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Effect of full-length (1-23ex) and short isoform (7-20ex) PIWIL2 expression in HEK293 cell line in result of knock-in (KI) procedure

ABSTRACT: To investigate the impact of full-length (1-23ex) and short isoform (7-20ex) PIWIL2 expression, we established by knock-in (KI) the HEK293 cell lines, expressed full-length (1-23ex) and short isoform (7-20ex) PIWIL2. KI_pCI is knock-in control.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213602 | GEO | 2026/09/01

REPOSITORIES: GEO

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Effect of full-length (1-23ex) and short isoform (7-20ex) PIWIL2 expression in HEK293 cell line in result of knock-in (KI) procedure

Project description:Effect of full-length (1-23ex) and short isoform (7-20ex) PIWIL2 expression in HEK293 cell line in result of knock-in (KI) procedure

| PRJNA881741 | ENA

Arabidopsis thaliana cultivar:Columbia

Project description:FLIC - Full-Length Isoform Constructor

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PIWIL2 downregulation in colon cancer promotes transposon activity and pro-tumorigenic phenotypes

Project description:Reactivation of transposable elements (TEs) in somatic tissues, particularly of LINE-1, is associated with disease by causing gene mutations and DNA damage. Previous work has shown that the PIWI pathway is crucial for TE suppression in the germline. However, the status and function of this pathway is not well characterized in differentiated somatic cells and there is lack of consensus on the role of the pathway in somatic tumorigenesis. To shed light on this conundrum, we examined the PIWI pathway in colon cancer through combining bioinformatic analyses and cell-based assays. Shifted Weighted Annotation Network (SWAN) analysis revealed that the pathway experiences significant allelic losses in colon cancer and that PIWIL2, the main catalytic component of the pathway responsible for TE silencing, experiences the highest percent deletions. PIWIL2 is downregulated in colon tumors of advanced stage, nodal metastasis, and in certain subtypes, correlating with poor survival, while it is also downregulated in ulcerative colitis, an inflammatory bowel disease that predisposes to colon cancer. PIWIL2 depletion in colon epithelial Caco2 cells leads to increased anchorage-independent growth, loss of transposon-targeting - non-canonical - piRNAs, increased LINE-1 levels and activity, and in DNA damage, altogether highlighting a tumor-suppressing role of PIWIL2 in the colon.

2025-07-31 | GSE303118 | GEO

The piRNAs bounding to Piwil2 in the CA1 region of the transient Global Cerebral Ischemia rats hippocampus

Project description:Purpose：To identify piRNAs bound to Piwil2 in Sham,transient Global Cerebral Ischemia(tGCI) and transient Global Cerebral Ischemia(tGCI) with Hypoxic Postconditioning (HPC). Methods: Samples from CA1 subregion were lysed in 500 μl lysis buffer and centrifuged. After centrifugation, supernatant was incubated with monoclonal mouse antibody against Piwil2 (Santa Cruz, California, CA, USA), preincubated with Protein A/G Agarose. The beads were washed twice with lysis buffer. After quality check by Western blot, the RNA was extracted from the magnetic beads using Trizol reagent (Invitrogen). Then, the immunoprecipitated RNA was analyzed with piRNAs sequencing. Results: After tGCI, a total of 423 piRNAs interacted with Piwil2 in CA1 was upregulated after 26 h of reperfusion. Of the 423 piRNAs, 317 were significantly upregulated by more than 1.5-fold. Of the 317 piRNAs, 258 showed ≥2-fold change. Comparison between tGCI and HPC groups revealed that 401 piRNAs interacted with Piwil2 in CA1 were significantly downregulated after HPC, whereas only 7 piRNAs were found to be altered in all 3 groups studied (≥1.5-fold change). Conclusions: In our study, we identified a cohort of piRNAs in CA1 of rats. We demonstrated directly contrast changes of piRNAs interacted with Piwil2 in CA1 after tGCI, as compared to those in HPC rats. The results of the prediction showed that DNMT3A may be a potential common target of the 7 differentially expressed piRNAs interacted with Piwil2. Therefore, we focused on the expression of DNMT3A in CA1 after tGCI with or without HPC.

2023-01-18 | GSE163299 | GEO

RNA sequencing of HSkM myotubes deficient in DMD, full-length dystrophin (DP427) and utrophin reveals common transcriptomic alterations

Project description:iRNA approaches were used to knock down the expression of dystrophin (DMD), including its full-length isoform DP427, and utrophin (UTRN) genes. Specifically, iRNA-mediated knockdown of both DMD (full-length dystrophin DP427) and UTRN was performed in HSkM myotubes. It is known that the shorter dystrophin isoform DP71 compensates for full-length dystrophin DP427 in the early stages of myofiber differentiation in cell models of Duchenne muscular dystrophy. Accordingly, DP427-deficient and DP71/DP427-deficient HSkM myotubes exhibit distinct changes in the expression of genes involved in membrane integrity and cytoskeletal functions. RNA-sequencing analyses revealed overlapping transcriptomic alterations in these HSkM cell lines, which corresponded to observed phenotypic abnormalities such as increased membrane permeability and intracellular calcium levels, mitochondrial aggregation, elevated reactive oxygen species (ROS), enhanced cyto- and genotoxicity, and induction of apoptosis.

2026-01-27 | GSE303672 | GEO

Effect of Piwil2-KO, Trp53KO and Dnmt3a/3b-DKO on gene expression in germline stem cells.

Project description:To investigate the effect of Piwil2-KO, Trp53-KO and Dnmt3a/3b-DKO in germ stem cells, we performed RNA-seq of germline stem cells.

2026-08-20 | GSE242728 | GEO

Project description:full-length isoform of endosperm from Nongda3672

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Project description:Full-length isoform sequencing of A17 grapevine

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SON and its alternatively spliced isoforms control MLL complex-mediated H3K4me3 and transcription of leukemia-associated genes (ChIP-seq data)

Project description:Dysregulation of MLL complex-mediated histone methylation plays a pivotal role in gene expression associated with diseases, but little is known about cellular factors modulating MLL complex activity. Here, we report that SON, previously known as an RNA splicing factor, controls MLL complex-mediated transcriptional initiation. SON binds to DNA near transcription start sites, interacts with menin, and inhibits MLL complex assembly, resulting in decreased H3K4me3 and transcriptional repression. Importantly, alternatively spliced short isoforms of SON are markedly upregulated in acute myeloid leukemia. The short isoforms compete with full-length SON for chromatin occupancy, but lack the menin-binding ability, thereby antagonizing full-length SON function in transcriptional repression while not impairing full-length SON-mediated RNA splicing. Furthermore, overexpression of a short isoform of SON enhances replating potential of hematopoietic progenitors. Our findings define SON as a fine-tuner of the MLL-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.

2016-03-24 | GSE76910 | GEO

Transcriptional profiling of striatum from a zQ175 KI mouse model of Huntington's disease treated with HTT-10150 siRNA targeting full-length Htt

Project description:In this study we conducted a comprehensive transcriptional profiling of the striatum utilizing a zQ175 knock-in (KI) mouse model of Huntington's disease, which was treated with HTT-10150 siRNA specifically designed to target the full-length huntingtin (Htt) mRNA. Our investigation aimed to assess the impact of this intervention across different time points.

2026-05-05 | GSE284497 | GEO

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