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。

• Single-cell RNA sequencing of appendiceal adenocarcinoma reveals a low proportion of epithelial cells and a fibroblast enriched tumor microenvironment
  GSE352702Homo sapiens4 个样本2026-10-31

  Appendiceal adenocarcinoma (AA) is an understudied gastrointestinal malignancy. Treatment is guided by its proximal counterpart, colorectal cancer (CRC), despite recent studies demonstrating AA’s unique mutational landscape and poor response to CRC chemotherapy. As the first application of single-cell technology to AA these data provide insight into the intratumor heterogeneity of AA and highlight the important contribution of the tumor microenvironment in this orphan disease. These results also reinforce multiple observations that AA is a unique disease entity from CRC and targeting the tumor microenvironment should be considered as a therapeutic strategy.

  单细胞
• Local and circulating cytotoxic CD4 T cells are early markers of disease activity in pediatric Crohn’s disease
  GSE352630Homo sapiens8 个样本2026-10-31

  Inflammatory bowel disease (IBD) requires improved molecular and cellular stratification to guide therapy. In the PREDICT study, we profiled intestinal and blood T cells from treatment-naïve pediatric patients with IBD, disorders of gut–brain interaction controls, and healthy donors using single-cell RNA sequencing. Across 107 participants, we identify a population of clonally expanded cytotoxic CD4 T cells (CD4 CTL) enriched in the inflamed gut of patients with Crohn's disease (CD) and ulcerative colitis. Cell–cell interaction analyses and validation in a mouse model implicate IL-27 in CD4 CTL differentiation. Elevated CD4 CTL frequencies in gut and peripheral blood at diagnosis are associated with subsequent poor outcome of anti-TNF therapy in pediatric CD. Findings in our identification cohort are validated in an independent cohort and through reanalysis of published datasets. Blood CD4⁺CXCR6⁺CD27⁻ T cells displayed a CD4 CTL transcriptional phenotype, supporting CD4 CTLs as a candidate blood-accessible biomarker for treatment stratification.

  单细胞
• Transcriptomic profiling of Gem-miR-15a treatment in parental and drug resistant HCT116 colorectal cancer cells
  GSE352606Homo sapiens4 个样本2026-10-31

  Resistance to 5-fluorouracil (5-FU)-based chemotherapy is a major obstacle in colorectal cancer (CRC). Gem-miR-15a, a gemcitabine-modified tumor-suppressor microRNA-15a mimic, was developed to overcome chemoresistance by combining the tumor-suppressive activity of miR-15a with the cytotoxic activity of gemcitabine in a single, vehicle-free molecule. To investigate the transcriptomic basis of its activity and its ability to reverse resistance-associated gene expression, RNA-sequencing was performed on parental and 5-FU-resistant HCT116 CRC cells under untreated and Gem-miR-15a-treated conditions. Analysis of these profiles identified modulation of key oncogenic and stress-response pathways and reversal of resistance-associated expression patterns following Gem-miR-15a treatment.
• Overexpression of IL-1Ra in MSCs Ameliorates Hepatic Injury via GGT5 and Improves Survival of aGVHD Mice
  GSE351748Homo sapiens6 个样本2026-10-31

  In conclusion, oeIL_x001E_1Ra_x001E_MSCs alleviate aGVHD_x001E_related hepatic lesions through anti_x001E_inflammatory effects and GGT5_x001E_dependent maintenance of redox and mitochondrial homeostasis, offering a promising cell_x001E_therapy strategy and theoretical foundation for targeted treatment of hepatic aGVHD.
• Spatial transcriptomic analysis of fibroblast therapy with collagen/PMMA in human skin [Xenium]
  GSE350895Homo sapiens3 个样本2026-10-31

  Xenium spatial transcriptomic analysis was performed to investigate cellular responses and tissue remodeling following fibroblast therapy with or without collagen/PMMA in human skin.

  空间转录组
• Collagen-PMMA scaffolds induce dermal remodeling and immune recruitment distinct from simple volar fibroblast therapy in human skin [scRNAseq]
  GSE350894Homo sapiens3 个样本2026-10-31

  Cellular therapy is promising but requires optimization in human subjects. Volar skin of the palms and soles is adapted to mechanical stress through a thick epidermis and dense extracellular matrix, whereas non-volar skin is vulnerable at high-pressure sites such as prosthetic limb interfaces. Because volar fibroblasts can partially reprogram non-volar skin, we tested whether collagen/polymethyl methacrylate (PMMA) could enhance volar fibroblast therapy. Healthy volunteers received vehicle, scalp fibroblast, or volar fibroblast injections, with or without collagen/PMMA, into non-volar skin. Durometer, optical coherence tomography, histology, and transcriptomic analyses showed volar-like structural changes and activation of skin-development, keratinocyte-differentiation, extracellular-matrix, and morphogenesis pathways. Collagen/PMMA promoted fibroblast, immune, and endothelial cell accumulation, consistent with a scaffold-associated tissue response. These findings distinguish volar fibroblast–associated skin identity changes from collagen/PMMA-induced stromal remodeling with foreign body, inflammatory, and fibrotic/myofibroblast-associated features.

  单细胞
• KLF16 and SIN3A facilitate endometrial cancer cell proliferation in association with CTD-2377D24.6
  GSE349296Homo sapiens6 个样本2026-10-31

  Endometrial cancer (EC) is the most common gynecological malignancy in developed countries. Pathogenetically, most cases arise from uncontrolled proliferative expansion of endometrial cells under prolonged estrogen stimulation, ultimately leading to malignant transformation within the glandular epithelium. Identifying key regulators of aberrant endometrial proliferation is therefore critical for developing novel therapeutic modalities against EC. In the present study, we characterized Kruppel-like factor 16 (KLF16), a transcription factor that drives proliferative signaling across multiple cellular components of the endometrium, including endothelial, epithelial, and smooth muscle cell types. Clinicopathological analysis revealed significantly elevated KLF16 expression in human EC tissues, which was positively associated with both advanced tumor stages and high histological grades. Genetic perturbation experiments demonstrated that knockdown of KLF16 robustly inhibited endometrial cancer cell proliferation in vitro and impeded tumor growth in vivo. Given its role as a master regulator controlling broad transcriptomic programs encompassing both protein-coding genes and non-coding RNAs, we performed unbiased screening and identified lncRNA CTD-2377D24.6 as a potential downstream mediator associated with KLF16 signaling. Notably, overexpression of CTD-2377D24.6 effectively counteracted the anti-proliferative effects induced by KLF16 depletion. Mechanistically, single-cell transcriptomics, coimmunoprecipitation, and functional assays demonstrated that SIN3A interacts with KLF16 and may contribute to the association between KLF16 and CTD-2377D24.6 expression, which is linked to enhanced endometrial cancer cell proliferation. Together, these findings established KLF16 contributes to endometrial cancer progression and highlight the KLF16/SIN3A/CTD-2377D24.6-associated regulatory axis as a potential molecular pathway relevant to EC proliferation.

  单细胞扰动筛选
• Targeting EGR1 Attenuates CCL2 Expression in Inflammatory Keratinocytes and Allergic Skin Inflammation
  GSE349203Homo sapiens5 个样本2026-10-31

  Early growth response 1 (EGR1) is a zinc-finger transcription factor involved in inflammatory gene regulation, but the extent to which pharmacological inhibition of EGR1 DNA-binding activity influences inflammatory transcriptional responses in keratinocytes remains incompletely understood. Here, we explored the transcriptional effects of pharmacological EGR1 inhibition in tumor necrosis factor-α (TNFα)-stimulated HaCaT keratinocytes. RNA sequencing was employed as an exploratory, hypothesis-generating screen using three structurally related EGR1 inhibitors (IT21, IT23, and IT25) to identify candidate genes showing concordant expression patterns across the three pharmacological perturbations. This analysis suggested broader changes in inflammation-associated transcriptional programs and identified several leukocyte-recruiting chemokines among the candidate genes. CCL2 was selected as a representative candidate for independent biological and mechanistic validation. IT25 treatment and EGR1 knockdown attenuated TNFα-induced CCL2 expression, while promoter-reporter analysis, EGR1-binding site mutagenesis, EGR1 overexpression, and chromatin immunoprecipitation supported EGR1-dependent transcriptional regulation of CCL2 in keratinocytes. Furthermore, topical IT25 treatment attenuated house dust mite-induced atopic dermatitis-like skin inflammation and was associated with reduced epidermal CCL2 expression and inflammatory cell infiltration in vivo. Collectively, these findings establish EGR1-dependent regulation of CCL2 in inflammatory keratinocytes and support further investigation of EGR1 DNA-binding activity as a pharmacological target in cutaneous inflammation.

  扰动筛选
• HNRNPH2-R114W remodels RNA splicing and neurodevelopmental gene programs in isogenic cerebral organoids
  GSE348913Homo sapiens4 个样本2026-10-31

  Autism spectrum disorder has been linked to disrupted RNA processing during corticogenesis, yet variant-specific mechanisms remain difficult to resolve. Isogenic cerebral organoids derived from a patient-derived induced pluripotent stem cell (iPSC) line carrying the HNRNPH2-R114W variant and its CRISPR-corrected counterpart serve as a human developmental model to investigate variant-associated RNA dysregulation. Imaging quantification and exploratory bulk RNA sequencing, performed at a single developmental time point using one pooled organoid RNA sample from each genotype, identify coordinated remodeling of neuronal and metabolic programs, along with junction-centered splicing dysregulation involving 6,310 differentially used junctions. Computational structural docking situates HNRNPH2 RNA recognition motifs (RRMs) 1-3 within a spliceosomal context and locates residue R114 near a predicted RNA-contact interface, indicating that the R114W substitution may alter RNA engagement. Integration of differential expression with event- and isoform-level analyses identifies regulatory hubs enriched for axon guidance and synaptic signaling pathways. Single-cell-reference-based deconvolution suggests modest compositional shifts that are unlikely to account for the extent of transcriptional and splicing alterations observed. Collectively, these findings implicate HNRNPH2-R114W in widespread RNA rewiring and define candidate isoform-level endpoints for mechanistic and therapeutic investigation in human cortical organoids. These molecular signatures open new avenues to examine how HNRNPH2-associated RNA dysregulation evolves across developmental time and recurs across independent biological contexts, providing a foundation for further mechanistic studies of this rare neurodevelopmental disorder.

  单细胞计算与 AI
• KIF1A p.T258M Impairs Neural Progenitor Differentiation and Axonal Transport Through Dysregulated Wnt/β-Catenin–BDNF Signaling
  GSE348793Homo sapiens6 个样本2026-10-31

  Human neural stem cells were derived from KIF1A p.T258M-mutant induced pluripotent stem cells and CRISPR-Cas9-corrected isogenic control cells. RNA sequencing was performed to compare global gene expression profiles between KIF1A-mutant and control neural stem cells. Differentially expressed genes were identified and used for downstream GO and KEGG pathway enrichment analyses to explore molecular pathways associated with KIF1A mutation-induced neural developmental defects.
• Single-cell regulatory genomics reveals coordinated myeloid and T-cell reprogramming in liver cirrhosis
  GSE348509Homo sapiens6 个样本2026-10-31

  We performed single-cell RNA sequencing (scRNA-seq) on liver tissues from 3 cirrhotic patients and 3 non-cirrhotic controls, analyzing 43,745 high-quality cells. We investigated cellular composition, SCENIC regulon activity, pseudotime trajectories, and CellChat communication. Cirrhosis was associated with Mono1 depletion, expansion of inflammatory macrophages and regulatory T cells, dysregulated YY1/ETV6 regulons in myeloid cells, altered EOMES/KLF6 programs in cytotoxic T cells, and increased EP300/SP3 in Tregs, along with fibrosis-biased ligand-receptor signaling. Note: Raw sequencing data are not available because the sequencing company routinely clears data after two years; only processed expression matrices are provided.

  单细胞
• Transcriptomic profiling of human lymphocytes treated with 2'-deoxyinosine reveals immunomodulatory mechanisms relevant to multiple sclerosis
  GSE347378Homo sapiens9 个样本2026-10-31

  2'-Deoxyinosine (2'-DI) is an endogenous nucleoside formed by the deamination of deoxyadenosine by adenosine deaminase, and nucleoside metabolism pathways are involved in the initiation and progression of Multiple Sclerosis (MS). Our previous study indicated that 2'-DI treatment alleviates disease severity in an MS mouse model. To explore the potential preventive therapeutic mechanism of 2'-DI, we performed RNA sequencing on human lymphocytes isolated from MS patients. Cells were stimulated with OKT3 and treated with 0, 0.5, or 1 mM 2'-DI. Results showed that 2'-DI exposure induced dose-dependent transcriptomic changes. Differentially expressed genes were significantly enriched in immune-related pathways, including chemokine signaling pathway, cytokine-cytokine receptor interaction, and IL-17 signaling pathway, suggesting that 2'-DI may exert a protective effect in MS by finely regulating inflammatory immune responses.
• Gene transcription and chromatin packing domains form a self-organizing system [RIP-Seq]
  GSE345114Homo sapiens6 个样本2026-10-31

  The human genome organizes into several thousand chromatin packing domains that couple euchromatin and heterochromatin into unified nanoscale volumes. Prior work suggested these domains form by transcriptionally driven loops that guide packing domain assembly. Here, we study the process of transcriptionally driven domain formation and maintenance. By pairing auxin-inducible degron technology with nanoscopic imaging, transcriptomics, and Hi-C, we show that Pol-II regulates conformationally defined interphase chromatin packing domains. Pol-II facilitates nascent domain generation and maintains mature domain integrity through the process of generating transcriptional loops. Mechanistically, Pol-II maintains the packing of intronic and intergenic chromatin within domains by transcribing exons within gene bodies. Consequently, polymerase loss disrupts genome connectivity, in situ packing domains, and gene expression, genome-wide. Our findings suggest chromatin packing domains and RNA synthesis are tightly coupled to optimize transcriptional responses in human cells.
• Gene transcription and chromatin packing domains form a self-organizing system [EU-Seq]
  GSE345113Homo sapiens7 个样本2026-10-31

  The human genome organizes into several thousand chromatin packing domains that couple euchromatin and heterochromatin into unified nanoscale volumes. Prior work suggested these domains form by transcriptionally driven loops that guide packing domain assembly. Here, we study the process of transcriptionally driven domain formation and maintenance. By pairing auxin-inducible degron technology with nanoscopic imaging, transcriptomics, and Hi-C, we show that Pol-II regulates conformationally defined interphase chromatin packing domains. Pol-II facilitates nascent domain generation and maintains mature domain integrity through the process of generating transcriptional loops. Mechanistically, Pol-II maintains the packing of intronic and intergenic chromatin within domains by transcribing exons within gene bodies. Consequently, polymerase loss disrupts genome connectivity, in situ packing domains, and gene expression, genome-wide. Our findings suggest chromatin packing domains and RNA synthesis are tightly coupled to optimize transcriptional responses in human cells.
• Gene transcription and chromatin packing domains form a self-organizing system [CUT&Tag]
  GSE345111Homo sapiens1 个样本2026-10-31

  The human genome organizes into several thousand chromatin packing domains that couple euchromatin and heterochromatin into unified nanoscale volumes. Prior work suggested these domains form by transcriptionally driven loops that guide packing domain assembly. Here, we study the process of transcriptionally driven domain formation and maintenance. By pairing auxin-inducible degron technology with nanoscopic imaging, transcriptomics, and Hi-C, we show that Pol-II regulates conformationally defined interphase chromatin packing domains. Pol-II facilitates nascent domain generation and maintains mature domain integrity through the process of generating transcriptional loops. Mechanistically, Pol-II maintains the packing of intronic and intergenic chromatin within domains by transcribing exons within gene bodies. Consequently, polymerase loss disrupts genome connectivity, in situ packing domains, and gene expression, genome-wide. Our findings suggest chromatin packing domains and RNA synthesis are tightly coupled to optimize transcriptional responses in human cells.
• PODXL regulates the neuronal entry of α-Synuclein aggregates
  GSE342465Homo sapiens6 个样本2026-10-31

  The spread of pathogenic α-synuclein assemblies between cells is thought to contribute to the progression of Parkinson’s disease, but the neuronal surface factors that control their uptake are still incompletely understood. To address this question, we established an arrayed CRISPR activation platform in human iPSC-derived cortical neurons and quantified the internalization of fluorescent α-synuclein preformed fibrils by high-throughput flow cytometry. Screening Parkinson’s disease genetics-prioritized surface proteins revealed podocalyxin-like protein 1 (PODXL) as a prominent negative regulator of fibril uptake.
• A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [RNA-seq]
  GSE341759Homo sapiens8 个样本2026-10-31

  Microglia are major targets of HIV-1 in the brain. Despite the effectiveness of antiviral therapy, infected microglia, including those containing a replication-defective provirus, can express viral RNA and proteins that contribute to neuroinflammation. However, the degree to which productive infection shapes the host response in microglia remains poorly defined. Using single cell RNA-seq of HIV-1-infected C20 microglia, we stratified cells by counts of HIV-1 reads with splice junctions into low- and high-infection groups, enabling us to resolve a graded rather than binary host transcriptional response. A core set of immune and cell-cycle pathways was induced regardless of infection level, but several programs reversed direction with increasing viral burden: interferon-α/γ and EMT/hypoxia signatures peaked at low infection, while high infection was marked by suppression of these signatures alongside induction of mTORC1/MYC signaling, ribosome biogenesis, RNA processing, and mitotic activity, accompanied by progressive loss of cytoskeletal, motility, and developmental gene programs. This pattern was reproduced in iPSC-derived microglia, supporting its generalizability beyond an immortalized line. Integration of differentially expressed miRNAs with differentially expressed genes from the low- and high-infection groups showing the canonical inverse miRNA-target relationship revealed miRNA/mRNA networks with strong representation of miRNAs previously implicated in HIV-1 replication (e.g., miR-33a-5p, miR-3065-3p) and in neurodegenerative and psychiatric disease (e.g., miR-107, let-7c-5p). These findings define a productive-infection-level continuum in microglial transcription, miRNA reprogramming, and identify candidate miRNA-mediated mechanisms, independent of the canonical Env/Nef/Tat pathway, by which HIV-1-infected microglia may contribute to neuroinflammation and neurocognitive impairment in people with HIV-1.

  单细胞
• A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [scRNA-seq]
  GSE341758Homo sapiens6 个样本2026-10-31

  Microglia are major targets of HIV-1 in the brain. Despite the effectiveness of antiviral therapy, infected microglia, including those containing a replication-defective provirus, can express viral RNA and proteins that contribute to neuroinflammation. However, the degree to which productive infection shapes the host response in microglia remains poorly defined. Using single cell RNA-seq of HIV-1-infected C20 microglia, we stratified cells by counts of HIV-1 reads with splice junctions into low- and high-infection groups, enabling us to resolve a graded rather than binary host transcriptional response. A core set of immune and cell-cycle pathways was induced regardless of infection level, but several programs reversed direction with increasing viral burden: interferon-α/γ and EMT/hypoxia signatures peaked at low infection, while high infection was marked by suppression of these signatures alongside induction of mTORC1/MYC signaling, ribosome biogenesis, RNA processing, and mitotic activity, accompanied by progressive loss of cytoskeletal, motility, and developmental gene programs. This pattern was reproduced in iPSC-derived microglia, supporting its generalizability beyond an immortalized line. Integration of differentially expressed miRNAs with differentially expressed genes from the low- and high-infection groups showing the canonical inverse miRNA-target relationship revealed miRNA/mRNA networks with strong representation of miRNAs previously implicated in HIV-1 replication (e.g., miR-33a-5p, miR-3065-3p) and in neurodegenerative and psychiatric disease (e.g., miR-107, let-7c-5p). These findings define a productive-infection-level continuum in microglial transcription, miRNA reprogramming, and identify candidate miRNA-mediated mechanisms, independent of the canonical Env/Nef/Tat pathway, by which HIV-1-infected microglia may contribute to neuroinflammation and neurocognitive impairment in people with HIV-1.

  单细胞
• A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [miRNA-seq]
  GSE341757Homo sapiens4 个样本2026-10-31

  Microglia are major targets of HIV-1 in the brain. Despite the effectiveness of antiviral therapy, infected microglia, including those containing a replication-defective provirus, can express viral RNA and proteins that contribute to neuroinflammation. However, the degree to which productive infection shapes the host response in microglia remains poorly defined. Using single cell RNA-seq of HIV-1-infected C20 microglia, we stratified cells by counts of HIV-1 reads with splice junctions into low- and high-infection groups, enabling us to resolve a graded rather than binary host transcriptional response. A core set of immune and cell-cycle pathways was induced regardless of infection level, but several programs reversed direction with increasing viral burden: interferon-α/γ and EMT/hypoxia signatures peaked at low infection, while high infection was marked by suppression of these signatures alongside induction of mTORC1/MYC signaling, ribosome biogenesis, RNA processing, and mitotic activity, accompanied by progressive loss of cytoskeletal, motility, and developmental gene programs. This pattern was reproduced in iPSC-derived microglia, supporting its generalizability beyond an immortalized line. Integration of differentially expressed miRNAs with differentially expressed genes from the low- and high-infection groups showing the canonical inverse miRNA-target relationship revealed miRNA/mRNA networks with strong representation of miRNAs previously implicated in HIV-1 replication (e.g., miR-33a-5p, miR-3065-3p) and in neurodegenerative and psychiatric disease (e.g., miR-107, let-7c-5p). These findings define a productive-infection-level continuum in microglial transcription, miRNA reprogramming, and identify candidate miRNA-mediated mechanisms, independent of the canonical Env/Nef/Tat pathway, by which HIV-1-infected microglia may contribute to neuroinflammation and neurocognitive impairment in people with HIV-1.

  单细胞
• GOLDEN: Gene expression and allele-informed decomposition for genetic heterogeneity in spatial transcriptomic data
  GSE341398Homo sapiens2 个样本2026-10-31

  Spatial transcriptomics (ST) enables exploration of cellular interactions, but current methods rely on pathologist annotation and face limitations in addressing genetic heterogeneity, where niches harbor non-clonal cells, as in placental or allograft tissues. To decipher such inter-individual heterogeneity in ST, we developed GOLDEN (Gene expression and allele-informed decomposition for genetic heterogeneity), an allele-aware multi-task network that encodes spot-level expression into shared latent representations. Incorporating allele features, it uses dual heads to classify spot identity (target, non-target, or mixed) and to estimate target fractions. For evaluation, we generated synthetic ST data via a Gamma-distribution model using semi-allogeneic single-cell profiles. On these synthetic benchmarks, GOLDEN achieved reliable deconvolution (Pearson's r = 0.977; MAE = 0.045) while maintaining consistent predictions across real-world STs, which were validated through genetic evidence.

  单细胞空间转录组计算与 AI
• The transcriptomic profile of wild-type HGC-27 cells treated with conditioned media from ANGPTL4-overexpressing or control HGC-27 cells
  GSE338826Homo sapiens4 个样本2026-10-31

  Given that ANGPTL4 is a secreted protein, we combined conditioned medium treatment with transcriptomic analysis to determine whether the activation of downstream signaling pathways by ANGPTL4 overexpression is dependent on its secretion.
• Single-cell atlas reveals shared early microenvironmental remodeling in colorectal polypogenesis
  GSE327909Homo sapiens6 个样本2026-10-31

  Colorectal polyps are the earliest precancerous lesions in colorectal carcinogenesis, but their common microenvironmental drivers remain incompletely defined. We performed single-cell RNA sequencing on paired normal mucosal and colorectal polyp tissues from 3 patients with unselected lesions, including hyperplastic polyps and tubular adenomas. After quality control, 31,147 high-quality cells were obtained. Comparative analysis revealed four conserved hallmarks of colorectal polyps relative to normal mucosa: disrupted epithelial homeostasis characterized by stem cell expansion, Paneth cell reduction, and Wnt pathway activation; pro-inflammatory polarization of CD4+ T cells with increased Th17 cells and activation of NF-kB/IL-17-related pathways; functional reprogramming of CD8+ T cell subsets, especially decreased IELs with specialized immune functions; and extensive remodeling of immune-epithelial intercellular communication, including CD55-ADGRE5, MIF-CD74, and GZMA-PARD3 signaling axes. These data provide a single-cell atlas of shared microenvironmental changes in early colorectal polypogenesis.

  单细胞细胞图谱
• A Single-Cell Atlas of Human Periodontal Ligament During Orthodontic Tooth Movement
  GSE327337Homo sapiens5 个样本2026-10-31

  Orthodontic tooth movement (OTM) requires coordinated remodeling of the periodontal ligament (PDL) and alveolar bone, yet the cellular architecture underlying this process in human tissues remains incompletely understood. Here, we generated the first single-cell transcriptomic atlas of the human PDL during OTM by profiling cells from the pressure and tension sides of teeth collected at day 3 and day 7 following force application. This atlas reveals the major stromal and immune cell populations and highlights spatial and temporal heterogeneity across force conditions and remodeling stages.

  单细胞空间转录组细胞图谱
• Upregulated TRPM1 is associated with apoptosis in Rs1 knockout mice and in ARPE19 cells through increased intracellular calcium
  GSE326551Homo sapiens8 个样本2026-10-31

  The pathological mechanism underlying retinal apoptosis in X-linked retinoschisis (XLRS), a disease caused by retinoschisin 1 (RS1) deficiency, remains incompletely understood. This study aimed to investigate the role of transient receptor potential melastatin 1 (TRPM1) in retinal tissues and cells. Retinal function and structure were assessed by electroretinography (ERG) and optical coherence tomography (OCT). Protein expression was evaluated by immunofluorescence staining and western blotting (WB). Retinal morphology was examined by hematoxylin and eosin (H&E) staining. Apoptotic retinal cells were detected by TUNEL staining. Key proteins were screened using proteomics data obtained by mass spectrometry. Intracellular calcium levels were measured using Rhod-2 AM. TRPM1 expression in Rs1-KO mice was 1.3-fold higher than that in wild-type mice (p < 0.05), whereas TRPM1-overexpressing ARPE19 cells exhibited approximately twofold higher expression than the empty vector control group. Mechanistically, TRPM1-mediated calcium influx promoted calcium/calmodulin-dependent protein kinase II (CAMKII) phosphorylation. Concomitantly, the accumulation of the autophagy-related proteins P62 and LC3B, increased BAX expression, and decreased BCL2 expression were observed in both Rs1-KO retinal tissues and TRPM1-overexpressing ARPE19 cells. These findings collectively suggest that TRPM1 may contribute to cell’s apoptosis. Our study provides new insight into the mechanism of retinal apoptosis in XLRS.
• Somatic TP53 Mutations Drive T and NK Cell Dysfunction and Create an Inflammatory Immune Niche in Acute Myeloid Leukemia
  GSE324592Homo sapiens2 个样本2026-10-31

  TP53-mutant acute myeloid leukemia (AML) is characterized by poor prognosis and limited response to immunotherapy, yet the mechanisms underlying immune failure in this setting remain unclear. Here, we integrate single-cell DNA sequencing with surface proteomics to demonstrate that somatic TP53 mutations arise not only in leukemic blasts but also in T and NK cells from patients with TP53-mutant AML. TP53-mutant T cells exhibit enhanced exhaustion phenotypes, impaired cytotoxic function, and altered clonal architecture. Mechanistically, mutant p53 reprograms T cells toward a pro-inflammatory yet dysfunctional state, reshaping cytokine networks and promoting a niche enriched in inflammatory and myeloid-supportive signals. These mutant T cells impair both intrinsic effector function and the functionality of surrounding immune cells. Introduction of TP53 mutations into healthy donor T cells recapitulates exhaustion and impaired tumor control, whereas elimination of mutant p53 restores effector function, normalizes cytokine programs, and improves disease control in a TP53-mutant AML xenograft model.

  单细胞
• Enhanced plasmin generation due to PAI-1 deficiency impairs regulated vascular endothelial cell motility.
  GSE320323Homo sapiens6 个样本2026-10-31

  Background: Plasminogen activator inhibitor-1 (PAI-1) plays a crucial role in the plasminogen activation system and fibrinolysis. Congenital PAI-1 deficiency in humans is characterized by severe bleeding and delayed wound healing, which is consistent with the altered regulation of the fibrinolytic regulation. Although plasmin influences various cellular processes, the mechanisms by which PAI-1-mediated control of plasminogen activation and regulates endothelial cell (EC) behavior, especially at the pericellular level, are not well understood. The aim of this study was to elucidate the specific cellular effects of enhanced plasminogen activator (PA) activity caused by PAI-1 deficiency in human ECs. Methods: PAI-1 deficient human ECs (PAIKO-ECs) were generated using CRISPR/Cas9-mediated gene editing and compared them with wild-type ECs (WT-ECs). We investigated the impact of plasminogen-induced pericellular plasmin activity and its impact on endothelial migration and angiogenic tube formation, conducting additional transcriptomic analysis. Results: PAIKO-ECs exhibited markedly increased PA activity, as demonstrated by elevated plasmin generation in the presence of plasminogen. In scratch assays, PAIKO-ECs exhibited increased overall uncoordinated motility with multidirectional migration trajectories and impaired directional wound closure in the presence of plasminogen; however, cell proliferation remained unaffected. This aberrant migratory phenotype was reversed by aprotinin, recombinant active PAI-1, or the lysine analog epsilon-aminocaproic acid (EACA). EACA notably reduced plasminogen accumulation on the cell surface while preserving fluid-phase plasmin generation. This indicates that enhanced EC motility is driven by pericellular rather than fluid-phase plasmin activity. In tube formation assays, PAIKO-ECs formed a higher number of extremities and branches, a phenotype that was reversed to the level of WT-ECs by EACA or aprotinin. Transcriptome analyses revealed differential gene expression related to fibrinolysis, angiogenesis, and endothelial-mesenchymal transition. Conclusions: These findings reveal that pericellular plasmin activity is essential for EC motility and angiogenic behavior under PAI-1-deficient conditions. This provides novel mechanistic insight into the spatial plasminogen activation systems in vascular remodeling.

  空间转录组
• ReprogRAM nanoplatform for direct conversion of fibroblasts into reprogrammed osteoblasts for bone regeneration
  GSE315875Homo sapiens4 个样本2026-10-31

  mRNA-based direct conversion offers an integration-free route for osteogenic cell-fate reprogramming, yet efficient reprogramming typically requires sustained expression of reprogramming factors. Here, we develop ReprogRAMs (Reprogrammable RNA Assemblies for Multi-factor expression), a self-assembled concatemeric mRNA nanoparticles synthesized by rolling-circle transcription and engineered for cap-independent translation. A single delivery of ReprogRAM to human dermal fibroblasts enabled cytosolic expression that persisted over time with minimal cytokine induction. By leveraging this long-acting expression profile, we encoded the osteogenic reprogramming factors Oct4 and Cbfβ and implemented a hybridized delivery strategy to enforce co-expression of both factors. ReprogRAM induced robust osteogenic conversion, as evidenced by increased mineralized matrix deposition, induction of osteoblast markers, and transcriptomic remodeling toward osteoblasts. Finally, transplantation of ReprogRAM-derived reprogrammed osteoblasts (rOBs) embedded in a gelatin scaffolds promoted bone repair in a critical-sized mouse calvarial defect model. Together, ReprogRAM provides a long-acting, integration-free mRNA modality for in situ cell-fate engineering and bone regeneration.
• Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells
  GSE280503Homo sapiens6 个样本2026-10-31

  In this study, transient transcriptome sequencing (TT-seq) was performed to dectect the impact of the overexpression of CTCF-s on nascent RNA and antisense RNA.
• BL-Hi-C, Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells
  GSE280419Homo sapiens8 个样本2026-10-31

  In this study, we performed BL-Hi-C to investigate the influence of the expression of CTCF/CTCF-s on higher-order chromatin structures.
• eCLIP-seq profiling of Flag-OTUD6B-associated RNA in HEK293T cells
  GSE352643Homo sapiens4 个样本2026-10-30

  RNA associated with Flag-OTUD6B was profiled by enhanced crosslinking and immunoprecipitation sequencing (eCLIP-seq) in human HEK293T cells. Two independent biological replicates were represented by two FLAG immunoprecipitation libraries and two corresponding size-matched input (SMInput) control libraries. This experiment and the OTUD6B-knockdown Ribo-seq experiment in MDA-MB-231 cells belong to the same research study.