详细内容（前10条）

1. ⭐ GSE335345 小鼠胸椎间盘 IVD2（D1 区）的 10X Visium 空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：10x、spatial、Visium、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Valeria Aceves ; Ziyi Xu ; Zhaoyang Liu ; Ryan S GraySeries Type : OtherOrganism : Mus musculusSpatial gene expression profiling of mouse thoracic spine tissue using the 10x Genomics Visium platform (FFPE, probe-based chemistry). Library IVD2 was profiled on Visium slide V11A19-364 capture area D1. This capture area contains both mutant and control tissue regions. Raw FASTQs comprise two sequencing lanes (L001 and L002) of the same IVD2 library (8 files total).
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2. ⭐ GSE299859 通过 BTK 抑制靶向 STING-NFκB 通路：一种缓解肌萎缩侧索硬化症中神经元和小胶质细胞功能障碍的双重机制治疗策略 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、RNA-seq、pathway
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAmyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder with limited therapeutic interventions. We identified the cGAS-STING-NFκB pathway as a dual therapeutic target that combats both neuronal degeneration and neurotoxic glial activity in ALS. Utilizing SOD1-mutant human iPSC-differentiated motor neurons(hiPSC-MNs) and microglia(hiPSC-MGs), we demonstrated that ALS hiPSC-MGs displayed a pronounced proinflammatory phenotype, characterized by significant inflammatory marker elevation (NLRP3 increased 0.66-fold, secreted IL-1β elevated 2.85-fold compared to controls) and compromised phagocytic capacity (48% reduction in bioparticle uptake). Concurrently, ALS hiPSC-MNs exhibit DNA damage, activating STING-NFκB signaling and triggering caspase-3-mediated apoptosis. Notably, co-culture experiments revealed that inflammatory hiPSC-MGs substantially increased neuronal apoptosis, indicating a toxic intercellular communication mechanism mediated through STING-NFκB signaling. Pharmacological inhibition of Bruton’s tyrosine kinase (BTK) - a critical upstream regulator of STING activation - effectively suppressed this inflammatory cascade. This intervention reduced DNA damage in ALS hiPSC-MNs by 61.4% and restored microglial phagocytic function to approximately 87.2% of normal levels. In vivo studies with SOD1-G93A ALS mice demonstrated that BTK inhibitor treatment significantly improved motor performance, extended median survival (183 days versus 158 days in untreated controls), and mitigated neuropathological progression. The treatment enhanced motor neuron survival, reduced microgliosis and astrogliosis, and modulated the PI3K-AKT-mTOR pathway without disrupting autophagy-lysosome dynamics. Our study presents a translational therapeutic strategy that simultaneously addresses neuron-intrinsic and glial-mediated mechanisms in ALS, providing a compelling rationale for repurposing BTK inhibitors in future ALS clinical trials.
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3. ⭐ GSE299856 通过 BTK 抑制靶向 STING-NFκB 通路：一种缓解肌萎缩侧索硬化症中神经元和小胶质细胞功能障碍的双重机制治疗策略 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、scRNA、pathway
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAmyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder with limited therapeutic interventions. We identified the cGAS-STING-NFκB pathway as a dual therapeutic target that combats both neuronal degeneration and neurotoxic glial activity in ALS. Utilizing SOD1-mutant human iPSC-differentiated motor neurons(hiPSC-MNs) and microglia(hiPSC-MGs), we demonstrated that ALS hiPSC-MGs displayed a pronounced proinflammatory phenotype, characterized by significant inflammatory marker elevation (NLRP3 increased 0.66-fold, secreted IL-1β elevated 2.85-fold compared to controls) and compromised phagocytic capacity (48% reduction in bioparticle uptake). Concurrently, ALS hiPSC-MNs exhibit DNA damage, activating STING-NFκB signaling and triggering caspase-3-mediated apoptosis. Notably, co-culture experiments revealed that inflammatory hiPSC-MGs substantially increased neuronal apoptosis, indicating a toxic intercellular communication mechanism mediated through STING-NFκB signaling. Pharmacological inhibition of Bruton’s tyrosine kinase (BTK) - a critical upstream regulator of STING activation - effectively suppressed this inflammatory cascade. This intervention reduced DNA damage in ALS hiPSC-MNs by 61.4% and restored microglial phagocytic function to approximately 87.2% of normal levels. In vivo studies with SOD1-G93A ALS mice demonstrated that BTK inhibitor treatment significantly improved motor performance, extended median survival (183 days versus 158 days in untreated controls), and mitigated neuropathological progression. The treatment enhanced motor neuron survival, reduced microgliosis and astrogliosis, and modulated the PI3K-AKT-mTOR pathway without disrupting autophagy-lysosome dynamics. Our study presents a translational therapeutic strategy that simultaneously addresses neuron-intrinsic and glial-mediated mechanisms in ALS, providing a compelling rationale for repurposing BTK inhibitors in future ALS clinical trials.
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4. GSE335275 从核心到边缘绘制胶质母细胞瘤的空间结构图，描绘出特定微环境的肿瘤细胞状态和细胞间相互作用 [xenium_cohort3]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial
• 📝 描述：Contributors : Saad M Khan ; Anthony Z Wang ; Rupen R Desai ; Colin R McCornack ; Rui Sun ; Sonika M Dahiya ; Jennifer A Foltz ; Ngima D Sherpa ; Lydia Leavitt ; Timothy West ; Alexander F Wang ; Aleksandar Krbanjevic ; Bryan D Choi ; Eric C Leuthardt ; Bhuvic Patel ; Albert H Kim ; Gavin P Dunn ; Allegra A PettiSeries Type : OtherOrganism : Homo sapiensTreatment resistance in glioblastoma (GBM) is largely driven by the extensive multi-level heterogeneity that typifies this disease. Despite significant progress toward elucidating GBM’s genomic and transcriptional heterogeneity, a critical knowledge gap remains in defining this heterogeneity at the spatial level. To address this, we employed spatial transcriptomics to map the architecture of the GBM ecosystem. This revealed tumor cell states that are jointly defined by gene expression and spatial localization, and multicellular niches whose composition varies along the tumor core-edge axis. Ligand-receptor interaction analysis uncovered a complex network of intercellular communication, including niche- and region-specific interactions. Finally, we found that CD8 +ve GZMK +ve T cells colocalize with LYVE1 positive CD163 positive myeloid cells in vascular regions, suggesting a potential mechanism for immune evasion. These findings provide novel insights into the GBM tumor microenvironment, highlighting previously unrecognized patterns of spatial organization and intercellular interactions, and novel therapeutic avenues to disrupt tumor-promoting interactions and overcome immune resistance.
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5. GSE298466 鳜鱼卵巢单细胞图谱揭示硬骨鱼卵子发生及其免疫微环境发育的轨迹

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、single-cell
• 📝 描述：Contributors : Feng Chen ; Yuting Wang ; Tilin Yi ; Yingbing Su ; Xuejun Gao ; Weiguang KongSeries Type : Expression profiling by high throughput sequencingOrganism : Siniperca chuatsiThe establishment of the immune microenvironment during oogenesis in teleosts plays an important role in individual survival and population continuation. However, the maternal influence on offspring immunity is poorly understood, particularly regarding the dynamic development and underlying mechanisms of the oocyte immune microenvironment. Here, we characterized the single-cell atlas of the mandarin fish ovary at the late stage IV, and identified three germ cells and five somatic cells. The distinctive features of the three germ cell types were further explored through the enrichment analysis, suggesting that the immune microenvironment of fish oocytes is formed during the mature oocyte stage. Subsequently, based on the pseudotemporal analysis of three germ cells, as well as the clustering analysis and the cell-cell communication analysis, we depicted the trajectories of oogenesis and its immune microenvironment formation in the mandarin fish ovary. Notably, we identified a high-low-high expression pattern in immune-related pathways across different development stages of oocytes. Furthermore, the spatiotemporal expression dynamics of six key markers were validated using RNA-FISH. These findings provide novel insights into oogenesis and the establishment of maternal/innate immunity in teleosts.
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6. GSE296507 纵向单细胞RNA测序揭示慢性粒细胞白血病微观和宏观状态的演变

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、sequencing
• 📝 描述：Contributors : David E Frankhouser ; Dandan Zhao ; Yu-Hsuan Fu ; Anupam Dey ; Ziang Chen ; Jihyun Irizarry ; Jennifer Rangel Ambriz ; Sergio Branciamore ; Denis O’Meally ; Lucy Ghoda ; Jeffery M Trent ; Stephen Forman ; Adam L MacLean ; Ya-Huei Kuo ; Bin Zhang ; Russell C Rockne ; Guido MarcucciSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSingle cell RNA sequencing (scRNA-seq) has revolutionized our understanding of cancer, yet identifying meaningful disease states from single cell data remains challenging. Here, we systematically explore the cancer specific information content encoded in single cell versus bulk transcriptomics to resolve this paradox and clarify how discrete disease-defining states emerge from inherently noisy single cell data. Using chronic myeloid leukemia (CML) progression as a model, we demonstrate that, while single cell transcriptomes exist along continuous transcriptional microstates, clinically relevant leukemia phenotypes clearly manifest only at the pseudobulk (macrostate) level. By leveraging state-transition theory, we reveal how robust disease phenotype state-transitions are governed by cell type specific contributions. Our results establish a theoretical framework explaining why discrete disease phenotypes remain hidden at the single cell scale but emerge clearly at the aggregated macrostate level, enabling previously inaccessible biological insights into leukemia evolution. Broadly applicable across cancers and other complex diseases, our approach fundamentally advances single cell analysis by clarifying how microscopic transcriptional variation collectively shapes macroscopic disease dynamics.
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7. GSE279309 Degos病患者的皮肤、血液和脑脊液（CSF）样本的单细胞TCR测序。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Goel Shubham ; Jin Seon-Pil ; Sakamoto Keiko ; Keisuke NagaoSeries Type : OtherOrganism : Homo sapiensSingle-cell TCR-sequencing was pefromed to identify clonal expansion of T cells in Skin, blood and CSF samples from Degos disease patients.
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8. GSE327701 非小细胞肺癌（NSCLC）患者脑转移组织、脑脊液（CSF）和血浆的甲基化谱分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、methylation
• 📝 描述：Contributors : Darin Dolezal ; Sampada Chande ; Giancarlo Bonora ; Yong Huang ; Myles Walsh ; Savannah Kandigian ; Wei Wei ; Anna Arnal-Estape ; Kurt Shalper ; Sarah Goldberg ; Darren Cross ; Massimo Squatrito ; Nicholas Blondin ; Pan Du ; Shidong Jia ; Veronica Chiang ; Don NguyenSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensThis project investigates genome-wide DNA methylation patterns in tumor, cerebrospinal fluid (CSF), and blood from patients with non-small cell lung cancer (NSCLC) brain metastasis. Brain metastasis tumor tissues obtained at the time of neurosurgical resection performed as part of routine clinical care were profiled alongside time-matched cell-free DNA (cfDNA) derived from CSF and plasma collected from the same patients. Additional longitudinal CSF and plasma cfDNA samples collected at the time of clinically suspected leptomeningeal metastasis were also analyzed. All samples were assessed using the PredicineEPIC whole-genome methylation analysis platform to identify CpG sites covered by differentially methylated fragments (DMFs). These data support the development of liquid biopsy approaches for the detection, monitoring, and risk stratification of central nervous system disease in patients with NSCLC brain metastases.
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9. GSE334772 NF1在雌激素受体阳性乳腺癌中的缺失诱导破骨细胞形成和免疫抑制，从而促进骨转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Zifan Zhao ; Ze-Yi Zheng ; Jonathan T Lei ; Matthew J Baik ; Yi-Hsuan Wu ; Lauren K Somes ; Andres F Mosquera Paternina ; Omar A Harb ; Owen A Chang ; Fengshuo Liu ; Matthew V Holt ; Junkai Wang ; Igor Bado ; Hai Wang ; George Miles ; Zbigniew Gugala ; Meenakshi Anurag ; Ahmed Elkhanany ; Yi Li ; Valentina Hoyos ; Xiang H Zhang ; Eric C ChangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEstrogen receptor-positive (ER⁺) breast cancer exhibits a marked propensity for skeletal metastasis; however, the molecular drivers of bone colonization remain incompletely defined. We investigated the tumor suppressor neurofibromin (NF1), a dual repressor for RAS and ER signaling, whose inactivation promotes endocrine therapy (ET) resistance and is associated with inferior relapse-free survival. NF1 copy number loss was detected in 62% of ER+ patients who subsequently developed metastases and was associated with an increased likelihood of bone metastases at initial diagnosis. In mouse xenograft models, NF1-depleted ER+ breast cancer cells demonstrated enhanced dissemination to skeletal sites following surgical resection of primary tumors. Furthermore, after intra-iliac injection, NF1-depleted cells generated significantly greater tumor burden in bone. Transcriptomic profiling revealed enrichment of bone-related gene signatures in NF1-depleted ER+ breast cancer cells, which more potently induced osteoclast differentiation and bone loss in co-culture systems. In parallel, low NF1 expression correlated with repressed T cell functional states in primary breast tumors and bone metastases. Consistent with these clinical observations, NF1-depleted ER+ breast cancer cells more effectively inhibited proliferation, interferon-γ secretion, and cytotoxicity of human primary CD8+ T cells. Collectively, these findings identify NF1 inactivation as a key driver of bone metastasis in a substantial subset of ER+ breast cancers. By amplifying the osteolytic “vicious cycle” and promoting immune evasion, NF1 loss remodels the microenvironment to favor tumor expansion. These results further suggest that NF1 loss functionally links therapy resistance with increased skeletal metastatic potential.
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10. GSE317620：RBP SYNCRIP 与 RNA 甲基化在决定 EV miRNA 载荷及其在细胞间通讯中的功能中的相互作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：methylation
• 📝 描述：Contributor : Luca QuattrocchiSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensSmall extracellular vesicles (sEVs) are critical mediators of tumour–microenvironment communication, largely through the selective transfer of microRNAs (miRNAs) that reprogram recipient cells. Active miRNA sorting into sEVs depends on RNA‑binding proteins, sequence determinants and RNA modifications. Here, a functional interplay between the RBP SYNCRIP and N6‑methyladenosine (m6A) RNA methylation in controlling miRNA loading into hepatocellular carcinoma (HCC)‑derived sEVs has been disclosed. It is reported that i) METTL3‑dependent m6A modification is required for efficient binding of SYNCRIP to specific miRNAs, thereby enabling their selective incorporation into sEVs; ii) silencing of SYNCRIP markedly reshapes the sEV miRNA-cargo and impairs the ability of HCC‑derived sEVs to induce epithelial–mesenchymal transition (EMT) in non‑tumorigenic hepatocytes. Notably, iii) depletion of METTL3 produces an even stronger effect, indicating that m6A methylation represents an upstream and essential determinant of SYNCRIP‑mediated miRNA export. Mechanistically, the data identify SYNCRIP as an m6A‑dependent miRNA reader, adding epitranscriptomic regulation to sequence‑based miRNA sorting into sEVs. Functionally, disruption of this interaction attenuates sEV‑driven EMT and pro‑tumorigenic signalling. Collectively, these findings uncover a novel regulatory axis governing sEV miRNA cargo selection and highlight the m6A–SYNCRIP interplay as a potential therapeutic target to interfere with EV‑mediated tumour progression and metastasis.
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详细内容（全部3条）

1. ⭐ Perturb-DBiT——利用空间CRISPR筛选和RNA测序绘制癌症生物学图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing、spatial
• 📝 描述：New spatial RNA sequencing technology links large-scale CRISPR perturbations to tumor growth, metastasis, immune responses, and complex RNA regulation within intact tissues… The post Perturb-DBiT – mapping cancer biology with spatial CRISPR screening and RNA sequencing appeared first on RNA-Seq Blog.
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2. 科学家发现癌症与阿尔茨海默病之间存在令人惊讶的联系

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、Alzheimer
• 📝 描述：Researchers discovered that mutations linked to blood cancers may help trigger Alzheimer’s disease by creating overly inflammatory immune cells in the brain. The unexpected finding could lead to new blood-based screening methods and potential treatments borrowed from cancer medicine.
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3. m6A-ARTR-DBiT – 利用空间 m6A 分析绘制组织中 RNA 修饰图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial
• 📝 描述：Spatial RNA sequencing and m6A profiling reveal how RNA modifications vary across tissues, uncovering region-specific patterns of gene regulation in developing and adult… The post m6A-ARTR-DBiT – mapping RNA modifications across tissues with spatial m6A profiling appeared first on RNA-Seq Blog.
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• GSE316378 小鼠 SINE B2 非编码 RNA 中腺苷到肌苷的差异性 RNA 编辑揭示了一种新型的表观转录组对淀粉样蛋白 β 神经毒性的反应
• GSE282375 LDB1 调控多能性和谱系分化中的基因表达和染色质结构 [ATAC-seq]
• GSE282372 LDB1 调控多能性和谱系分化中的基因表达和染色质结构 [RNA-seq]
• GSE278838 Degos 病患者的皮肤、血液和脑脊液 (CSF) 单细胞 RNA 转录组谱。
• GSE335338 EphA4 通过对头颈部鳞状细胞癌中 AKT 的上游负调控介导促肿瘤和抗肿瘤效应 - EphA4 敲除对 HNSCC 细胞系中 RNA 表达的影响。
• GSE335176 醋酸甲羟孕酮相关脑膜瘤的基因组特征[甲基化]
• GSE335175 醋酸甲羟孕酮相关脑膜瘤的基因组特征 [RNA-seq]
• GSE329566 CDK8 抑制解除融合驱动的肺泡横纹肌肉瘤中的肌肉分化阻滞 [ChIP-Seq]
• GSE320348 细胞内在的糖皮质激素生物合成和感知回路维持 Th17 细胞的稳态 [ATAC-seq]
• GSE304450 评估microRNA遗传变异在胃癌易感性和病理生理学中的作用
• GSE303149 CDK8 抑制解除融合驱动的肺泡状横纹肌肉瘤中的肌肉分化阻滞 [ATAC-seq]
• GSE300974 CDK8 抑制解除融合驱动的肺泡横纹肌肉瘤中的肌肉分化阻滞 [RNA-seq]
• GSE298401 心肌细胞蛋白O-GlcNAc糖基化水平的瞬时升高增强了压力超负荷诱导的心脏重塑的易感性
• GSE296490 体外极化的 Th0 细胞群体 ATAC-seq 数据
• GSE296482 细胞内在的糖皮质激素生物合成和感知回路维持 Th17 细胞的稳态 [RNA-seq]
• GSE245937 G1期适当的核区室重组对于DNA复制控制至关重要[Hi-C]
• GSE334865 过度活跃的 BMP 和机械信号重塑染色质以驱动进行性骨化性纤维发育不良中的异常骨生成 (ATAC-Seq)
• GSE334754 宿主感染选择驱动细菌社会欺骗的sRNA变体
• GSE334731 过度活跃的 BMP 和机械信号重塑染色质以驱动进行性骨化性纤维发育不良中的异常骨生成（RNA-Seq）
• GSE334648 发育和炎症挑战期间胆汁酸代谢的改变
• GSE334646 ATAC-seq 测序数据来自新生和成年野生型小鼠的近端和远端结肠上皮细胞。
• GSE234820 全外显子组测序揭示肥厚型心肌病的突变特征