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.
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2-induced gene expression [Myc_RNA]
  GSE352602Mus musculus6 个样本2026-10-31

  The transcription factor Foxp3, with its singular role in the differentiation and function of regulatory T (Treg) cells, is thought to modulate their responses to activatory extracellular cues. However, the underlying mechanisms remain largely unknown. Beyond its requirement for Foxp3 induction during Treg differentiation, STAT5 activation downstream of interleukin-2 (IL-2) signaling is essential for the fitness, activation, and suppressive capacity of mature Treg cells. Here, we demonstrate that IL-2-induced phospho-STAT5 directly binds Foxp3, endowing Foxp3 with a new binding specificity and enabling its recruitment to a distinct set of GAS motif-enriched cis-regulatory elements. Using acute chemogenetic and pharmacological protein degradation strategies, we show that Foxp3 selectively modulates STAT5-dependent transcriptional responses of activated Treg cells to IL-2, including a Myc-dependent gene module. These results suggest that Foxp3-STAT5 complexes “customize” transcriptional responses of activated Treg cells to IL-2 stimulation to support their fitness and functionality.
• The CRISPR-Cas system functions as a regulatory module in Salmonella enterica serovar Typhi
  GSE352555Salmonella enterica subsp. enterica serovar Typhi str. CT18; Salmonella enterica subsp. enterica serovar Typhi; Salmonella enterica subsp. enterica serovar Typhimurium str. LT27 个样本2026-10-31

  Transcriptional profile of Salmonella enterica serovar Typhi IMSS-1 mutants lacking individual components of the Type I-E CRISPR-Cas system. Strains carrying deletions of cas1, cas2, cas3, casB (cse2), casD (cas5), casE (cas6e) or the cas3-CRISPR region were compared with the wild-type strain, which was used as control. All strains were grown in N-minimal medium at 37 °C to an OD600 of 0.6. CRISPR-Cas systems are best known as adaptive immune systems of bacteria against phages and plasmids, but they are increasingly recognized as regulators of endogenous gene expression. The aim of the experiment was to learn if the loss of CRISPR-Cas components was able to modify the overall mRNA expression profile of S. Typhi. Here, we demonstrate that the Type I-E CRISPR-Cas system in S. Typhi modulates the expression of the key transcriptional regulator TviA.
• Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition [pADam]
  GSE352286Mus musculus8 个样本2026-10-31

  The cut-and-paste DNA transposon Sleeping Beauty (SB) is widely used for genome engineering, mutagenesis and gene delivery. When mobilized from a genomic donor position (“launch site”), SB preferentially reintegrates locally (< 2 Mb), but factors governing its transposition from genomic sites remain incompletely understood. Here we analysed local transposition experiments in mouse embryonic stem cells to determine the influence of chromatin context and transposon cargo on SB transposition. Transposons in launch sites with transcriptionally active, accessible chromatin showed lower transposition efficiency. Large cargo and cargo with higher transcriptional activity also result in reduced transposition efficiency. After excision, local reintegration patterns closely resembled 3D contact frequencies of the launch site. This indicates that chromosome folding is a major determinant of the transposition pattern. Surprisingly, we did not detect any effect of the destination chromatin composition on reintegration efficiency. Cargo sequence modified the reintegration patterns: promoter-containing cargo increased both very proximal (<10kb) and interchromosomal transpositions, while CTCF binding sites in the cargo increased reintegration on the launch chromosome. Together, these results define key determinants of SB transposition in chromosomes and inform the design of SB-based genome engineering strategies.
• Investigating the transcriptional response of PSC2 deletion and overexpression in C. neoformans
  GSE352234Cryptococcus neoformans6 个样本2026-10-31

  Adaptation to CO2 is necessary for virulence in Cryptococcus neoformans. The regulation of Ace2p activity and cellular morphogenesis (RAM) pathway is essential for growth under high temperature and high CO2 conditions. We identified PSC2 (CNAG_01335) as a suppressor of the RAM pathway in H99 cbk1 deletion mutant. To investigate the role of Psc2, RNA sequencing was performed on the wild-type H99, PSC2 deletion, and Psc2 over expression strains.
• Age-associated hsa_piR_020485 inhibits osteogenic differentiation of bone marrow stromal cells and promotes macrophage migration
  GSE351871Rattus norvegicus6 个样本2026-10-31

  Age-related decline in bone marrow stromal cell (BMSC) function and inflammatory changes contribute to osteoporosis. We investigated the age-associated PIWI-interacting RNA hsa_piR_020485 and its effects on BMSC function, macrophage responses, and trabecular bone volume fraction.
• 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.
• Liver Kinase B1 depletion disrupts the pantothenic acid: coenzyme A pathway in astrocytes
  GSE351587Mus musculus8 个样本2026-10-31

  Previous studies showed conditional knockout of Liver Kinase B1 (LKB1) from astrocytes exacerbated disease severity and glial cell activation in a mouse model of Multiple Sclerosis (MS). A major function of LKB1 is to maintain energy supplies under conditions of metabolic stress, suggesting that loss of LKB1 could alter astrocytic metabolic processes. Following siRNA mediated knockdown (KD) of LKB1 from primary mouse astrocytes, untargeted metabolomic screening identified significant increases in Pantothenic Acid (PA) and related metabolites; and pathway analysis showed the PA:Coenzyme A (PA:CoA) pathway was significantly modified. This pathway was also identified by bulk RNA sequencing. In LKB1 KD cells, relative mRNA levels of enzymes in the PA:CoA pathway were reduced, and PA Kinase 2 (Pank2, which converts PA to phosphoPA) expression was reduced. Deficiencies in Pank2 are known to cause iron accumulation, which we confirmed occurs in LKB1 KD astrocytes. The KD cells also showed increased sensitivity to induction of ferroptosis. Measurement of serum PA levels showed a positive correlation with age at diagnosis in relapsing remitting MS patients harboring a variant in the gene encoding LKB1. Together, these results indicate that metabolic disturbance leads to dysregulation of the PA:CoA pathway in astrocytes and suggest that plasma PA levels could provide a novel biomarker for MS disease.
• Twenty-Hour Hypothermic Oxygenated Perfusion Preserves Myocardial Viability and Bioenergetics with No Primary Graft Dysfunction After Porcine Heart Transplantation
  GSE351179Sus scrofa8 个样本2026-10-31

  Background: Hypothermic oxygenated perfusion (HOPE) may extend donor heart preservation beyond conventional storage durations. We evaluated early graft function and myocardial cellular and metabolic integrity following porcine heart transplantation after 20 hours of HOPE. Methods: Ten donor hearts underwent various preservation conditions: static cold storage (SCS) for 4 hours (n=2), HOPE for 4 hours (n=3), and HOPE for 20 hours (n=5), followed by heart transplantation (HT) in recipient pigs. Following implant and reperfusion, graft function was assessed over 3 hours by serial echocardiography, invasive hemodynamics, optical flow analysis, and vasoactive support scoring; myocardial tissue was analyzed by histopathology, flow cytometry, mitochondrial respirometry, transcriptomics, and proteomics. Results: Ejection fraction, right atrial pressure and systolic blood pressure did not differ significantly between groups, and no graft met criteria for primary graft dysfunction. LV contractility was within normal range with comparable vasoactive support among all groups. Preservation-associated weight gain was greatest after HOPE 20h, and histopathology showed comparable findings with edema present in all cohorts, without fibrosis, thrombosis, or necrosis. Cardiomyocyte viability was preserved across all groups (HOPE 20h, 86%, HOPE 4h, 81%, and SCS 4h, 77%). Maximal oxygen consumption rate was elevated in HOPE 20h versus HOPE 4h and SCS 4h (p<0.01), while basal and non-mitochondrial respiration were similar. Transcriptomics and proteomics revealed minimal differences in gene and pathway expression among groups. Conclusions: HOPE preserves donor heart viability, mitochondrial integrity, and ventricular function after 20 hours of ischemia in a porcine model, without evidence of primary graft dysfunction, supporting extended preservation for heart transplantation. Edema, recovery of function, and metabolic responses warrant further investigation with longer-term monitoring.
• 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
• Single-cell analysis reveals sex-specific ERβ regulation of neurovascular protection in the AppNL-G-F mouse model of Alzheimer’s disease
  GSE350656Mus musculus4 个样本2026-10-31

  Alzheimer’s disease (AD) exhibits pronounced sex differences, but the molecular mechanisms underlying this dimorphism remain unclear. To investigate the role of estrogen receptor beta (ERβ; Esr2) in modulating sex-specific amyloid pathology, single-cell RNA sequencing was performed on hippocampal tissue from six-month-old male and female AppNL-G-F and AppNL-G-F/Esr2KO mice. Loss of Esr2 induced sex-dependent alterations in amyloid burden, glial activation states, and endothelial-centered intercellular communication networks, with more pronounced transcriptomic remodeling in males. Transthyretin (Ttr) emerged as a strongly sex-modulated gene associated with increased amyloid pathology in male Esr2-deficient mice. These data provide a sex-stratified transcriptomic resource for understanding ERβ-dependent regulation of cellular programs in AD-related pathology

  单细胞
• Gene Expression in the Glioblastoma Cell Line (GL261) Transcriptome Following Treatment with Magnetic Nanoparticles (MNPQ)
  GSE349688Mus musculus9 个样本2026-10-31

  GL261 cells are a widely used glioma tumor model system; following in situ transplantation, they stably form glioblastoma and are extensively utilized as a preclinical evaluation model for brain gliomas. Magnetic nanomedicines (MNPQ), with their advantages of magnetically responsive targeted enrichment and locally controlled release, have demonstrated effective antitumor potential against gliomas; however, how they reshape the gene expression profile of tumor cells at the transcriptomic level remains unclear. Our study has one primary objective: to identify differentially expressed genes and their enriched signaling pathways in the GL261 cell transcriptome before and after MNPQ treatment, thereby elucidating the molecular mechanisms underlying its antitumor effects.
• Gene expression in pericental and periportal hepatocytes
  GSE349461Mus musculus4 个样本2026-10-31

  Hepatic metabolic zonation enables periportal (PP) and pericentral (PC) hepatocytes to perform distinct metabolic functions. To characterize spatial differences in hepatic gene expression, we isolated PP and PC hepatocytes from mouse liver and performed RNA sequencing. This dataset provides transcriptomic profiles of PP and PC hepatocytes and enables identification of genes and pathways differentially regulated across the portal-to-central vein axis.

  空间转录组
• 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.
• Id2 orchestrates IL-33-driven metabolic reprogramming in pathogenic Th2 cells (RNA-seq)
  GSE344612Mus musculus8 个样本2026-10-31

  The transcription factor Id2 licenses the transition of stem‑like Th2 cells to pathogenic ST2⁺ Tpath2 cells by orchestrating IL‑33‑ST2 signaling to drive glycolytic reprogramming. Id2 transcriptionally represses Pten by sequestering E proteins at its promoter, amplifying PI3K‑AKT signaling and glycolytic flux, which supports histone acetylation at Il1rl1 and Il5. Id2‑deficient Th2 cells fail to establish this epigenetic state; pyruvate supplementation rescues the defect. Pharmacological Id2 inhibition attenuates Tpath2 responses and airway inflammation in vivo, and cross‑species analysis confirms conserved PTEN dynamics in human asthma. Thus, the IL‑33–Id2–PI3K‑AKT axis represents a metabolic–epigenetic checkpoint and therapeutic target for allergic airway disease.
• Local effect of Ixodes scapularia TNFBP gene silence on transcriptome of bitten skin of mouse
  GSE344220Mus musculus9 个样本2026-10-31

  To explore their potential role in tick-host interactions, RNA-seq was performed on the skin of mice bitten by TNFBP1 and TNFBP2 silenced ticks. The transcriptome was altered after feeding on gene silenced ticks compared with control ticks, and defined pathways including legionellosis, HIF-1TNF, IL-17 signaling pathway, phagosome were significantly enriched in the downregulated genes.
• 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.
• Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Nr2f2_ecko P5bm]
  GSE342123Mus musculus6 个样本2026-10-31

  The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.
• Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Tek_ecko P3bm]
  GSE342122Mus musculus8 个样本2026-10-31

  The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.