GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• Effect of tPA and Annexin A2 receptor inhibition on neutrophils gene expression after ischemic stroke
  GSE246580Rattus norvegicus9 个样本2026-10-29

  Acute ischemic stroke is a life-threating disease worldwide and tissue plasminogen activator (tPA) is currently the only drug approved for thrombolytic treatment. tPA has been reported to interact with neutrophils and have an impact on its activity. The project carried out the RNA sequencing on neutrophils, which aimed to investigate the mRNA expression change of neutrophils in response to tPA infusion and Annexin A2 receptor inhibition after ischemic stroke.
• Transcriptomic profiling of ECV304 cells under normoxic, hypoxic, and hypoxia-tolerant conditions
  GSE352293Homo sapiens9 个样本2026-10-28

  This study investigated transcriptomic changes in ECV304 cells under normoxic, hypoxic, and hypoxia-tolerant conditions. Cells were assigned to three groups, each with three biological replicates. The hypoxia group was exposed to 3% O2 for 24 h, whereas hypoxia tolerance was established by repeated hypoxia-reoxygenation cycles (cycle details to be confirmed). Total RNA was subjected to paired-end RNA sequencing on an Illumina NovaSeq 6000. The dataset supports comparisons of gene expression patterns associated with acute hypoxia and hypoxia tolerance.
• Long-read sequencing reveals transcriptome diversity in the development
  GSE352002Mus musculus3 个样本2026-10-28

  The thymus is recognized as one of the most pivotal endocrine and immune organs within the human body. This study investigated the thymus transcriptome using PacBio single-molecule long-read sequencing technology, addressing the limitations of current transcriptome analyses. By sequencing mouse thymus tissue at critical postnatal developmental stages (7 days, 4 weeks, and 4 months), we performed the first long-read full-length isoform survey of postnatal mouse thymus development. A total of 136,104 transcripts were identified and mapped to 16,667 annotated genes and 22,465 previously unannotated transcript loci. Comparative analysis across the three datasets revealed differences in transcript composition, alternative splicing patterns, and fusion transcript detection. These comparisons provide a descriptive overview of transcriptome diversity across postnatal developmental stages, while the biological mechanisms underlying these differences require further investigation. Selected exon skipping events and RNA fusion events were experimentally validated. In addition, more long non-coding RNAs were characterized, offering new perspectives on the regulatory networks underlying immune function and development. In summary, PacBio long-read sequencing provides a valuable resource for characterizing full-length transcript isoforms and transcriptome complexity in the postnatal mouse thymus.
• Super-enhancer NR125945 drives prostate cancer malignancy via long-range chromatin interactions [CUT&Tag]
  GSE346319Homo sapiens3 个样本2026-10-28

  Genetic susceptibility plays an essential role in prostate cancer (PCa) risk, while the functional mechanisms underlying several classic risk loci remain largely uncharacterized. Here, we identified a PCa specific super-enhancer within 1q42.3 locus, termed NR125945-SE. Through comparative H3K27ac ChIP-seq analysis, we observed that NR125945-SE is highly active in PCa cells compared to normal controls. NR125945-SE contributes to PCa malignant progression. Mechanistically, integrative analysis combining RNA-seq and 4C-seq data revealed that NR125945-SE regulates the expression of CAPN2 and KRT19 through long-range chromatin interactions. Furthermore, we demonstrated that NR125945-SE activity is mediated by the cooperative binding of multiple transcription factors. In summary, our findings provide insights into a functional epigenetic element within a classic genetic risk locus, proposing a mechanism by which super-enhancer-mediated regulation promotes prostate cancer progression.
• Super-enhancer NR125945 drives prostate cancer malignancy via long-range chromatin interactions [4C-Seq]
  GSE346318Homo sapiens3 个样本2026-10-28

  Genetic susceptibility plays an essential role in prostate cancer (PCa) risk, while the functional mechanisms underlying several classic risk loci remain largely uncharacterized. Here, we identified a PCa specific super-enhancer within 1q42.3 locus, termed NR125945-SE. Through comparative H3K27ac ChIP-seq analysis, we observed that NR125945-SE is highly active in PCa cells compared to normal controls. NR125945-SE contributes to PCa malignant progression. Mechanistically, integrative analysis combining RNA-seq and 4C-seq data revealed that NR125945-SE regulates the expression of CAPN2 and KRT19 through long-range chromatin interactions. Furthermore, we demonstrated that NR125945-SE activity is mediated by the cooperative binding of multiple transcription factors. In summary, our findings provide insights into a functional epigenetic element within a classic genetic risk locus, proposing a mechanism by which super-enhancer-mediated regulation promotes prostate cancer progression.
• Transcriptomic Analysis Identifies Candidate Molecular Mechanisms Underlying SCF+G-CSF-Reduced Neuropathology in Aged APP/PS1 Mice
  GSE345694Mus musculus8 个样本2026-10-28

  Alzheimer’s disease (AD) is characterized by amyloid pathology, neuroinflammation, and cognitive decline. Our previous studies demonstrated that combined treatment with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) reduces AD pathology in APP/PS1 mice. In this study, we performed transcriptomic analysis to investigate candidate molecular mechanisms underlying the effects of SCF+G-CSF in aged APP/PS1 mice. Aged APP/PS1 mice received daily subcutaneous injections of SCF+G-CSF or vehicle for 12 days, and age-matched wild-type mice served as controls. Gene-chip analysis identified 27 differentially expressed genes in SCF+G-CSF-treated versus vehicle-treated APP/PS1 mice and 89 differentially expressed genes in APP/PS1 versus wild-type mice. The findings identify treatment-associated transcriptional changes involving immune regulation, metal ion homeostasis, and other molecular pathways potentially relevant to AD pathology.
• Real-world river water organic pollutant mixture induces ovarian hyperandrogenism via aryl hydrocarbon receptor activation
  GSE343592Mus musculus9 个样本2026-10-28

  Humans are exposed to complex mixtures of endocrine-disrupting chemicals (EDCs) in the real world. Most prior studies, however, focus on individual EDCs. Here, we investigated the ovarian impact of organic pollutant mixtures extracted from the Raritan River, a heavily industrialized watershed in central New Jersey, using a three-dimensional (3D) in vitro ovarian follicle culture system. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UHPLC-HRMS) identified organic pollutant mixtures dominated by alkylphenols, pharmaceuticals, per- and polyfluoroalkyl substances (PFAS), and phthalates, together with previous reports demonstrating that the Raritan River also contains hydrophobic persistent organic pollutants (POPs), including polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and dioxins. In vitro exposure to the Raritan River-derived EDC mixture did not affect follicle growth and ovulation but dose-dependently increased preovulatory testosterone secretion while suppressing postovulatory progesterone production. Transcriptomic analysis, Gene set enrichment analysis (GSEA), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and in situ RNA hybridization revealed widespread reprogramming of follicular somatic cell gene expression, including altered steroidogenic pathways and activation of aryl hydrocarbon receptor (AhR) signaling. An established AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), reproduced the phenotype of EDC mixture-induced hyperandrogenism, which was reversed by a selective AhR inhibitor. Together, this study demonstrates that real-world EDC mixtures, particularly AhR-activating chemicals, disrupt ovarian steroidogenesis and induce hyperandrogenism, highlighting EDC mixtures as an underrecognized mechanism linking aquatic pollution to impaired women’s reproductive health.
• ChipExo to determine sites of Wor1 binding Candida tropicalis opaque cells
  GSE343266Candida tropicalis4 个样本2026-10-28

  The fungal human pathobionts Candida albicans and Candida tropicalis exhibit switching between the sterile "white" state and the mating-competent "opaque" state. In C. albicans, extensive differences in gene expression are observed between white and opaque states. Here, we examined the global gene expression programs in C. tropicalis white and opaque states in strain AM2005/0093. We also examined gene expression programs in a second C. tropicalis isolate (ATCC3419 ST-120) that exhibits tristable switching between white, hybrid and opaque states. Our results reveal both similarities and differences between white-opaque programs between the two C. tropicalis strains.
• Hypoxia-Driven CA2 Promotes Trophoblast Dysfunction in Preeclampsia
  GSE342874Homo sapiens6 个样本2026-10-28

  Objective: Explore the potential function of Carbonic Anhydrase 2 (CA2) in the pathophysiology of preeclampsia. Methods: Peripheral blood and placental samples were collected from healthy pregnant women and patients with preeclampsia. Placental CA2 expression was validated in independent clinical cohorts and experimental mouse models. HTR-8/SVneo cells was cultured and transfected with a CA2 overexpression plasmid to evaluate trophoblast dysfunction. Bulk RNA sequencing was performed to identify downstream genes associated with CA2 overexpression, followed by VEGFA rescue experiments. Hypoxia-related regulation of CA2 was investigated. Lipid nanoparticle (LNP)-encapsulated siRNA against CA2 was constructed in an L-NAME-induced PE model to evaluate therapeutic effects. Results: CA2 expression was significantly increased in placental tissues and maternal serum from women with PE and was also elevated in experimental PE mouse models.CA2 predominantly localized in trophoblast cells, and correlated positively with serum creatinine and urea and correlated negatively with fetal birth weight. CA2 overexpression markedly suppressed trophoblast proliferation, migration, and invasion, without affecting apoptosis. Transcriptomic analysis suggested that vascular endothelial growth factor A (VEGFA) acted as a downstream mediator of CA2, and VEGFA overexpression partially rescued CA2-induced trophoblast dysfunction. CA2 expression was upregulated under hypoxic conditions and regulated by hypoxia-inducible factor-1α (HIF-1α). LNP-mediated CA2 silencing partially improved placental structure and fetal outcomes in vivo. Conclusion: CA2 is upregulated in the preeclamptic placenta and is associated with placental dysfunction and adverse fetal outcomes. Mechanistically, CA2 may act downstream of HIF-1α and contribute to trophoblast dysfunction partly through modulation of VEGFA signaling, and CA2 silencing partially improved maternal and fetal outcomes, highlighting CA2 as a potential therapeutic target for preeclampsia.
• Glutamine Metabolism as a Rheostat of CD4+ T cell Pathogenic Function in Metabolic Dysfunction-Associated Steatotic Liver Disease
  GSE341871Mus musculus7 个样本2026-10-28

  Metabolic dysfunction-associated steatotic liver disease (MASLD) severity is independently linked with pathogenic CD4+ T cell responses and skewed hepatic glutamine (Gln) metabolism. Whether these processes interact to drive disease progression remains unclear. Here, we identify hepatic Gln depletion as a key feature of steatohepatitis that is linked with increased hepatic CD4+ T cell inflammation and hepatocellular damage in humans. In complementary mouse models, both total hepatic and hepatic CD4+ T cell Gln levels were similarly reduced. Restoration of hepatic Gln through supplementation selectively restrained hepatic CD4+ T cell inflammatory programs and alleviated hepatocellular damage and disease severity. Mechanistically, T cell-intrinsic Gls1-mediated glutaminolysis limited O-GlcNAcylation to dampen pathogenic CD4+ T cell inflammation. Importantly, Gln treatment dampened CD4+ T cell-mediated injury in human liver organoids. Together, these findings establish hepatic CD4+ T cell-intrinsic Gln metabolism as a critical rheostat of pathogenic inflammation in MASLD and invoke metabolism-targeted strategies to restrict disease progression.
• TFIIIC regulates SMC complex binding and 3D DNA contacts between tRNA genes [Hi-C]
  GSE338222Caenorhabditis elegans7 个样本2026-10-28

  Transcription factor IIIC (TFIIIC) is a multi-subunit protein complex that recruits RNA polymerase III (Pol III) to the majority of its target genes. Evolutionarily conserved overlap between TFIIIC binding sites and the structural maintenance of chromosomes (SMC) complexes suggested a role for TFIIIC in SMC regulation and 3D organization of eukaryotic genomes; but the evidence has remained largely correlational due to the essential role of TFIIIC in recruiting RNA Pol III for transcription initiation. Here, we directly tested the function of TFIIIC in SMC complex regulation by using auxin inducible protein degradation in C. elegans. We performed Hi-C and ChIP-seq analyses upon acute depletion of TFTC-3, an essential TFIIIC subunit, and RPC-1, the catalytic subunit of RNA Pol III. Our results showed that TFIIIC is required for cohesin and condensin complexes binding to tRNA genes. TFIIIC is also required for increasing 3D contacts between distant tRNA genes located on the same or different chromosomes. Depletion of individual SMC complexes did not significantly reduce the tRNA gene contacts, suggesting redundancy or an independent mechanism mediating these contacts. Together, our study supports an RNA Pol III independent function for TFIIIC in regulating multiple SMC complexes, as well as the 3D organization of tRNA genes.
• Transcriptomic profiling of primary rat nucleus pulposus cells following MDL-800 treatment
  GSE337900Rattus norvegicus7 个样本2026-10-28

  Intervertebral disc degeneration is associated with age-related molecular and epigenetic alterations in nucleus pulposus (NP) cells. SIRT6 is an NAD⁺-dependent histone deacetylase implicated in chromatin regulation, DNA repair, and cellular homeostasis. MDL-800 is a selective allosteric activator of SIRT6. To investigate the transcriptional effects of SIRT6 activation, primary rat nucleus pulposus cells were treated with MDL-800 or vehicle control, and genome-wide RNA sequencing was performed. Differential gene expression analysis was used to identify transcriptional changes associated with pharmacological activation of SIRT6 in nucleus pulposus cells.
• ATAC-seq analysis of chromatin accessibility in rat nucleus pulposus cells following MDL-800 treatment
  GSE337792Rattus norvegicus6 个样本2026-10-28

  Intervertebral disc degeneration is associated with altered cellular homeostasis and epigenetic regulation. To investigate chromatin accessibility changes induced by SIRT6 activation, primary rat nucleus pulposus cells were treated with the SIRT6 activator MDL-800 and analyzed by ATAC-seq. Three biological replicates were generated for untreated control cells and MDL-800-treated cells. Raw sequencing data were deposited in the Sequence Read Archive (SRA), and processed differential chromatin accessibility results are provided.
• A circRNA platform for safe partial reprogramming and rejuvenation of mesenchymal stem cells without pluripotent conversion
  GSE333770Homo sapiens9 个样本2026-10-28

  Mesenchymal stem cells (MSCs) are widely used in cell therapies; however, replicative senescence during in vitro expansion limits their potency and consistency. Partial reprogramming has emerged as a promising strategy to rejuvenate aged cells, yet concerns regarding unintended pluripotent conversion have hindered its translational application. Here we developed a circular RNA (circRNA)-based platform enabling safe partial reprogramming and rejuvenation of MSCs. We generated a lipid nanoparticle (LNP)-delivered circRNA co-expressing OCT4, SOX2, and KLF4 (circ-OSK) to achieve transient and coordinated expression of partial reprogramming factors without genomic modification in MSCs.
• Immune landscape and intercellular crosstalk in the cornea of an autoimmune-mediated dry eye disease
  GSE333335Mus musculus2 个样本2026-10-28

  We have employed a single cell sequencing approach using 10x genomis scRNAseq to study the immune composition in autoimmune induced dry eye cornea. This study found a diverse immune cell composition, including T cells, B cells, neutrophils and macrophages. Moreover, we characterized cell signaling communication networks between immune and epithelial and stormal cells.

  单细胞
• Tissue engineering polymeric formulations enable lymphangiogenesis for myocardial repair
  GSE330459Rattus norvegicus6 个样本2026-10-28

  We performed single-cell RNA sequencing (scRNA-seq) to profile the transcriptional landscape of ventricular tissue in a Sprague-Dawley rat model of myocardial ischemia/reperfusion (I/R). Two groups were analyzed: an I/R control group and a group treated with the pro-lymphangiogenic polymeric formulation PD-DN. Ventricular tissues were collected from both groups at three time points post-injury — 3, 5, and 7 days — to capture the temporal dynamics of cardiac repair. Single-cell suspensions were processed using the 10x Genomics Chromium platform with Illumina NovaSeq sequencing. Our analysis revealed temporally orchestrated changes in endothelial, immune, and fibroblast cell populations. The data provide insights into how PD-DN-driven lymphangiogenesis reprograms the cardiac microenvironment to facilitate functional recovery.

  单细胞
• Molecular mechanism of augmentation of oncogenic activity of MYC by TAF2 in HCC
  GSE329914Homo sapiens6 个样本2026-10-28

  The oncogenes MYC and TAF2 (TATA-box binding protein associated factor 2) are frequently overexpressed and co-amplified in many cancers, including Hepatocellular Carcinoma (HCC). We recently demonstrated that overexpression of TAF2 in mouse liver markedly augments MYC -induced HCC. MYC is a transcription factor. TAF2 is a component of transcription factor IID (TFIID) and functions as a transcription co-factor. We hypothesized that TAF2 modulates gene regulation by MYC, contributing to augmentation of MYC’s oncogenic activity. To test this hypothesis, we generated stable HepG2 cell lines overexpressing TAF2, MYC, or both. Combined overexpression significantly augmented in vitro proliferation, migration and invasion compared to the overexpression of either gene alone. We performed RNA-sequencing and CUT&RUN (cleavage under targets & release using nuclease) to identify MYC-regulated genes that are induced only by TAF2 overexpression. RASGEF1A (RasGEF domain family member 1A), a guanine exchange factor activating Ras, was significantly induced by TAF2 and MYC overexpression. Consequently, the MEK/ERK pathway was robustly activated in cells co-overexpressing TAF2 and MYC, rendering them uniquely sensitive to MEK inhibitor Trametinib. These findings suggest that HCC patients with TAF2 and MYC overexpression might benefit from targeted treatment with MEK inhibitors.
• The Circadian Clock controls Hepatic Inflammation in Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) [Multi-omics]
  GSE327440Mus musculus6 个样本2026-10-28

  The circadian clock dictates time-of-day dependent gene, protein expression, and metabolite levels to ensure liver homeostasis. Circadian misalignment is implicated in the development of various metabolic disorders, but its contribution to the progression of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) toward Metabolic dysfunction-Associated Steatohepatitis (MASH) remains poorly understood. Here, we aimed to dissect the role of the circadian clock in MASH development. Using an environmental model of chronic circadian misalignment, combined with metabolic and immune phenotyping, single nuclei transcriptomics and lipidomic profiling, we investigated the role of the clock in MASLD development and hepatic inflammation. To dissect the specific contribution of the immune clock, we used a genetic model overexpressing the clock component Rev-erbα in myeloid cells. Chronic circadian misalignment combined with a high-fat, high-sucrose, cholesterol-enriched (HFHSC) diet markedly amplified hepatic inflammation, characterized by the upregulation of pro-inflammatory genes and increased immune cell infiltration, including the expansion of lipid-associated macrophages (LAMs). Although circadian misalignment did not worsen glucose intolerance or hepatic steatosis, it altered hepatic metabolic gene expression, reflecting a broad reprogramming of immune and metabolic pathways. The circadian clock controls both FA profile and inflammatory process, and its misalignment aggravates MASLD by increasing liver inflammation. Targeting circadian regulators such as Rev-erbα in myeloid cells may offer a promising therapeutic avenue for controlling liver inflammation in MASLD.

  多组学
• Gene expression analysis of HepG2 cells overexpressing MYC or TAF2 and MYC
  GSE327282Homo sapiens6 个样本2026-10-28

  Taf2 is a transcription co-factor and a member of TFIID complex. MYC is a transcription factor. Overexpression of TAF2 markedly augments MYC-induced hepatocellular carcinoma (HCC) in mice. It is hypothesized that overexpression of TAF2 might modulate MYC-regulated gene expression and thereby increase oncogenic function of MYC. To test this hypothesis, we generated an in vitro system in which we established stable clones in HepG2 cells overexpressing MYC and both TAF2 and MYC (Hep-MYC and Hep-TAF2-MYC, respectively). The analysis shows that overexpression of TAF2 results in a significant increase in MYC-mediated expression of genes with oncogenic properties.
• Periplocin Targets Low Density Lipoprotein Receptor-Related Protein 4 and Protects Against Osteoarthritis
  GSE325883Homo sapiens9 个样本2026-10-28

  Osteoarthritis (OA) is recognized as the most common chronic joint disease, characterized primarily by the degeneration of articular cartilage. Periplocin, a cardiotonic steroid isolated from Periploca forrestii, has been proven to be involved in anti-inflammatory responses. However, the role and mechanism of periplocin in OA have not been confirmed.
• Nanostring transcriptomics profiling of wild type and PIK3CA knockin bladder cancer cells
  GSE323369Homo sapiens6 个样本2026-10-28

  Profiling of metabolic genes using nanostringtargeted transcriptomics to determine oncogenic metabolic rewiring of PIK3CA mutation in bladder cancer cells
• Impact of sacubitrilat-cGMP-PRKG1 signaling on microtubule detyrosination in cardiomyocytes
  GSE317137Homo sapiens8 个样本2026-10-28

  Microtubule detyrosination (dTyr-tub) and re-tyrosination (Tyr-tub) on the C-terminal residue of alpha-tubulin are mediated by the vasohibin (VASH)-small vasohibin-binding protein (SVBP) complex and tubulin tyrosine ligase (TTL), respectively. The level of dTyr-tub is elevated in heart failure (HF), and reducing this modification improves cardiac function, suggesting HF therapies may modulate it. We investigated whether components of the angiotensin receptor–neprilysin inhibitor LCZ696 affect dTyr-tub in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and explored the underlying mechanisms. Endothelin-1 (ET1) induced hypertrophy and increased dTyr-tub in wild-type but not in SVBP-deficient hiPSC-CMs and did not further enhance hypertrophy in TTL-deficient hiPSC-CMs. Both sacubitrilat and valsartan blocked ET1-induced hypertrophy, but only sacubitrilat prevented dTyr-tub accumulation. Sacubitrilat modestly stabilised atrial natriuretic peptide in culture medium, increased intracellular guanosine 3',5'-cyclic monophosphate (cGMP), augmented the phosphorylation of vasodilator stimulated phosphoprotein (Ser239), a substrate of cGMP-dependent protein kinase 1 (PRKG1), and lowered dTyr-tub level in hiPSC-CMs. Conversely, PRKG1 inhibition or knockdown increased dTyr-tub level. PRKG1A phosphorylated VASH1-WT but not a phosphomimetic VASH1 (VASH1-7E) in vitro. In addition, VASH1-7E did not interact with microtubules and did induce detyrosination. We overexpressed VASH1-WT, -7E and a dephosphorylated form of VASH1 (VASH1-7A) in newly generated VASH1-deficient hiPSC-CMs. The level of dTyr-tub was lower in VASH1-7E- than in VASH1-WT or VASH1-7A-expressing cells. In conclusion, sacubitrilat reduced dTyr-tub levels via PRKG1 activation and VASH1 phosphorylation, a mechanism that may contribute to the therapeutic benefit of LCZ696 in patients with HF.
• Med1 Deletion Reprograms Dental Epithelium into Primitive Hair-Forming Epidermal Architecture via Trp63 Driven Epigenetic Alterations
  GSE316847Mus musculus1 个样本2026-10-28

  Ectodermal fate decisions between tooth enamel and skin hair are governed by transcription factors, epigenetic mechanisms, and tissue architecture. Deletion of the Mediator subunit Med1, which links enhancer activity to transcriptional output, induces a striking lineage conversion characterized by ectopic hair formation in mouse incisors. Here, we define the cellular, transcriptional, and epigenetic mechanisms underlying this process. Single-cell and spatial transcriptomic analyses reveal extensive remodeling of the incisor epithelium following Med1 deletion, whereby dental pre-ameloblasts and SI cells convert into hair germ–like populations resembling ancestral hair-initiating cells while retaining dental identity. Epidermal fate is driven by the master regulator Trp63, enabling hair formation without follicles distinguishing this process from canonical skin hair regeneration. Mechanistically, epigenetic changes occur in which TRP63 co-localized with alternative MED12-containing enhancers to activate itself and downstream epidermal genes. Together, these findings suggest that Med1 loss promotes hair formation through unique reprogramming to an evolutionarily primitive epidermal state rather than direct trans-differentiation to skin epithelium, providing new insights in ectodermal plasticity.

  单细胞空间转录组
• Soundwave Priming Enhances the Therapeutic Efficacy of Mesenchymal Stromal Cell–Derived Extracellular Vesicles in Acute Respiratory Distress Syndrome
  GSE316041Mus musculus8 个样本2026-10-28

  Our findings provide a robust model in which the UC-EVs cargo modulated by pFUS priming drives improved mitochondrial energetics, barrier protection, and resolution of inflammation, supporting the translational potential of pUC-EVs.
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7
  GSE314741synthetic construct8 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [incellSHAPEPool1]
  GSE314422Homo sapiens4 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [invitroSHAPEPool1]
  GSE314421Homo sapiens2 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [directRNA]
  GSE314420Homo sapiens7 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [invitroSHAPEPool1]
  GSE314419Homo sapiens4 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [invitroBIDpool2]
  GSE314391Homo sapiens8 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

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