详细内容（前10条）

1. ⭐ GSE328460 利用 CosMX 对粘液性管状梭形细胞癌进行单细胞分辨率空间转录组学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Ariel Madrigal ; Minjun Kim ; Zohreh Mehrjoo ; Tamiko Nishimura ; Yasser Riazalhosseini ; Hamed S NajafabadiSeries Type : OtherOrganism : Homo sapiensThis dataset investigates the spatial organization of a human mucinous tubular and spindle cell carcinoma using single-cell resolution spatial transcriptomics. The dataset comprises 22 fields of view from a primary tumor specimen profiled using the CosMX Human 1K panel. Gene program activity scores were estimated using gene programs previously identified from single-cell RNA sequencing data. Local malignant cell density, defined as the fraction of neighboring cells classified as malignant, was quantified and analyzed in relation to gene program activity to assess spatial associations within the tumor microenvironment.
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2. ⭐ GSE314940 粘连蛋白突变抑制 HLA II 类基因表达，从而促进唐氏综合征患儿在发展为急性白血病过程中的免疫逃逸 [Hi-C]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA、Hi-C
• 📝 描述：Contributors : Austin C Boucher ; Wojciech Rosikiewicz ; Yichao Li ; Yong Cheng ; Beisi Xu ; John D CrispinoSeries Type : OtherOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
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3. ⭐ GSE314929 粘连蛋白突变抑制 HLA II 类基因表达，从而促进唐氏综合征患儿在发展为急性白血病过程中的免疫逃逸 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA、ChIP-seq
• 📝 描述：Contributors : Austin C Boucher ; Wojciech Rosikiewicz ; Lahiri Konada ; John D CrispinoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
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4. ⭐ GSE314928 黏连蛋白突变抑制HLA II类基因表达，从而促进唐氏综合征患儿在发展为急性白血病过程中的免疫逃逸。[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA、RNA-seq
• 📝 描述：Contributors : Austin C Boucher ; Wojciech Rosikiewicz ; John D CrispinoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
• 🔗 查看原文

5. ⭐ GSE314926 研究表明，在唐氏综合征患儿中，黏连蛋白突变会抑制HLA II类基因表达，从而促进免疫逃逸，最终发展为急性白血病。[ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA、ATAC-seq
• 📝 描述：Contributors : Austin C Boucher ; Wojciech Rosikiewicz ; John D CrispinoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
• 🔗 查看原文

6. ⭐ GSE314930 粘连蛋白突变抑制 HLA II 类基因表达，从而促进唐氏综合征患儿在发展为急性白血病过程中的免疫逃逸 [CUT&Run]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA
• 📝 描述：Contributors : Austin C Boucher ; Wojciech Rosikiewicz ; Te Ling ; John D CrispinoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
• 🔗 查看原文

7. ⭐ GSE314927 研究表明，在唐氏综合征患儿中，黏连蛋白突变会抑制 HLA II 类基因表达，从而促进免疫逃逸，最终发展为急性白血病。[CRISPR]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、HLA
• 📝 描述：Contributors : Austin C Boucher ; Shilpa Narina ; Shondra M Pruett-Miller ; John D CrispinoSeries Type : OtherOrganism : Homo sapiensChildren with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.
• 🔗 查看原文

8. ⭐ GSE289138 胰腺癌异质性和免疫逃逸中的 PAI-巨噬细胞轴

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、macrophage
• 📝 描述：Contributors : Chiara Falcomatà ; Brian D BrownSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPancreatic ductal carcinoma (PDAC) is characterized by a highly immunosuppressive, ECM-rich microenvironment, yet tumors display striking heterogeneity. This raises the question of whether immune resistance is a global tumor property or organized within spatially restricted niches. Using Perturb-map spatial functional genomics, we determine how different genes shape the growth and cellular environments of PDAC clones across space and time. This revealed early gene-driven remodeling of local immune neighborhoods preceding late-stage spatial clonal dominance. We identify SERPINE1 (PAI1) and SERPINB2 (PAI2) as dominant regulators of tumor microenvironment control and immune evasion. These SERPINs promote stabilization of fibrin-rich ECM niches that spatially retain and program macrophages toward immunosuppressive states while excluding cytotoxic T cells. Loss of Serpine1 or Serpinb2, or pharmacologic inhibition of PAI1 or CD18, improves tumor control and synergizes with anti-PD-1. Multimodal spatial analysis of patient tumors revealed that immunosuppressive niches form around rare SERPINB2- and SERPINE1-expressing PDAC subpopulations, dominated by SPP1+MARCO+ macrophages. These findings identify cancer-derived SERPINE1/B2 as local spatial organizers of immune suppression, linking tumor-intrinsic heterogeneity to local microenvironmental control and immunotherapy resistance in PDAC.
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9. GSE326211 活性组蛋白修饰限制脱靶 6mA 沉积并维持根霉中的转录稳定性 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、histone
• 📝 描述：Contributors : Carlos Lax ; Macario Osorio ; Natalia Nicolás ; Ghizlane Tahiri ; Stephen Mondo ; Vivian Ng ; Eusebio Navarro ; Igor Grigoriev ; Francisco Nicolás ; Victoriano GarreSeries Type : Expression profiling by high throughput sequencingOrganism : Rhizopus microsporusEpigenetic mechanisms provide sophisticated regulatory layers that modulate gene expression across diverse organisms, yet their organization and crosstalk remain poorly understood in non-dikarya fungi. Here, we characterize the genome-wide landscape of chromatin organization in Rhizopus microsporus, revealing a compartmentalized architecture where active histone modifications (H3K4me1, H3K4me3, H3K27ac) define transcriptionally active euchromatin distinct from H3K9me3-marked constitutive heterochromatin. Through comprehensive ChIP-seq analysis, we demonstrate that these modifications exhibit distinct distribution patterns over gene bodies and co-localize with 6-methyladenine (6mA) clusters, the predominant DNA modification in this fungus. We identified functional specialization among Set1 and Gcn5 paralogs, where Set1a primarily deposits H3K4me3, Set1b regulates H3K4me1, and both Gcn5 variants function redundantly in H3K27ac deposition. Knockout analysis reveals that these enzymes are critical for sporulation, stress resistance, and pathogenicity. Importantly, we uncover a hierarchical crosstalk where histone modifications restrict off-target 6mA deposition, regulate methylation cluster stability, and buffer transcriptional variation. Our findings establish R. microsporus as a model for understanding epigenetic compartmentalization in non-dikarya fungi and reveal conserved principles of epigenetic crosstalk that may be fundamental to eukaryotic chromatin regulation.
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10. GSE326209 活性组蛋白修饰限制脱靶 6mA 沉积并维持根霉中的转录稳定性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、histone
• 📝 描述：Contributors : Carlos Lax ; Macario Osorio ; Natalia Nicolás ; Ghizlane Tahiri ; Stephen Mondo ; Vivian Ng ; Eusebio Navarro ; Igor Grigoriev ; Francisco Nicolás ; Victoriano GarreSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Rhizopus microsporusEpigenetic mechanisms provide sophisticated regulatory layers that modulate gene expression across diverse organisms, yet their organization and crosstalk remain poorly understood in non-dikarya fungi. Here, we characterize the genome-wide landscape of chromatin organization in Rhizopus microsporus, revealing a compartmentalized architecture where active histone modifications (H3K4me1, H3K4me3, H3K27ac) define transcriptionally active euchromatin distinct from H3K9me3-marked constitutive heterochromatin. Through comprehensive ChIP-seq analysis, we demonstrate that these modifications exhibit distinct distribution patterns over gene bodies and co-localize with 6-methyladenine (6mA) clusters, the predominant DNA modification in this fungus. We identified functional specialization among Set1 and Gcn5 paralogs, where Set1a primarily deposits H3K4me3, Set1b regulates H3K4me1, and both Gcn5 variants function redundantly in H3K27ac deposition. Knockout analysis reveals that these enzymes are critical for sporulation, stress resistance, and pathogenicity. Importantly, we uncover a hierarchical crosstalk where histone modifications restrict off-target 6mA deposition, regulate methylation cluster stability, and buffer transcriptional variation. Our findings establish R. microsporus as a model for understanding epigenetic compartmentalization in non-dikarya fungi and reveal conserved principles of epigenetic crosstalk that may be fundamental to eukaryotic chromatin regulation.
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1. 对转移性骨髓神经母细胞瘤样本的单细胞和批量RNA测序数据进行比较研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：RNA sequencing reveals how neuroblastoma reshapes the bone marrow environment, identifying immune interactions and new tumor-specific targets that may improve…
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2. 细胞类型特征揭示了不同人群中阿尔茨海默病共同的特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：RNA sequencing reveals cell-specific molecular signatures of Alzheimer’s disease shared across diverse populations, providing new insights into disease mechanisms and potential therapeutic targets…
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3. 阿尔茨海默病研究取得突破性进展：科学家无需清除脑斑块即可恢复两小时睡眠

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have uncovered a surprising culprit behind sleep loss in Alzheimer’s disease: the brain’s own immune cells. In mice with amyloid plaques, overactive microglia triggered inflammation that kept the brain from getting enough deep, restorative sleep. Temporarily removing most of these cells restored more than two hours of sleep per day, even though the plaques remained unchanged.
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4. 科学家发现一种能保护大脑免受阿尔茨海默病损害的蛋白质

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：A protein called SORLA may act as a powerful defense against the toxic tau tangles involved in Alzheimer’s disease. Mice with extra SORLA had less tau accumulation, less brain atrophy, and healthier connections between neurons, while mice without it experienced more severe damage. The findings also revealed a possible drug target that could help control harmful activity in supporting brain cells.
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• GSE325753 靶向 EHMT2 增强 NK 细胞成熟和抗肿瘤活性 [RNA-Seq]
• GSE282152 利用二维和三维hiPSC-神经元模型解析Parkin (PRKN)相关帕金森病转录组
• GSE272377 老年 Grn KO 小鼠分选小胶质细胞的单细胞 RNA 测序 [HEX000661]
• GSE339154：肝细胞特异性 ADK 过表达小鼠和对照小鼠肝脏非实质细胞的单细胞 RNA 测序
• GSE330528 骨髓微环境中 Latexin 的缺失通过 LIFR 信号通路下调和免疫激活抑制白血病
• GSE328692 单细胞基因程序定义了肾细胞癌的亚型特征和转移轨迹
• GSE272740 SUCLG1 缺陷导致过度琥珀酰化并损害白血病发展 [RNA-seq]
• GSE272739 SUCLG1 缺陷导致过度琥珀酰化并损害白血病发展 [ChIP-seq]
• GSE337264 CALB2 是转移性前列腺癌中的一种机械抗性基因
• GSE327962 CRISPR介导的Mitf、Tfe3和Tfeb敲除对WT和Grn KO小鼠BMDM转录组的影响[hex001130]
• GSE325754 靶向 EHMT2 增强 NK 细胞成熟和抗肿瘤活性 [CUT&Tag]
• GSE308598 病毒RNA和RNase L驱动的内含子保留的整合感知协调抗痘病毒免疫
• GSE272363 溶酶体酸化对 Grn 敲除原代小胶质细胞转录组的影响 [HEX000747_MG]
• GSE272358 组成型 Grn KO 对 BMDM 转录组的影响 [HEX000747_BMDM]
• GSE339279 人类衰老大脑中环状和线性非编码RNA的特征及其与痴呆症的关联
• GSE328575 肾细胞癌单细胞基因表达谱分析
• GSE328454 HIF1A 和 HIF2A 敲低后 A498 透明细胞肾细胞癌细胞的基因表达谱分析
• GSE339044 巨型增强子将大脑中转录活跃的长基因分隔开来 [RNA-Seq]
• GSE339018 巨型增强子将大脑中转录活跃的长基因分隔开来 [Hi-C]
• GSE339012 巨型增强子将大脑中转录活跃的长基因分隔开来 [ChIP-Seq]
• GSE338907 肝组织来源的细胞外囊泡 miRNA 通过重编程代谢来维持肝脏稳态，从而调节 Pelteobagrus vachellii 的缺氧耐受性
• GSE311678 抗CD20抗体清除B细胞可促进多发性硬化症中黏膜来源的调节性IgA分泌细胞的生成
• GSE305971 整合单细胞分析揭示多发性骨髓瘤中的恶性原型和增殖层级
• GSE295540 RNA-seq 结果来自银屑病患者和健康对照者的皮肤样本。