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。

• Spatially resolved heterogeneity of lymphatic vasculature in the adult lung
  GSE325297Mus musculus2 个样本2026-10-29

  Background. Lung lymphatic drainage of interstitial fluid is essential for preventing pulmonary edema, a condition characterized by the accumulation of extravascular fluid that impedes respiratory gas exchange and can be fatal. Beyond fluid regulation, lung lymphatics also serve as conduits for immune cell trafficking, supporting both surveillance and mounting of host immune responses during lung infection. Despite their essential roles, the cellular and functional heterogeneity of lung lymphatic endothelial cells (LECs) remains poorly defined. Methods. Leveraging single nucleus sequencing technology, we investigated LEC heterogeneity in the homeostatic adult mouse lung. Results. We identified Stabilin-2 (Stab2), a Class H scavenger receptor, as a unique marker of a distinct subset of LECs in lymphatic vessels adjacent to pulmonary veins and in alveolar regions. A separate distinct subset of LECs is defined by expression of Polycystic Kidney and Hepatic Disease 1-Like-1 (Pkhd1l1), a component of stereocilia, and these lymphatic vessels are localized to the bronchovascular bundle. Conclusions. Our findings suggest that lung LECs are not a uniform population but instead compromise molecularly distinct and spatially organized lymphatic vessels, possibly with specialized functions. These results lay the groundwork for further studies geared towards understanding the roles of cellular origin in lung LEC heterogeneity, whether lymphatics in other organs have analogous spatial organization, and whether these disparate cells and vessels have functional differences in fluid homeostasis and immune regulation during pulmonary disease pathogenesis.

  单细胞空间转录组
• Smad4/SKI/SKIL-mediated repression of TGF-β signature is essential for a robust CD8 T cell response [viral vectors RNA-seq]
  GSE325275Mus musculus24 个样本2026-10-29

  Transforming growth factor-β (TGF-β) is an immunosuppressive cytokine that regulates both innate and adaptive immune responses. Earlier studies have shown that TGF-β plays a role in promoting T cell exhaustion during the later stages of chronic viral infection. In this study we examined the role of Smad4, a transcription factor downstream of TGF-β signaling, in regulating CD8 T cell responses during chronic lymphocytic choriomeningitis virus (LCMV) infection of mice. Surprisingly, we found that Smad4 acts as an intracellular repressor of TGF-β regulated genes during the early effector phase of the CD8 T cell response. Deletion of Smad4 in CD8 T cells resulted in a striking collapse of the virus-specific CD8 T cell response between day 5 to day 8 after LCMV clone 13 infection, with a 50–100-fold reduction in the number of LCMV-specific CD8 T cells at day 8. Both the stem-like and effector CD8 T cells generated in the absence of Smad4 have a dysregulated transcriptional and epigenetic program with elevated TGF-β signature. We show that Smad4 directly binds to several TGF-β target genes and other key genes involved in T cell survival and differentiation and regulates histone modifications and chromatin accessibility at these loci. Deletion of both TGF-β receptor II and Smad4 in antigen-specific CD8 T cells did not rescue the CD8 T cell response. This demonstrates that TGF-β target genes must be actively repressed by Smad4 intracellularly during the effector phase of the CD8 T cell response even in the absence of extracellular TGF-β signaling. By enforced expression of WT and mutant Smad4 in Smad4-KO CD8 T cells using retrovirus vectors, we show that the interaction between Smad4 and the TGF-β signaling repressors, SKI/SKIL, plays a critical role in antigen-specific CD8 T cells during the effector phase by turning off the TGF-β signature, whereas the interaction between Smad4 with TGF-β-induced phospho-Smad2/3 is dispensable at this stage. Consistent with this essential role of Smad4 during the effector phase, Smad4/SKI/SKIL interaction is also required for a robust CD8 T cell response against tumors and acute viral infection. Our findings documenting the striking requirement for Smad4-SKI-SKIL mediated restraint of TGF-β-associated program during the effector phase of the CD8 T cell response have implications for developing immunotherapeutic approaches against chronic viral infections and cancer.
• Smad4/SKI/SKIL-mediated repression of TGF-β signature is essential for a robust CD8 T cell response [kockout infection RNA-seq]
  GSE325274Mus musculus18 个样本2026-10-29

  Transforming growth factor-β (TGF-β) is an immunosuppressive cytokine that regulates both innate and adaptive immune responses. Earlier studies have shown that TGF-β plays a role in promoting T cell exhaustion during the later stages of chronic viral infection. In this study we examined the role of Smad4, a transcription factor downstream of TGF-β signaling, in regulating CD8 T cell responses during chronic lymphocytic choriomeningitis virus (LCMV) infection of mice. Surprisingly, we found that Smad4 acts as an intracellular repressor of TGF-β regulated genes during the early effector phase of the CD8 T cell response. Deletion of Smad4 in CD8 T cells resulted in a striking collapse of the virus-specific CD8 T cell response between day 5 to day 8 after LCMV clone 13 infection, with a 50–100-fold reduction in the number of LCMV-specific CD8 T cells at day 8. Both the stem-like and effector CD8 T cells generated in the absence of Smad4 have a dysregulated transcriptional and epigenetic program with elevated TGF-β signature. We show that Smad4 directly binds to several TGF-β target genes and other key genes involved in T cell survival and differentiation and regulates histone modifications and chromatin accessibility at these loci. Deletion of both TGF-β receptor II and Smad4 in antigen-specific CD8 T cells did not rescue the CD8 T cell response. This demonstrates that TGF-β target genes must be actively repressed by Smad4 intracellularly during the effector phase of the CD8 T cell response even in the absence of extracellular TGF-β signaling. By enforced expression of WT and mutant Smad4 in Smad4-KO CD8 T cells using retrovirus vectors, we show that the interaction between Smad4 and the TGF-β signaling repressors, SKI/SKIL, plays a critical role in antigen-specific CD8 T cells during the effector phase by turning off the TGF-β signature, whereas the interaction between Smad4 with TGF-β-induced phospho-Smad2/3 is dispensable at this stage. Consistent with this essential role of Smad4 during the effector phase, Smad4/SKI/SKIL interaction is also required for a robust CD8 T cell response against tumors and acute viral infection. Our findings documenting the striking requirement for Smad4-SKI-SKIL mediated restraint of TGF-β-associated program during the effector phase of the CD8 T cell response have implications for developing immunotherapeutic approaches against chronic viral infections and cancer.
• Two-phase NEUROD1 pioneer activity regulates temporal differentiation and subtype specification of auditory neurons [scRNA-Seq]
  GSE317781Mus musculus2 个样本2026-10-29

  The transcriptional and epigenetic mechanisms that govern neuronal subtype differentiation and diversification remain poorly defined, with auditory neurons among the least understood. Here, we investigate the role of the proneural factor NEUROD1 using a delayed, self terminating conditional knockout (Neurod1ST) mouse model that bypasses the early neuronal loss observed in germline mutants. By integrating NEUROD1 chromatin binding and histone profiling at E11.5 with transcriptomic analyses at E11.5, E14.5, and E18.5, we show that NEUROD1 is essential for coordinating the timing of neuronal differentiation. Neurod1 deletion prolongs progenitor-like states while prematurely accelerating differentiation and axonogenesis programs, reflecting the collapse of NEUROD1-dependent transcriptional networks and recruitment of compensatory pathways. NEUROD1 preferentially binds enhancers of neuronal differentiation genes and promotes their transition to active chromatin states, consistent with a pioneer factor function. Loss of Neurod1 disrupts these epigenomic transitions, alters neuronal migration and innervation trajectories, and ultimately leads to neuronal instability and apoptosis. During spiral ganglion neuron diversification, Neurod1ST neurons prematurely activate maturation markers and fail to generate Type Ic, instead adopting a Type Ib-like identity. These findings establish NEUROD1 as a central regulator that synchronizes differentiation, stabilizes neuronal identity, and shapes auditory neuron subtype diversity in the developing inner ear

  单细胞
• A CRISPR-Based Humanized Model Reveals Cooperative Role of STAG2 Loss in Familial GATA2-Deficient MDS Progression
  GSE317264Homo sapiens6 个样本2026-10-29

  Myelodysplastic syndrome is a heterogeneous myeloid malignancy driven by hematopoietic stem cell dysfunction, leading to ineffective hematopoiesis and cytopenias. Familial GATA2 deficiency is the most common cause of Myelodysplastic syndrome in adolescents, with progression often accelerated by co-occurring mutations, notably STAG2 loss-of-function. Using CRISPR/Cas9-mediated genome engineering in primary human fetal liver-derived hematopoietic stem cells and xenotransplantation in mice, we modeled GATA2-deficient Myelodysplastic syndrome with acquired STAG2 loss to investigate disease initiation and progression. While GATA2 deficiency alone had minimal short-term impact in our model, combined GATA2 and STAG2 loss increased hematopoietic stem cell maintenance and self-renewal, induced a myeloid-lineage bias, and expanded primitive progenitors. Single-cell transcriptional profiling revealed upregulation of stemness genes and inflammatory pathways, alongside downregulation of MYC targets. This humanized model faithfully recapitulates high-risk GATA2-deficient Myelodysplastic syndrome, providing mechanistic insight into how cooperative mutations drive stem cell expansion, inflammatory signaling, and myeloid skewing.

  单细胞
• Two-phase NEUROD1 pioneer activity regulates temporal differentiation and subtype specification of auditory neurons [snRNA-Seq]
  GSE315741Mus musculus2 个样本2026-10-29

  The transcriptional and epigenetic mechanisms that govern neuronal subtype differentiation and diversification remain poorly defined, with auditory neurons among the least understood. Here, we investigate the role of the proneural factor NEUROD1 using a delayed, self terminating conditional knockout (Neurod1ST) mouse model that bypasses the early neuronal loss observed in germline mutants. By integrating NEUROD1 chromatin binding and histone profiling at E11.5 with transcriptomic analyses at E11.5, E14.5, and E18.5, we show that NEUROD1 is essential for coordinating the timing of neuronal differentiation. Neurod1 deletion prolongs progenitor-like states while prematurely accelerating differentiation and axonogenesis programs, reflecting the collapse of NEUROD1-dependent transcriptional networks and recruitment of compensatory pathways. NEUROD1 preferentially binds enhancers of neuronal differentiation genes and promotes their transition to active chromatin states, consistent with a pioneer factor function. Loss of Neurod1 disrupts these epigenomic transitions, alters neuronal migration and innervation trajectories, and ultimately leads to neuronal instability and apoptosis. During spiral ganglion neuron diversification, Neurod1ST neurons prematurely activate maturation markers and fail to generate Type Ic, instead adopting a Type Ib-like identity. These findings establish NEUROD1 as a central regulator that synchronizes differentiation, stabilizes neuronal identity, and shapes auditory neuron subtype diversity in the developing inner ear

  单细胞
• Two-phase NEUROD1 pioneer activity regulates temporal differentiation and subtype specification of auditory neurons [CUTTag_E115]
  GSE315627Mus musculus12 个样本2026-10-29

  The transcriptional and epigenetic mechanisms that govern neuronal subtype differentiation and diversification remain poorly defined, with auditory neurons among the least understood. Here, we investigate the role of the proneural factor NEUROD1 using a delayed, self terminating conditional knockout (Neurod1ST) mouse model that bypasses the early neuronal loss observed in germline mutants. By integrating NEUROD1 chromatin binding and histone profiling at E11.5 with transcriptomic analyses at E11.5, E14.5, and E18.5, we show that NEUROD1 is essential for coordinating the timing of neuronal differentiation. Neurod1 deletion prolongs progenitor-like states while prematurely accelerating differentiation and axonogenesis programs, reflecting the collapse of NEUROD1-dependent transcriptional networks and recruitment of compensatory pathways. NEUROD1 preferentially binds enhancers of neuronal differentiation genes and promotes their transition to active chromatin states, consistent with a pioneer factor function. Loss of Neurod1 disrupts these epigenomic transitions, alters neuronal migration and innervation trajectories, and ultimately leads to neuronal instability and apoptosis. During spiral ganglion neuron diversification, Neurod1ST neurons prematurely activate maturation markers and fail to generate Type Ic, instead adopting a Type Ib-like identity. These findings establish NEUROD1 as a central regulator that synchronizes differentiation, stabilizes neuronal identity, and shapes auditory neuron subtype diversity in the developing inner ear
• Two-phase NEUROD1 pioneer activity regulates temporal differentiation and subtype specification of auditory neurons [scRNAseq_E115]
  GSE315597Mus musculus2 个样本2026-10-29

  The transcriptional and epigenetic mechanisms that govern neuronal subtype differentiation and diversification remain poorly defined, with auditory neurons among the least understood. Here, we investigate the role of the proneural factor NEUROD1 using a delayed, self terminating conditional knockout (Neurod1ST) mouse model that bypasses the early neuronal loss observed in germline mutants. By integrating NEUROD1 chromatin binding and histone profiling at E11.5 with transcriptomic analyses at E11.5, E14.5, and E18.5, we show that NEUROD1 is essential for coordinating the timing of neuronal differentiation. Neurod1 deletion prolongs progenitor-like states while prematurely accelerating differentiation and axonogenesis programs, reflecting the collapse of NEUROD1-dependent transcriptional networks and recruitment of compensatory pathways. NEUROD1 preferentially binds enhancers of neuronal differentiation genes and promotes their transition to active chromatin states, consistent with a pioneer factor function. Loss of Neurod1 disrupts these epigenomic transitions, alters neuronal migration and innervation trajectories, and ultimately leads to neuronal instability and apoptosis. During spiral ganglion neuron diversification, Neurod1ST neurons prematurely activate maturation markers and fail to generate Type Ic, instead adopting a Type Ib-like identity. These findings establish NEUROD1 as a central regulator that synchronizes differentiation, stabilizes neuronal identity, and shapes auditory neuron subtype diversity in the developing inner ear

  单细胞
• Two-phase NEUROD1 pioneer activity regulates temporal differentiation and subtype specification of auditory neurons
  GSE315509Mus musculus12 个样本2026-10-29

  The transcriptional and epigenetic mechanisms that govern neuronal subtype differentiation and diversification remain poorly defined, with auditory neurons among the least understood. Here, we investigate the role of the proneural factor NEUROD1 using a delayed, self terminating conditional knockout (Neurod1ST) mouse model that bypasses the early neuronal loss observed in germline mutants. By integrating NEUROD1 chromatin binding and histone profiling at E11.5 with transcriptomic analyses at E11.5, E14.5, and E18.5, we show that NEUROD1 is essential for coordinating the timing of neuronal differentiation. Neurod1 deletion prolongs progenitor-like states while prematurely accelerating differentiation and axonogenesis programs, reflecting the collapse of NEUROD1-dependent transcriptional networks and recruitment of compensatory pathways. NEUROD1 preferentially binds enhancers of neuronal differentiation genes and promotes their transition to active chromatin states, consistent with a pioneer factor function. Loss of Neurod1 disrupts these epigenomic transitions, alters neuronal migration and innervation trajectories, and ultimately leads to neuronal instability and apoptosis. During spiral ganglion neuron diversification, Neurod1ST neurons prematurely activate maturation markers and fail to generate Type Ic, instead adopting a Type Ib-like identity. These findings establish NEUROD1 as a central regulator that synchronizes differentiation, stabilizes neuronal identity, and shapes auditory neuron subtype diversity in the developing inner ear
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain
  GSE314268Mus musculus1,449 个样本2026-10-29

  This SuperSeries is composed of the SubSeries listed below.

  单细胞SuperSeries
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [scRNA-seq]
  GSE314217Mus musculus491 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [5mC]
  GSE314211Mus musculus479 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [5hmC]
  GSE314195Mus musculus479 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• Intestinal SAA1 and SAA2 regulate the balance between host inflammatory responses and metabolism
  GSE286869Mus musculus40 个样本2026-10-29

  Since their discovery as acute phase reactants, the SAA proteins have been an important focus of innate immunity research. Most SAA production is in the liver, and despite recent findings of their roles in promoting intestinal immunity, the precise functions of intestinal SAAs have not been well-studied. Validating and using an SAA1/2 double knock-out mouse, we found protective effects of SAA1 and SAA2 mitigating systemic and local inflammatory challenges, along with gene-, sex-, and location-specific responses to gut microbiota perturbations. SAA1 and SAA2 expression supports immunological protection in homeostasis but prioritizes metabolic activities under stress. From this work, we propose a new model in which SAA functions to regulate and integrate the interface between metabolism and host responses to inflammatory insults.

  扰动筛选
• Non-canonical RNA binding of the MYBL2 transcription factor promotes melanoma (CLIP-seq)
  GSE284545Homo sapiens3 个样本2026-10-29

  Melanoma originates from melanocytes, and the process of melanocyte malignant transformation is affected by various factors, including non-mutational gene alterations. MYBL2 is a transcription factor primarily known for its role in regulating cell cycle progression. In this study, we characterized that MYBL2 gain or amplification occurs in one fifth of the melanoma patients, and the aberrantly upregulated MYBL2 promotes melanoma growth while representing a melanoma vulnerability. Notably, MYBL2 can also binds RNA, and its oncogenic effect is mediated through its RNA binding function. Crosslinking-immunoprecipitation followed by high-throughput sequencing revealed that MYBL2 primarily binds protein-coding genes and introns. Interestingly, MYBL2 does not affect the RNA metabolism of its direct targets. Instead, its RNA binding function influences its association with chromatin and thereby rewiring the transcription program favoring poor patient survival. Surprisingly, we observed that MYBL2 binds RNA exclusively in melanoma cells, but not in melanocytes. This phenomenon is primarily due to the altered RNA background developed following melanoma transformation, while alternations within MYBL2 itself also involved in a lesser extent. Therefore, our work identified a novel oncogenic function of MYBL2 through its RNA binding activity, extending our current understanding of MYBL2 and highlighting a critical mechanism in melanoma progression.
• Non-canonical RNA binding of the MYBL2 transcription factor promotes melanoma (RNA-seq)
  GSE284544Homo sapiens12 个样本2026-10-29

  Melanoma originates from melanocytes, and the process of melanocyte malignant transformation is affected by various factors, including non-mutational gene alterations. MYBL2 is a transcription factor primarily known for its role in regulating cell cycle progression. In this study, we characterized that MYBL2 gain or amplification occurs in one fifth of the melanoma patients, and the aberrantly upregulated MYBL2 promotes melanoma growth while representing a melanoma vulnerability. Notably, MYBL2 can also binds RNA, and its oncogenic effect is mediated through its RNA binding function. Crosslinking-immunoprecipitation followed by high-throughput sequencing revealed that MYBL2 primarily binds protein-coding genes and introns. Interestingly, MYBL2 does not affect the RNA metabolism of its direct targets. Instead, its RNA binding function influences its association with chromatin and thereby rewiring the transcription program favoring poor patient survival. Surprisingly, we observed that MYBL2 binds RNA exclusively in melanoma cells, but not in melanocytes. This phenomenon is primarily due to the altered RNA background developed following melanoma transformation, while alternations within MYBL2 itself also involved in a lesser extent. Therefore, our work identified a novel oncogenic function of MYBL2 through its RNA binding activity, extending our current understanding of MYBL2 and highlighting a critical mechanism in melanoma progression.
• 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.
• TFIIIC regulates SMC complex binding and 3D DNA contacts between tRNA genes
  GSE352553Caenorhabditis elegans94 个样本2026-10-28

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• TFIIIC regulates SMC complex binding and 3D DNA contacts between tRNA genes [RNA-seq]
  GSE352551Caenorhabditis elegans15 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, ChIP-seq and mRNA-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.
• Lobe-specific liver transcriptional responses to portal vein ligation in wild-type and TNFR-knockout mice
  GSE352371Mus musculus22 个样本2026-10-28

  One-color mouse microarray expression profiles from untreated wild-type liver, ligated left and non-ligated right liver lobes after portal vein ligation, and an immediate postoperative sham reference. TNFR-knockout samples provide exploratory genotype comparisons.
• Drinking-Water 4,4'-Methylenedianiline Establishes a Longitudinally Tractable Mouse Model of Cholestatic Liver Injury
  GSE352312Mus musculus72 个样本2026-10-28

  This study examines time-dependent hepatic responses to 4,4'-methylenedianiline (MDA), a cholestatic hepatotoxicant, administered to male C57BL/6JJcl mice in drinking water. Liver RNA sequencing was performed in separate terminal cohorts sampled on Days 1, 2, 3, 4, and 8 after exposure to control tap water, thioacetamide (TAA; 300 mg/L), or MDA (750 mg/L). The dataset comprises 72 poly(A)-selected liver RNA-seq libraries and provides gene-level expression measurements for characterizing temporal transcriptional changes and comparing the MDA model with the TAA reference condition.
• 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.
• The analysis of mRNA and miRNA clarified the immune regulation mechanism of rainbow trout ( Oncorhynchus mykiss ) head kidney under IHNV infection
  GSE352277Oncorhynchus mykiss12 个样本2026-10-28

  The head kidney is a multifunctional organ that integrates hematopoiesis, antigen processing, immune signal transduction, antibody production and endocrine regulation to maintain the immune homeostasis of fish and resist pathogens. Several studies indicate that AS can produce functionally diverse protein isoforms and has become a vital regulatory mechanism in fish antiviral innate immunity. However, the mechanism of AS in antiviral response of head kidney is still unclear in rainbow trout. Accordingly, this study analyzed AS events in the head kidney of rainbow trout though RNA-seq. This study provided a theoretical basis for the study of AS response mechanism of rainbow trout antiviral, and also provided potential molecular targets for in-depth understanding of fish interferon signal transduction.
• QUAIL-100 Induces Distinct, Multifunctional γδ T Cell Responses with Enhanced Durability Compared to Zoledronic Acid in Post-HSCT Pediatric Leukemia Patients
  GSE352026Homo sapiens21 个样本2026-10-28

  γδ T cells mediate potent anti-leukemic and anti-infective immunity following allogeneic hematopoietic stem cell transplantation (HSCT); however, standard Vγ9Vδ2 activation with zoledronic acid (ZOL) induces rapid terminal differentiation and functional exhaustion, limiting sustained therapeutic efficacy. Pathogen-driven γδ T cell responses, including those elicited by cytomegalovirus (CMV), exhibit greater functional diversity and durability, providing a conceptual framework for multimodal activation strategies. QUAIL-100, a quadruple-attenuated Listeria monocytogenes strain (Lm ΔactA/ΔinlB/ΔribC/ΔribF), was evaluated as a novel γδ T cell activator that engages combinatorial signals including phosphoantigens, pathogen-associated molecular patterns, and co-stimulatory pathways.
• 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.
• Sodium butyrate alleviates metabolic dysfunction-associated steatotic liver disease by activating PPAR-γ/FUNDC1‑mediated mitophagy to inhibit ferroptosis
  GSE351765Mus musculus18 个样本2026-10-28

  This study aims to elucidate the protective effects and underlying molecular mechanisms of sodium butyrate (NaB), a gut microbiota-derived metabolite, against metabolic dysfunction-associated steatotic liver disease (MASLD). Using high-fat diet (HFD)-fed mice and palmitic acid (PA)-treated hepatocytes, the study seeks to determine whether NaB alleviates hepatic steatosis and injury by restoring iron and redox homeostasis, upregulating glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), and suppressing ferroptosis. It further aims to investigate whether these protective effects depend on FUN14 domain-containing protein 1 (FUNDC1)-mediated mitophagy, and to identify peroxisome proliferator-activated receptor gamma (PPAR-γ) as an upstream regulator of FUNDC1 expression and mitophagy. Collectively, this study aims to define a PPAR-γ/FUNDC1-mitophagy-ferroptosis axis through which NaB protects against MASLD, thereby linking a gut microbial metabolite to hepatic mitochondrial quality control and providing a potential therapeutic target and nutritional intervention strategy for MASLD.
• Tau A152T risk variant drives distinct cell type transcriptional signatures in AD and PSP
  GSE350921Homo sapiens28 个样本2026-10-28

  The A152T point mutation is a rare genetic variant in the tau gene (MAPT) that is linked to risk of Alzheimer’s disease (AD) and frontotemporal dementia spectrum disorders, including progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). To uncover mechanisms through which the A152T variant contributes to risk of tauopathy, we performed single-nucleus RNA sequencing (snRNA-seq) on postmortem brain tissue collected from A152T carriers and pathology-matched non-carriers with either AD or PSP, along with age-matched controls. These efforts revealed that despite similar cell type composition across groups, A152T carriers exhibited distinct cell type-specific transcriptional changes in both AD and PSP. Differential expression analysis identified excitatory neurons, oligodendrocytes and astrocytes as the most affected cell populations in AD and PSP, and these same cell types showed the strongest A152T-specific changes. These findings identify transcriptional alterations that differentiate sporadic AD and sporadic PSP from AD-A152T and PSP-A152T, as well as shared molecular signatures unique to A152T carriers in both PSP and AD. Donor-level pseudobulk analyses showed broad directional support with the single-nucleus findings, although the proportion of donor-supported genes varied across cell type and comparison. Importantly, merging sporadic and A152T cases into a single disease group was found to mask transcriptional differences in several cell types in both AD and PSP, indicating divergence in transcriptional signature and highlighting the importance of screening for genetic risk variants like A152T in snRNA-seq data from human cohorts.

  单细胞
• Bulk RNA-seq profiling of regulatory and effector T cells of C57BL/6 mice
  GSE350087Mus musculus12 个样本2026-10-28

  Regulatory T cells (Tregs) maintain immune tolerance, whereas effector T cells (Teffs) mediate immune responses. Imbalance between Tregs and Teffs may contribute to immune dysregulation in type 1 diabetes mellitus (T1DM). Here, we performed bulk RNA sequencing of splenic Tregs and Teffs from control and streptozotocin-induced diabetic C57BL/6 mice to characterize disease-associated transcriptional alterations. Tregs in T1DM exhibited enhanced proliferative, effector-associated, and metabolic transcriptional programs, alongside reduced expression of genes involved in immunoregulation, lineage maintenance, tissue homing, metabolic fitness, and stress adaptation. Meanwhile, Teffs adopted a hyperactivated, but functionally imbalanced transcriptional state characterized by enhanced proliferative and inflammatory programs alongside dysregulated metabolic, signaling, and migratory functions. This study identified transcriptional alterations of splenic Tregs and Teffs in control and STZ-induced diabetic C57BL/6 mice, providing candidate molecular markers for further investigation of T-cell dysregulation in T1DM.
• Paired Transcriptomic Profiling Identifies Shared Liver Metas-tasis-Associated Molecular Features in Colorectal Cancer
  GSE347316Homo sapiens12 个样本2026-10-28

  Colorectal cancer liver metastasis (CCLM) is closely associated with poor patient prognosis, yet patient-specific molecular heterogeneity complicates the identification of recurrent molecular changes during metastasis. To address this, we performed RNA sequencing on paired primary tumors and liver metastases synchronously resected from six patients and analyzed gene expression changes using a paired design that accounted for interpatient variability. This analysis identified differentially expressed genes (DEGs) and metastasis-associated pathways through functional enrichment analysis and Gene Set Enrichment Analysis (GSEA). The reproducibility of these changes was further assessed across multiple independent publicly available transcriptomic datasets from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). Selected candidate genes were additionally evaluated in a metastasis-selected colorectal cancer cell model, in which several genes showed expression changes consistent with the transcriptomic findings. Together, these results indicate that recurrent molecular changes accompany CCLM despite substantial interpatient heterogeneity and provide a strategy for identifying metastasis-associated molecular features and potential therapeutic targets

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• Furan fatty acids reprogram hepatic lipid metabolism via acyl-CoA conjugates in obesity.
  GSE347256Mus musculus24 个样本2026-10-28

  Dietary fish oil (FO) and omega-3 fatty acids are associated with cardiometabolic benefits, yet their molecular mediators remain incompletely defined. Furan fatty acids (FuFAs), a distinct lipid class enriched in FO, have emerged as potential regulators of metabolic health. Here, we identify and quantify FuFA species in prescription omega-3 formulations and natural fish oils, and synthesize structurally engineered analogs designed to isolate antioxidant activity and β-oxidation susceptibility from FuFA bioactivity. In a diet-induced obesity mouse model, both natural and synthetic FuFAs reduced fat accumulation and inflammatory markers, while 11U3-2M additionally produce significant improvement in glucose tolerance, dyslipidemia, and hepatic steatosis. The superior activity of 11U3-2M reflects the stable accumulation of its acyl-CoA conjugate that activates peroxisome proliferator-activated receptor alpha (PPARα) signaling and allosterically inhibits acetyl-CoA carboxylases (ACCs) to reprogram hepatic lipid metabolism. These findings position FuFAs as functional dietary lipids contributing to fish oil’s metabolic effects and define fatty acid structural determinants that govern hepatic metabolic activity.