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SRRM4 knockout helps the human mesenchymal stem cell line to intrude into decellularized bone

ABSTRACT: SRRM4 knockout helps the human mesenchymal stem cell line to intrude into decellularized bone

PROVIDER: PRJNA1290247 | ENA |

REPOSITORIES: ENA

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SRRM4 knockout helps the human mesenchymal stem cell line to intrude into decellularized bone

Project description:Analysis of the human bone marrow microenvironment requires an in vivo model that reflects this microenvironment. We introduced a human bone marrow mesenchymal stem cell (MSC) line into decellularized bone. Using the CRISPR Knock Out library, we identified serine/arginine repetitive matrix 4 knockout in an MSC cell line, as a candidate factor for bone intruding, which may be applied to the analysis of hematological diseases such as myelodysplastic neoplasm.

2025-07-16 | GSE302358 | GEO

Identification of the factor to lead human mesenchymal stem cell line into decellularized bone

Project description:Identification of the factor to lead human mesenchymal stem cell line into decellularized bone

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Role of SRRM4 in regulating microexons in Circular RNAs

Project description:Stduying the role of splicing factor SRRM4 on circular RNAs in human cells

2020-12-07 | GSE148813 | GEO

AmpliSeq Transcriptome Analysis of Human Prostate Cancer Cells With or Without Overt SRRM4 Expression

Project description:Prostate adenocarcinoma (AdPC) cells can undergo lineage switching to neuroendocrine cells and develop into therapy-resistant neuroendocrine prostate cancer (NEPC). While genomic/epigenetic alterations are shown to induce neuroendocrine differentiation via an intermediate stem-like state, RNA splicing factor SRRM4 can transform AdPC cells into NEPC xenografts through a direct neuroendocrine transdifferentiation mechanism. Whether SRRM4 can also regulate a stem-cell gene network for NEPC development remains unclear. Here, we use the Ion AmpliSeqTM Transcriptome Human Gene Expression Kit (AmpliSeq) to analyze the transcriptome of human AdPC cell line DU145 overexpressing SRRM4 via lentiviral transduction compared to the control, empty vector-transduced DU145 cells. This study reveals that SRRM4 induces a pluripotency gene network consisting of the stem-cell differentiation gene, SOX2. In summary, we report a novel mechanism by which SRRM4 drives NEPC progression via a pluripotency gene network.

2018-08-14 | GSE118104 | GEO

MJAY analysis of cortical RNA obtained from Srrm3-Srrm4 double mutant mice and wild-type mice

Project description:The Bronx waltzer mutation in Srrm4, a gene that encodes a neuronal Ser/Arg (SR)-rich splicing factor, disrupts the expression of several alternative exons specifically in the inner ear. Here we show that the expression of SRRM3 in neurons limits the distribution of SRRM4-dependent splicing. In vitro, SRRM3 and SRRM4 regulated the same alternative exons, yet in vivo Srrm3 deficiency caused neuronal splicing alterations and motor dysfunction, indicating that SRRM3 has non-redundant functions. Mice harboring mutations in both Srrm3 and Srrm4 failed to breathe, and their neuromuscular junctions (NMJ) were malformed. Transcriptome-wide analysis revealed a large network of SRRM3/SRRM4-dependent splicing changes, including the skipping of key exons in the NMJ organizer Agrin. Furthermore, SRRM3/SRRM4 regulated gene expression through neuron-specific switches in chromatin regulatory complexes and by altering the reading frame in several mRNAs. Our findings reveal that the SRRM3/SRRM4 subfamily of SR proteins is central to regulation of the neuronal transcriptome. In this dataset, we include probe-set level data obtained from brain cortex samples. The processed data represent probe-set intensities that have been normalized to gene expression levels.

2018-07-01 | GSE71480 | GEO

Role of SRRM4 in regulating microexons in Circular RNAs in brain tissue

Project description:Studying the role of splicing factor SRRM4 on circular RNAs in human cells

2020-12-07 | GSE159260 | GEO

Alternative splicing of LSD1+8a is mediated by SRRM4 in Neuroendocrine Prostate Cancer

Project description:Neuroendocrine prostate cancer (NEPC) is the most virulent subtype. Currently, there is an urgent need to identify new biomarkers and therapeutic targets in NEPC. The splicing factor SRRM4 was previously demonstrated to be highly expressed in NEPC, to promote expression of genes linked to neuroendocrine differentiation and cancer progression, and to promote alternate splicing of genes, including REST. One of REST’s binding protein is lysine specific demethylase 1 (LSD1). Importantly, a transcript variant of LSD1 called LSD1+8a is expressed in neuronal tissues and promotes neuronal gene expression. However, there was no information about LSD1+8a’s importance in prostate cancer. Using adenocarcinoma and NEPC patient-derived xenografts and clinical specimens, we determined that LSD1+8a was expressed exclusively in NEPC. Furthermore, LSD1+8a expression was significantly correlated with elevated mRNA expression of SRRM4. Using SRRM4-overexpressing prostate cancer cell lines, we determined that alternative splicing of LSD1+8a is directly mediated by SRRM4 and that LSD1+8a and SRRM4 co-regulate a unique program of cancer-promoting genes that is not regulated by canonical LSD1. Our findings demonstrate that measurement of LSD1+8a expression is a promising NEPC biomarker and suggest that targeting LSD1+8a in NEPC may be a useful strategy to block expression of genes linked to cancer progression.

2020-05-19 | GSE132062 | GEO

Whole transcriptome analysis of control human fibroblasts, TGFβ-induced human fibroblasts, and fibroblasts co-cultured with normal lung decellularized scaffolds and fibroblasts co-cultured with bleomycin-induced lung decellularized scaffolds.

Project description:Fibrosis refers to the abnormal proliferation and excessive accumulation of fibrous tissue in an organ or tissue, typically caused by chronic injury or inflammation. Fibroblasts play a crucial role in the initiation and progression of fibrosis, with their excessive activation and overproduction of ECM being key mechanisms in fibrotic diseases. In this study, we constructed decellularized lung scaffolds from normal mice and bleomycin-induced lung decellularized scaffolds to analyze and compare the differential gene expression in control human fibroblasts, TGFβ-induced human fibroblasts, fibroblasts co-cultured with normal lung decellularized scaffolds, and fibroblasts co-cultured with bleomycin-induced lung decellularized scaffolds. This investigation aims to explore the impact of ECM on fibroblast activation and its underlying mechanisms.

2025-08-20 | GSE275625 | GEO

A mutation in the Srrm4 gene causes pre-mRNA splicing defects and deafness in Bronx waltzer mice.

Project description:The spontaneous mutant Bronx waltzer (bv) mouse line is characterized by deafness and balance defect. We located the bv mutation to the Srrm4 gene which encodes a regulator of alternative pre-mRNA splicing. We found that Srrm4 is expressed in balance and hearing organs (i.e. in the vestibular maculas and the cochlea). Srrm4 is also expressed in the central nervous system including the cerebellum. To identify potential splicing defects in bv/bv mice, we analyzed RNA samples from the vestibular maculas and cerebellums of bv/bv mice and control (bv/+) littermates, using mouse exon junction microarrays (MJAY). In this dataset, we include probe-set level data obtained from cerebellar samples. The processed data represent probe-set intensities that have been normalized to gene expression levels. 8 total samples were analyzed in this series: cerebellums from 4 heterozygous (bv/+) and 4 homozygous (bv/bv) mice at P15.

2012-10-21 | E-GEOD-33589 | biostudies-arrayexpress

A mutation in the Srrm4 gene causes pre-mRNA splicing defects and deafness in Bronx waltzer mice.

2012-10-21 | GSE33589 | GEO