represent global gene expression patterns in human TSCs upon knockdown of protein arginine methyla transferase 1 (PRMT1).

ORGANISM(S): Homo sapiens

PROVIDER: GSE295904 | GEO | 2026/06/15

REPOSITORIES: GEO

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			Action	DRS
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	GSE295904_PRMT1KD_CT27_count.txt.gz	Txt
	GSE295904_PRMT1KD_vs_CT27_DESeq2Out.csv.gz	Csv

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Similar Datasets

Single cell RNAseq analysis in CT27 human TSC with and without PRMT1 Knockdown

Project description:The study reports single cell RNA seq analyses of gene expression dynamics in human TSCs. Protein Arginine Methyl Transferase 1 (PRMT1) regulates cellular function via methylation of arginine residues on its target proteins. In this study we depleted PRMT1 in CT27 human TSCs via RNAi. Loss of PRMT1 affects human TSC self-renewal process. We performed single cell RNA-seq with control and PRMT1-knocked down CT27 human TSCs to capture gene expression dynamics at a single cell resolution.

2026-06-15 | GSE295665 | GEO

Global Transcriptome analyses in Human Trophoblast Stem Cells (human TSCs) derived from placental tissues from patients suffering from idopathic recurrent pregnancy losses (RPLS).

Project description:We established RPL-Patient specific TSC lines from placental tissues collected after patients undergoing procedures at the REI clinic at the University of Kansas Medical Center. Two groups of RPL-TSC lines were established. A control RPL-TSC group, which were established from placental tissues without any apparent defect in placental ultratructure and trophoblast layers and also maintained high expressions of protein arginine methyl transferase 1 (PRMT1) in villous cytotrophoblast cells (CTBs). The second group is the experimental RPL-TSC group, which were established from RPL-Placentae with defects in placental villi structure and trophoblast layers and showed strong repression of PRMT1 expression in villous CTBs. The established RPL-TSCs were tested for PRMT1 expression. TSCs showed similar expression patterns of PRMT1 with respect to CTBs, from which they were established. Thus, RPL-TSC lines with high expression of PRMT1 are called PRMT1_high RPL-TSCs and The experimental RPL TSCs are called PRMT1_low RPL-TSCs. Four RPL-TSC lines from each group were used for global RNA-sequencing to identify global gene expression patterns.

2026-06-15 | GSE318854 | GEO

PRMT1-dependent Arginine methylation regulates replication stress response through DNA-protein kinase

Project description:PRMT1 is the major Arginine methyltransferase in mammalian cells and its over-expression in human cancer has been linked to poor response to cancer therapy. Here, combining mass spectrometry-based global methyl-proteomics with genome-wide mRNA expression profiling, we identify PRMT1 and its associated Arginine methylation as a regulatory hubs controlling cancer cell response to replicative stress agents. We show that DNA-PK binds to PRMT1 and regulates both its subcellular localization and activity, leading to PRMT1 recruitment to drug-stalled replication forks and channelling its methyl-transferase activity from its soluble targets towards Arginine 3 of histone H4. This DNA-PK-PRMT1 axis is required for the induction of the Senescence-Associated Secretory Phenotype, which sustains cell cycle arrest and protects cells from apoptosis. Our data show that Arginine-methylation regulates the adaptive response of cancer cell to replicative stress agents and might be targeted to sensitize cancer cells to genotoxic chemotherapeutics

2020-01-14 | GSE106609 | GEO

PRMT1 recruitment and H3R4Me32a modfification in control and PRMT1-depleted trophoblast progenitors

Project description:To understand PRMT1 recruitment and associated changes in histone H4 arginine3 di-methylation at the chromatin region in trophoblast progenitors, we performed CUT&RUN experiments in CT27 human trophoblast stem cells (CT27 hTSCs) and in primary trophoblast stem and progenitor cells (TSPCs) in mouse embryonic day (E) 7.5 ectoplacental cone region (EPC). For CT27 hTSCs, experiments were done in both control and PRMT1-knockdown CT27 hTSC. We also tested RNA polymerase II recruitment in these cells.

2026-06-15 | GSE295846 | GEO

Global Transcriptome analyses in METTL3_high and METTL3_Low Human Trophoblast Stem Cells from idiopathic recurrent pregnancy losses (RPLs)

Project description:We established RPL-Patient specific TSC lines from placental tissues collected after patients undergoing procedures at the REI clinic at the University of Kansas Medical Center. Two groups of RPL-TSC lines were established. A control RPL-TSC group, which were established from placental tissues without any apparent defect in placental ultra-structure and trophoblast layers and also maintained high expressions of Methyl Transferase-Like3 (METTL3) in villous cytotrophoblast cells (CTBs). The second group is the experimental RPL-TSC group, which were established from RPL-Placentae with defects in placental villi structure and trophoblast layers and showed strong repression of PRMT1 expression in villous CTBs. The established RPL-TSCs were tested for PRMT1 expression. TSCs showed similar expression patterns of METTL3 with respect to CTBs, from which they were established. Thus, RPL-TSC lines with high expression of METTL3 are called METTL3_high RPL-TSCs and The experimental RPL TSCs are called METTL3_low RPL-TSCs. Six METTL3_high RPL TSC lines and three METTL3_low RPL-TSC lines were used for global RNA-sequencing to identify global gene expression patterns.

2026-05-26 | GSE319502 | GEO

Transcription profiling of human HeLa cells follwing siRNA mediated knock down of the arginine methyltransferases CARM1 and/or PRMT1

Project description:siRNA mediated knockdown of the arginine methyltransferases CARM1 and/or PRMT1 in HeLa cells

2007-08-30 | E-MEXP-1173 | biostudies-arrayexpress

The arginine methyltransferase PRMT1 establishes transcriptomic homeostasis essential for spermatogonial differentiation and male fertility

Project description:Protein arginine methyltransferase 1 (Prmt1) is known as the major Type-I protein arginine methyltransferase that deposits asymmetrical dimethylarginine (ADMA) in both histone and non-histone substrates. Nonetheless, how Prmt1 and its downstream signalling through substrate methylation function in the male germline development remains poorly understood. In this study, we discovered that Prmt1 is predominantly present in the spermatogonial population during mouse spermatogenesis. Using three Cre-mediated conditional Prmt1 knockout mouse lines, we observed that Prmt1 is essential for the maintenance of spermatogonial cells and Prmt1-deposited ADMA marks coordinate an inherent homeostasis among three types of substrate methylation. In conjunction with high-throughput Cut&Tag and modified mini-bulk Smart-seq2 analyses, we unveiled that Prmt1-mediated H4R3me2a mark enriched in the promoter region, together with other histone arginine methylations, drives a global transcriptomic landscape that maintains the regular gene expression and alternative splicing. Collectively, we provide the genetic evidence showing the essential role of Prmt1-deposited arginine methylation in the establishment of transcriptional homeostasis, and shed light on the methylarginine signalling pathway in orchestrating spermatogonial development in the mammalian germline.

2023-03-31 | GSE227857 | GEO

Targeting PRMT1-mediated SRSF1 Methylation to Suppress Exon Inclusion within Oncogenic Transcripts and Breast Tumorigenesis

Project description:PRMT1 is highly expressed in breast tumors, and has been suggested to play a vital role in breast tumorigenesis, but the underlying molecular mechanisms remain to be fully characterized. Here, we reveal that PRMT1 exhibits a wide-spreading role in RNA alternative splicing based on transcriptome analysis, with a preference for exon inclusion in a large cohort of oncogenic genes. Profiling PRMT1 methylome reveals that the arginine/serine-rich splicing factor SRSF1 is heavily arginine-methylated by PRMT1, which is critical for SRSF1 phosphorylation, SRSF1 binding with RNA, and PRMT1-induced exon inclusion. In breast tumors, the overexpression of PRMT1 is associated with high levels of SRSF1 arginine methylation and aberrant exon inclusion in those oncogenic genes. Accordingly, PRMT1-mediated SRSF1 methylation and exon inclusion events are found to be critical for the malignant behaviors of breast cancer cells. Furthermore, we identified and characterized a selective PRMT1 inhibitor iPRMT1, which is potent in inhibiting PRMT1-mediated SRSF1 methylation and exon inclusion events, and breast cancer cell growth both in vitro and in vivo. Combination treatment with iPRMT1 and inhibitor targeting SRSF1 phosphorylation, SPHINX31 or SRPIN340, exhibits synergistic effects on suppressing breast cancer cell growth, strengthening the cross-talk between arginine methylation and phosphorylation in SRSF1. In conclusion, our data uncover a key mechanism underlying PRMT1-mediated gene alternative splicing, demonstrating targeting PRMT1 has great potential to treat breast cancer in clinic.

2023-10-02 | GSE212049 | GEO

PRMT1 inhibition activates the interferon pathway to potentiate antitumor immunity and enhance checkpoint blockade efficacy in melanoma

Project description:Despite the immense success of immune checkpoint blockade (ICB) in cancer treatment, many tumors, including melanoma, exhibit innate or adaptive resistance. Tumor-intrinsic T-cell deficiency and T-cell dysfunction have been identified as essential factors in the emergence of ICB resistance. Here, we found that protein arginine methyl transferase 1 (PRMT1) expression was inversely correlated with the number and activity of CD8+ T cells within melanoma specimen. PRMT1 deficiency or inhibition with DCPT1061 significantly restrained refractory melanoma growth and increased intratumoral CD8+T cells in vivo. Moreover, PRMT1 deletion in melanoma cells facilitated formation of double-stranded RNA (dsRNA) derived from endogenous retroviral elements (ERVs) and stimulated an intracellular interferon response. Mechanistically, PRMT1 deficiency repressed the expression of DNA methyltransferase 1 (DNMT1) by attenuating modification of H4R3me2a and H3K27ac at enhancer regions of DNMT1, and DNMT1 downregulation consequently activated ERV transcription and the interferon signaling. Importantly, PRMT1 inhibition with DCPT1061 synergized with PD-1 blockade to suppress tumor progression and increase the proportion of CD8+T cells as well as IFNγ+CD8+T cells in vivo. Together, these results reveal an unrecognized role and mechanism of PRMT1 in regulating antitumor T-cell immunity, suggesting PRMT1 inhibition as a potent strategy to increase the efficacy of ICB.

2023-11-07 | GSE240258 | GEO

Comprehensive transcriptome analysis of the brain in CNS-specific PRMT1 knockout mice.

Project description:Arginine methylation is a common post-translation modification that is catalyzed by protein arginine methyltransferases (PRMTs). We generated the central nervous system-specific PRMT1 deficient (PRMT1-CKO) mice by Cre-loxP recombination system. Recently, we have discovered that PRMT1 is essential for development of CNS, and it is especially crucial for oligodendrocyte lineage progression and the subsequent myelination. In this study, we performed a comprehensive analysis of gene expression changes in whole brains, cortices or cerebella of wild type (WT) and PRMT1-CKO mice using RNA sequencing (RNA-seq). Filtering characteristics were used to identify the differentially expressed genes using the CLC Genomics Workbench software

2020-08-14 | GSE126127 | GEO

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