详细内容（前10条）

1. ⭐ GSE327406：冷冻组织切片中转录组和表观基因组靶标的空间分辨、整合的单细胞多组学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatially、transcriptome
• 📝 描述：Contributors : Ting Zhang ; Saba Farassati ; Alejandro Quiroz ; Yuanhang Liu ; Tamas Ordog ; Jeong-Heon LeeSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe present a spatial Trekker–CUT&Tag multiome protocol that combines direct spatial barcoding of a frozen tissue section with subsequent single-cell multiome analysis. This approach enables integrated single-cell and spatial profiling of histone H3K27ac modification and gene expression, revealing mechanistic and anatomical cell-type organization across the tissue.
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2. ⭐ GSE312281 MicroRNA-200 家族通过破坏 SOX9 功能抑制皮脂腺命运决定 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Arpan Das ; Rui YiSeries Type : OtherOrganism : Mus musculusHair follcile (HF) are known as mini-organs because of their cycling capability. They also provide an excellent system to study the developmental timeline of these appendages, regulated by multiple factors. However, how another skin appendage, sebaceous gland (SG), associated with the HFs gets specified from the HF-cells is largely unknown. Here using an integrated method we demonstrate how SOX9+ early progenitor cells regulate the fate specification of the SG.
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3. ⭐ GSE296563 DNMT3A 突变通过协调急性髓系白血病 (WGBS) 中的 BCAA 代谢来协调表观遗传和翻译调控

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、metabolism、epigenetic
• 📝 描述：Contributors : Chengyang Xu ; Yongjia Wei ; Chenxi Han ; Jian Li ; Jia Yu ; Fang WangSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) harboring DNMT3A mutation exhibits epigenetic dysregulation, chemoresistance and poor outcome, but the underlining mechanism remains elusive. Here, inspired by the unexpected finding that DNMT3A-mutated AML patients exhibit a unique translatome landscape, we connected this epigenetic mutation to translational dysregulation through reprogrammed branched-chain amino acid (BCAA) metabolism. Particularly, DNMT3A mutation induces DNA hypomethylation-dependent activation of BCAT1, a rate-limiting aminotransferase gene for BCAA metabolism. Thereafter, the accumulation of intracellular BCAA more profoundly alters translation of a select subset of transcripts with higher BCAA codon ratios. Accordingly, deficiency in BCAA availability reduces the translation of target genes and attenuated the proliferative advantages of DNMT3A-mutated AML cells. More importantly, the pharmacological inhibition of BCAT1 with Gabapentin normalized BCAA levels, reversed target genes translation and repressed leukemia cell growth specifically in DNMT3A-mutated AML cells. Collectively, these findings uncovered a novel epigenetics-metabolism axis, in which DNMT3A mutation boosts BCAA metabolism thereby not only forming a positive feedback loop to enhance DNA hypomethylation through alpha ketoglutarate (α-KG)-dependent ten-eleven translocation (TET) activation, but also affecting gene translation in a BCAA codon-biased manner. Moreover, the efficacy of Gabapentin in suppressing AML cell proliferation highlights the clinical relevance of targeting BCAA metabolism to improve outcomes of DNMT3A-mutated AML.
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4. ⭐ GSE296332 DNMT3A 突变通过调控急性髓系白血病中的支链氨基酸代谢来协调表观遗传和翻译调控

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、metabolism、epigenetic
• 📝 描述：Contributors : Chengyang Xu ; Yongjia Wei ; Chenxi Han ; Jian Li ; Jia Yu ; Fang WangSeries Type : Other ; Expression profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) harboring DNMT3A mutation exhibits epigenetic dysregulation, chemoresistance and poor outcome, but the underlining mechanism remains elusive. Here, inspired by the unexpected finding that DNMT3A-mutated AML patients exhibit a unique translatome landscape, we connected this epigenetic mutation to translational dysregulation through reprogrammed branched-chain amino acid (BCAA) metabolism. Particularly, DNMT3A mutation induces DNA hypomethylation-dependent activation of BCAT1, a rate-limiting aminotransferase gene for BCAA metabolism. Thereafter, the accumulation of intracellular BCAA more profoundly alters translation of a select subset of transcripts with higher BCAA codon ratios. Accordingly, deficiency in BCAA availability reduces the translation of target genes and attenuated the proliferative advantages of DNMT3A-mutated AML cells. More importantly, the pharmacological inhibition of BCAT1 with Gabapentin normalized BCAA levels, reversed target genes translation and repressed leukemia cell growth specifically in DNMT3A-mutated AML cells. Collectively, these findings uncovered a novel epigenetics-metabolism axis, in which DNMT3A mutation boosts BCAA metabolism thereby not only forming a positive feedback loop to enhance DNA hypomethylation through alpha ketoglutarate (α-KG)-dependent ten-eleven translocation (TET) activation, but also affecting gene translation in a BCAA codon-biased manner. Moreover, the efficacy of Gabapentin in suppressing AML cell proliferation highlights the clinical relevance of targeting BCAA metabolism to improve outcomes of DNMT3A-mutated AML.
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5. ⭐ GSE292303 犬和人肝细胞癌肿瘤微环境的多组学比较评估

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment
• 📝 描述：Contributors : Yulia Nussbaum ; Edward Ricemeyer ; Wesley WarrenSeries Type : Expression profiling by high throughput sequencingOrganism : Canis lupus familiarisBackground: Liver cancer remains a leading cause of death in humans. Its primary form, hepatocellular carcinoma (HCC) is frequently resistant to chemotherapy and radiation and often shows insufficient response to immunotherapy. HCC in dogs can arise from various factors but is not typically associated with viral infections, cirrhosis, or alcohol consumption, the more common triggers of spontaneous HCC in humans. This distinction offers a unique comparative perspective on the intrinsic genetic drivers of the disease.Methods: Using whole exome sequencing (WES) and single nucleus RNA sequencing (snRNA-seq) in tandem, we perform a multi-omic analysis of the dog HCC tumor.Results: Mutational analysis of impactful polymorphisms revealed a conserved cross-species landscape with genes such as CTNNB1, known for highly recurrent mutations in human HCC, showing similar alterations in dogs. In dog HCC tumors, we identified major cell types commonly observed in human HCC, including T lymphocyte, endothelial, macrophage, fibroblast, hepatocyte, malignant, and non-specific proliferating types. A comparative analysis of intercellular interactions across human and dog HCC cell types revealed intriguing parallels, particularly in macrophage functionality.Conclusions: These findings underscore the need for expanded genetic studies of dog HCC to further elucidate cross-species commonalities, offering deeper insights into key aspects of HCC biology and identifying novel therapeutic targets.
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6. ⭐ GSE282096 转录活性降低和剪接变化驱动衰老转录组中基因长度偏向的重编程（RNA-Seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、RNA-seq、transcriptome
• 📝 描述：Contributors : Saeid M Parast ; Madhurima Das ; Marta Iwanaszko ; Ali ShilatifardSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTranscription by RNA polymerase II (RNAPII), which is essential for protein-coding gene expression and cellular function, is increasingly understood to become dysregulated with aging. Here, we use a multi-modal approach to comprehensively characterize age-dependent changes in RNAPII-mediated transcription in both mouse and human tissues. Short-read total RNA sequencing (RNA-seq) to profile nascent transcription reveals a global reduction in overall transcriptional activity/frequency in aged tissues, without apparent change in elongation rates. Transcriptomic analysis reveals a shift toward preferential expression of short genes in aged tissues, with notable upregulation of short stress-response genes and downregulation of long neurodevelopmental genes in the aged mouse brain. These results are recapitulated by analysis of total RNA-seq data from human tissues. Leveraging long-read RNA-seq, we determine that the representation of aberrant mono-exonic and intron-retention splice isoforms is increased in the aged mouse brain. Finally, we characterize the composition of RNAPII transcriptional machinery, finding that interactions between RNAPII and the Mediator complex are decreased in the chromatin of aged mouse liver and brain. Collectively, these analyses provide insight for future aging studies and reveal potential transcriptional control targets for anti-aging drug development.
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7. ⭐ GSE282010 转录活性降低和剪接变化驱动衰老转录组中基因长度偏向的重连（ChIP-seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、ChIP-seq、transcriptome
• 📝 描述：Contributors : Saeid M Parast ; Madhurima Das ; Marta Iwanaszko ; Ali ShilatifardSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTranscription by RNA polymerase II (RNAPII), which is essential for protein-coding gene expression and cellular function, is increasingly understood to become dysregulated with aging. Here, we use a multi-modal approach to comprehensively characterize age-dependent changes in RNAPII-mediated transcription in both mouse and human tissues. Short-read total RNA sequencing (RNA-seq) to profile nascent transcription reveals a global reduction in overall transcriptional activity/frequency in aged tissues, without apparent change in elongation rates. Transcriptomic analysis reveals a shift toward preferential expression of short genes in aged tissues, with notable upregulation of short stress-response genes and downregulation of long neurodevelopmental genes in the aged mouse brain. These results are recapitulated by analysis of total RNA-seq data from human tissues. Leveraging long-read RNA-seq, we determine that the representation of aberrant mono-exonic and intron-retention splice isoforms is increased in the aged mouse brain. Finally, we characterize the composition of RNAPII transcriptional machinery, finding that interactions between RNAPII and the Mediator complex are decreased in the chromatin of aged mouse liver and brain. Collectively, these analyses provide insight for future aging studies and reveal potential transcriptional control targets for anti-aging drug development.
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8. ⭐ GSE234209：接受PD-1抗体治疗的2例胃癌患者的多点活检样本中免疫细胞和胃癌细胞的单细胞水平基因表达谱分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、antibody
• 📝 描述：Contributors : Chenfei Zhou ; Liting Guo ; Qu Cai ; Wenqi Xi ; Fei Yuan ; Huan Zhang ; Chao Yan ; Lei Huang ; Zhenggang Zhu ; Jun ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo analyze the correlation between the neutrophil-to-lymphocyte ratio (NLR) and prognosis of advanced gastric cancer (AGC) patients treated by PD-1 antibody-based therapy and to delineate molecular characteristics of circulating neutrophils by single-cell RNA sequencing (scRNA-seq).
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9. GSE333425 原发性神经母细胞瘤肿瘤细胞的 RNA-seq 分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、RNA-seq
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate the transcriptional effects of Paics, we performed RNA-seq on primary tumor cells isolated from Th-MYCN+/+Th-IGF2BP1+/+ mice.
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10. GSE332838 范可尼贫血通路激活将癌基因诱导的衰老转化为促肿瘤状态

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、pathway
• 📝 描述：Contributors : Yue Qiu ; Jingjie Mu ; Yifan Guo ; Jin-Yu Lu ; Xiaoqin Li ; Wenahn Liu ; Wenyan Xu ; Sha Song ; Xianjue MaSeries Type : Expression profiling by arrayOrganism : Drosophila melanogasterDNA repair pathways are canonically tumor-suppressive, yet emerging evidence suggests their upregulation can promote cancer progression, a paradox whose mechanisms remain poorly understood. Here, we report that activation of the Fanconi Anemia (FA) DNA repair pathway drives malignant tumor progression by reprogramming cellular senescence from a tumor-suppressive to a pro-tumorigenic state. Through an unbiased genetic screen in Drosophila, we identified that loss of Sras (homologous to human RCE1) cooperates with oncogenic RasV12 to induce slow-progressing yet highly malignant tumors. Bioinformatics analysis revealed marked upregulation of the FA pathway and Hippo signaling in these tumors. Genetic manipulation demonstrates that FA pathway activation is required for tumor growth and invasion. Mechanistically, we show that FA pathway upregulation enhances cellular senescence and triggers secretion of senescence-associated secretory phenotype (SASP) factors, particularly the cytokine Unpaired-1 (Upd1; IL-6 homolog), which in turn activates JAK-STAT signaling within tumor cells through an autocrine loop, thereby promoting tumor progression. Notably, p53 activation is dispensable for this pro-tumorigenic senescence program. FA pathway activation and its pro-tumorigenic function are conserved across multiple RasV12-driven malignant tumor models. Our findings reveal a previously unrecognized mechanism by which DNA repair machinery is co-opted to convert oncogene-induced senescence into a tumor-promoting state, with broad implications for understanding cancer progression and developing therapies targeting Ras-driven malignancies.
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💡 该来源还有 54 条内容，详见 文末

• GSE328967 多种感染模型表明结核分枝杆菌对先天免疫具有强大的抵抗力
• GSE327621 里氏木霉 Nsd3 转录因子：在发育、应激反应、次级代谢和纤维素酶产生中的多效性作用 [ATAC-seq]
• GSE318803 转录活性降低和剪接变化驱动衰老转录组中基因长度偏向的重连（CUT&Run）
• GSE298039 利用 RNA 测序对 CT26 细胞和通过强制表达 Oct4 和 SOX2 诱导的去分化 CT26 细胞进行转录组分析。
• GSE294249 BACH1 协调巨噬细胞状态转变以协调再生性炎症 [嵌合 BMT]
• GSE294248 BACH1 协调巨噬细胞状态转变以协调再生性炎症 [Individualmouse]
• GSE293856 甲型病毒 M1 破坏骨肉瘤中超级增强子驱动的致癌转录 [RNA-seq]
• GSE293855 甲型病毒 M1 破坏骨肉瘤中超级增强子驱动的致癌转录 [ChIP-seq]
• GSE282097 转录活性降低和剪接变化驱动衰老转录组中基因长度偏向性重编程
• GSE276811 果糖对 Asxl1 突变克隆造血的影响 [单细胞 RNA 测序]
• GSE240533 RNA-Seq 分析 CRISPR/Cas9 靶向乳腺癌细胞 AGR2 揭示其表达和分泌的潜在调节因子
• GSE313520 多细胞衰老会损害衰老过程中废用后骨骼肌的恢复
• GSE333548 ZNHIT1 依赖的 H2A.Z 在减数分裂前期 I 的沉积是雄性减数分裂粗线期基因表达和减数分裂进程的基础 [H2A.Z ChIP-seq]
• GSE333547 ZNHIT1 依赖的 H2A.Z 在减数分裂前期 I 的沉积是雄性减数分裂粗线期基因表达和减数分裂进程的基础 [scRNA-seq]
• GSE333466 用于高效人类 iPSC 重编程和分化的无病毒纳米颗粒-3D 支架平台 [WTC0011 RNA-Seq]
• GSE333429 原发性神经母细胞瘤肿瘤细胞的 RIP-seq 分析。
• GSE333428 TT-seq 分析原发性神经母细胞瘤肿瘤细胞。
• GSE333427 IGF2BP1 在 17q 扩增中与 MYCN 协同作用，调节神经母细胞瘤中的嘌呤生物合成和免疫治疗疗效
• GSE333317 肾上腺衍生因子驱动骨硬化性前列腺癌的进展
• GSE333246 感染柯萨奇病毒 B1 的人类肠道类器官的单细胞 RNA 测序
• GSE331489 哺乳动物衰老中细胞类型特异性时间动态的全球视角[II]
• GSE331488 哺乳动物衰老过程中细胞类型特异性时间动态的全球视角 [I]
• GSE330915 msf基因导致流感嗜血杆菌中与细胞表面修饰和代谢感知相关的环境特异性转录变化
• GSE330905 靶向钙调磷酸酶同源蛋白 1 (CHP1)-跨膜蛋白 87A (TMEM87A) 机械感受复合物：转移性卵巢癌的可药物靶点
• GSE330418 RNA-seq 分析了 P7 至 P21 时皮质 CD51+ 星形胶质细胞表达 hM3D-mCherry 的情况，注射生理盐水或 cno 后
• GSE330283 年轻和衰老间充质干细胞对内皮细胞转录组的重塑取决于共培养模式、细胞外基质和分泌因子
• GSE329791 骨骼肌干细胞中机械调控的转录和DNA甲基化程序
• GSE329437 骨骼肌干细胞中机械调控的转录和DNA甲基化程序
• GSE328452 里氏木霉 Nsd3 转录因子：在发育、应激反应、次级代谢和纤维素酶产生中的多效性作用
• GSE326404 急性及持续性人博卡病毒1型感染诱导人呼吸道上皮细胞转录组改变
• GSE324491 人类胚胎干细胞成骨模型中microRNA网络对发育性骨毒性的调控[RNA-Seq]
• GSE315093 核ERK-ATF5轴协调棕色脂肪细胞中的线粒体代谢和产热基因表达
• GSE312278 MicroRNA-200 家族通过破坏 SOX9 功能抑制皮脂腺命运决定 [scRNA-seq]
• GSE312276 MicroRNA-200 家族通过破坏 SOX9 功能抑制皮脂腺命运决定 [scATAC-seq]
• GSE311983 心内膜 HAND2 协调缺氧和 TGFβ 信号传导以调节冠状动脉形成 [scRNA-seq]
• GSE311982 心内膜 HAND2 协调缺氧和 TGFβ 信号传导以调节冠状动脉形成 [RNA-Seq]
• 利用单核RNA测序技术对甜叶菊叶片进行细胞类型特异性基因表达谱分析（GSE311951）
• GSE310986 AMPK对SPHK2的磷酸化将能量应激与乳腺癌中的核S1P信号传导联系起来
• GSE310304 UXS1 或 MRPL42 对肝细胞癌细胞系 HCCLM3 中 mRNA 表达的影响
• GSE299373 中华绒螯蟹眼柄在正常和高温条件下的转录组分析
• GSE298436 诺比列汀靶向 CHEK1-H3K27ac-CENPM 轴并抑制结直肠癌的恶性进展
• GSE298213 巨噬细胞在METTL1介导的m7G再急性炎症中的作用
• GSE297304 ClpX 和 PstB 的协同调控通过感受态驱动的代谢适应调节戈登链球菌对季铵化合物的敏感性
• GSE295094：代谢功能障碍小鼠模型在禁食和进食状态下肝脏对葡萄糖摄入反应的转录组分析
• GSE294445 调控星形胶质细胞中非经典WNT5B-NFATc2通路依赖的MMP14表达可改善亨廷顿病小鼠的神经病理学和运动行为
• GSE290362 α卫星RNA标记原始人类ESC的核周区室并抑制rRNA表达（染色体RNA测序）
• GSE290080 α卫星RNA标记原始人类ESC的核周区室并抑制rRNA表达（RNA-Seq）
• GSE281038 3D增强子动力学决定T细胞急性淋巴细胞白血病的治疗反应
• GSE268123 地塞米松预处理的CD4阳性CAR T细胞的测序分析
• GSE266639 研究发现，BMI1 水平降低可通过表观遗传增强 CSTA 和 TGFB2 来抑制自发性流产中滋养层细胞的增殖和迁移。
• GSE266348 TNF介导的细胞死亡：T细胞急性淋巴细胞白血病免疫治疗的可操作靶点
• GSE266346 TNF介导的细胞死亡：T-ALL免疫治疗的一个可操作靶点[2]
• GSE266344 TNF介导的细胞死亡：T-ALL免疫治疗的一个可操作靶点[1]
• GSE201682 Chinmo 通过直接调控 Doublesex 和胰岛素信号通路来维持成体干细胞的性别特性 [bulk RNA-seq]