详细内容（前10条）

1. ⭐ GSE324058 快速转录动力学在急性髓系白血病阿糖胞苷耐药性中的作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、ATAC-seq
• 📝 描述：Contributors : Goichi Tatsumi ; Rajni Kumari ; Yutaro Suzuku ; Shuting Li ; Russell Scharf ; Samuel Taylor ; Sriram Sundaravel ; Amit Verma ; Justin Wheat ; Ulrich SteidlSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy resistance remains a critical challenge in the treatment of patients with cancer including acute myeloid leukemia (AML). While genetic alterations contribute to chemotherapy resistance, rapid-adaptive non-genetic mechanisms, particularly transcription dynamics, remain poorly understood. Given the role of cell-intrinsic transcriptional variability in cell fate decisions, understanding and targeting chemotherapy-induced changes in transcription dynamics could offer new strategies to prevent chemotherapy resistance. In this study, we demonstrate that short-term treatment with the widely used chemotherapeutic cytarabine (AraC) leads to the rapid emergence of RNA-induced AML cells with increased AraC resistance in both cell lines as well as primary patient samples. Mechanistically, through global transcriptomic analyses and targeted high-resolution analysis of transcription dynamics using single-molecule RNA FISH, we found rapid induction of transcriptional dynamics and upregulation of key transcription factors (TFs) - which we term “AraC rapid response TFs (ARR-TFs)” and which include PU.1 and GATA1 – following chemotherapy treatment. At a functional level, short-term pre- and co-treatment with RNA transcription inhibitors effectively suppressed chemotherapy-induced RNA induction and prevented resistance acquisition, in both in vitro and in vivo models. Furthermore, we found that CRISPR-mediated suppression of PU.1 and GATA1 induction significantly attenuated AraC resistance. In summary, our findings reveal a previously unrecognized role of rapid and early adaptive transcriptional dynamics in AML chemotherapy resistance, highlighting master TFs as key regulators of drug resistance. These insights offer a novel, pharmacologically targetable and accessible approach to alleviate chemotherapy resistance, and encourage further testing with the ultimate goal to improve AML treatment outcomes.
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2. ⭐ GSE324057 快速转录动力学在急性髓系白血病阿糖胞苷耐药性中的作用 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、RNA-seq
• 📝 描述：Contributors : Goichi Tatsumi ; Rajni Kumari ; Yutaro Suzuki ; Shuting Li ; Russell Scharf ; Taylor Samuel ; Sriram Sundaravel ; Amit Verma ; Justin Wheat ; Ulrich SteidlSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy resistance remains a critical challenge in the treatment of patients with cancer including acute myeloid leukemia (AML). While genetic alterations contribute to chemotherapy resistance, rapid-adaptive non-genetic mechanisms, particularly transcription dynamics, remain poorly understood. Given the role of cell-intrinsic transcriptional variability in cell fate decisions, understanding and targeting chemotherapy-induced changes in transcription dynamics could offer new strategies to prevent chemotherapy resistance. In this study, we demonstrate that short-term treatment with the widely used chemotherapeutic cytarabine (AraC) leads to the rapid emergence of RNA-induced AML cells with increased AraC resistance in both cell lines as well as primary patient samples. Mechanistically, through global transcriptomic analyses and targeted high-resolution analysis of transcription dynamics using single-molecule RNA FISH, we found rapid induction of transcriptional dynamics and upregulation of key transcription factors (TFs) - which we term “AraC rapid response TFs (ARR-TFs)” and which include PU.1 and GATA1 – following chemotherapy treatment. At a functional level, short-term pre- and co-treatment with RNA transcription inhibitors effectively suppressed chemotherapy-induced RNA induction and prevented resistance acquisition, in both in vitro and in vivo models. Furthermore, we found that CRISPR-mediated suppression of PU.1 and GATA1 induction significantly attenuated AraC resistance. In summary, our findings reveal a previously unrecognized role of rapid and early adaptive transcriptional dynamics in AML chemotherapy resistance, highlighting master TFs as key regulators of drug resistance. These insights offer a novel, pharmacologically targetable and accessible approach to alleviate chemotherapy resistance, and encourage further testing with the ultimate goal to improve AML treatment outcomes.
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3. ⭐ GSE304115 免疫疗法、化疗、厄洛替尼或曲美替尼治疗的遗传多样性三阴性乳腺癌小鼠模型的批量 RNA 测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、RNA-seq
• 📝 描述：Contributor : Charles M PerouSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate the molecular determinants of response to therapy, we profiled 26 genetically diverse murine models of mammary cancer using bulk RNA sequencing. Tumors were harvested from mice that were either untreated or treated with immunotherapy (anti-PD-1 and anti-CTLA-4), chemotherapy (Carboplatin + Paclitaxel), EGFR inhibition (Erlotinib), or MEK inhibition (Trametinib) for 7 days. Each model represents a distinct transcriptional subtype and genetic background, enabling the assessment of intertumoral heterogeneity in treatment response. This dataset includes RNA-seq from 2-9 biological replicates per model per condition. Tumor samples were collected prior to or during treatment response assessment, and are accompanied by corresponding survival from similarly-treated tumors. All sequencing was performed on polyA-selected RNA using Illumina platforms.
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4. ⭐ GSE324069 转录组学和实验证实，虾青素通过抑制 Toll 样受体信号通路减少缺血性脑卒中中神经细胞的凋亡。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Toll-like receptor、transcriptomics、pathway
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusBackground and Objective. Inflammation is an important pathological process in ischemic stroke (IS). Astaxanthin (ATX) is a natural product with neuroprotection effects. However, the mechanism of ATX on anti-inflammatory after IS is not clear. The aim of this study was to investigate the mechanism of ATX on anti-inflammatory after IS.Methods. Male Sprague-Dawley rats were used to establish a model of middle cerebral artery occlusion (MCAO) on one side, and were pre-treated with gavage of ATX for 7 days. One day after MCAO, the brain tissues were collected. Transcriptomic sequencing, flow cytometry, brain water content, western blot, HE staining and ELISA were analyzed to evaluated the brain damage.Results. ATX treatment has improved the neurological deficits, reduced brain edema, and apoptosis. Also, ATX has reduced inflammation and apoptosis related proteins such as TLR4, MyD88, NFκB, IL1β, IL6, Cyt C and Caspsae3.Conclusions. ATX can improve nerve damage after IS, and these protective effects were realized by anti-inflammatory and anti-apoptosis. This protective mechanism involves the TLR4/MyD88/NF-κB signaling pathway
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5. ⭐ GSE318875 单细胞分析揭示出芽酵母中相互竞争决定细胞命运的独立衰老过程——scRNA-seq

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、single-cell、scRNA
• 📝 描述：Contributors : Manuel Hotz ; Rachel G Kroll-Ling ; Nathaniel H Thayer ; Daniel E GottschlingSeries Type : Expression profiling by high throughput sequencingOrganism : Saccharomyces cerevisiaePhenotypic heterogeneity is prevalent during aging, yet its underlying molecular drivers remain poorly understood. In budding yeast, two distinct aging trajectories, characterized by either ribosomal DNA (rDNA) instability or mitochondrial decline, have been proposed to be mutually exclusive. Here, we systematically dissect the heterogeneity among aging yeast cells by combining single-cell transcriptomics with longitudinal fluorescence microscopy. Our data reveals distinct transcriptional responses that emerge in aging cells, highlighted by loss of rDNA silencing, a hypoxia response, and the Environmental Stress Response (ESR). Contrary to expectation, we establish that ESR induction is not caused by rDNA instability but is instead a consequence of an early decline in mitochondrial membrane potential (MMP). However, the ESR is merely a biomarker of this decline and not itself a determinant of lifespan. While rDNA instability and mitochondrial dysfunction are anti-correlated as terminal phenotypes, we find that they are not necessarily mutually exclusive and can instead proceed concurrently within individual cells. Targeted genetic perturbations that are specific for one pathway do not impinge on the other, which is in contradiction to the idea of mutual inhibition between the two. We therefore propose a “competing hazards model”, where independent aging processes progress in parallel, and the observed mode of death is determined by which process first reaches a catastrophic failure point. Our work untangles the causal links between several aging pathways and provides a new framework for understanding how distinct aging trajectories emerge from independent molecular events.
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6. ⭐ GSE318874 单细胞分析揭示出芽酵母中相互竞争决定细胞命运的独立衰老过程——批量RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、RNA-seq、single-cell
• 📝 描述：Contributors : Manuel Hotz ; Rachel G Kroll-Ling ; Nathaniel H Thayer ; Daniel E GottschlingSeries Type : Expression profiling by high throughput sequencingOrganism : Saccharomyces cerevisiaePhenotypic heterogeneity is prevalent during aging, yet its underlying molecular drivers remain poorly understood. In budding yeast, two distinct aging trajectories, characterized by either ribosomal DNA (rDNA) instability or mitochondrial decline, have been proposed to be mutually exclusive. Here, we systematically dissect the heterogeneity among aging yeast cells by combining single-cell transcriptomics with longitudinal fluorescence microscopy. Our data reveals distinct transcriptional responses that emerge in aging cells, highlighted by loss of rDNA silencing, a hypoxia response, and the Environmental Stress Response (ESR). Contrary to expectation, we establish that ESR induction is not caused by rDNA instability but is instead a consequence of an early decline in mitochondrial membrane potential (MMP). However, the ESR is merely a biomarker of this decline and not itself a determinant of lifespan. While rDNA instability and mitochondrial dysfunction are anti-correlated as terminal phenotypes, we find that they are not necessarily mutually exclusive and can instead proceed concurrently within individual cells. Targeted genetic perturbations that are specific for one pathway do not impinge on the other, which is in contradiction to the idea of mutual inhibition between the two. We therefore propose a “competing hazards model”, where independent aging processes progress in parallel, and the observed mode of death is determined by which process first reaches a catastrophic failure point. Our work untangles the causal links between several aging pathways and provides a new framework for understanding how distinct aging trajectories emerge from independent molecular events.
• 🔗 查看原文

7. GSE324170 快速转录动力学在急性髓系白血病阿糖胞苷耐药性中的作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance
• 📝 描述：Contributors : Goichi Tatsumi ; Rajni Kumari ; Yutaro Suzuki ; Shuting Li ; Russell Scharf ; Samuel Taylor ; Sriram Sundaravel ; Amit Verma ; Justin Wheat ; Ulrich SteidlSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy resistance remains a critical challenge in the treatment of patients with cancer including acute myeloid leukemia (AML). While genetic alterations contribute to chemotherapy resistance, rapid-adaptive non-genetic mechanisms, particularly transcription dynamics, remain poorly understood. Given the role of cell-intrinsic transcriptional variability in cell fate decisions, understanding and targeting chemotherapy-induced changes in transcription dynamics could offer new strategies to prevent chemotherapy resistance. In this study, we demonstrate that short-term treatment with the widely used chemotherapeutic cytarabine (AraC) leads to the rapid emergence of RNA-induced AML cells with increased AraC resistance in both cell lines as well as primary patient samples. Mechanistically, through global transcriptomic analyses and targeted high-resolution analysis of transcription dynamics using single-molecule RNA FISH, we found rapid induction of transcriptional dynamics and upregulation of key transcription factors (TFs) - which we term “AraC rapid response TFs (ARR-TFs)” and which include PU.1 and GATA1 – following chemotherapy treatment. At a functional level, short-term pre- and co-treatment with RNA transcription inhibitors effectively suppressed chemotherapy-induced RNA induction and prevented resistance acquisition, in both in vitro and in vivo models. Furthermore, we found that CRISPR-mediated suppression of PU.1 and GATA1 induction significantly attenuated AraC resistance. In summary, our findings reveal a previously unrecognized role of rapid and early adaptive transcriptional dynamics in AML chemotherapy resistance, highlighting master TFs as key regulators of drug resistance. These insights offer a novel, pharmacologically targetable and accessible approach to alleviate chemotherapy resistance, and encourage further testing with the ultimate goal to improve AML treatment outcomes.
• 🔗 查看原文

8. GSE319448 DNA甲基化随机性与转录变异性相关，并识别出AML基因定义的亚型中趋同的表观遗传破坏[CellCulture_WGBS]

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic、methylation
• 📝 描述：Contributors : Eleanor A Hilgart ; Michael A Koldobskiy ; Andrew P FeinbergSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensEpigenetic regulators are frequently mutated in acute myeloid leukemia (AML). We investigated DNA methylation stochasticity in genetic subtypes of AML using WGBS data and publicly-available ERRBS data, and identified transcriptional dysregulation and altered chromatin accessibility related to methylation entropy using single-cell RNA-seq and single-cell ATAC-seq data. We demonstrated that the hypomethylating drug decitabine (DAC) leads to reduction of DNA methylation entropy specifically in IDH2-mutant AML cells.
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9. GSE319447 DNA甲基化随机性与转录变异性相关，并识别出AML基因定义的亚型中趋同的表观遗传破坏[PrimaryAML_scATACseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic、methylation
• 📝 描述：Contributors : Eleanor A Hilgart ; Michael A Koldobskiy ; Andrew P FeinbergSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensEpigenetic regulators are frequently mutated in acute myeloid leukemia (AML). We investigated DNA methylation stochasticity in genetic subtypes of AML using WGBS data and publicly-available ERRBS data, and identified transcriptional dysregulation and altered chromatin accessibility related to methylation entropy using single-cell RNA-seq and single-cell ATAC-seq data.
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10. GSE319444 DNA甲基化随机性与转录变异性相关，并识别出AML基因定义的亚型中趋同的表观遗传破坏[PrimaryAML_WGBS]

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic、methylation
• 📝 描述：Contributors : Eleanor A Hilgart ; Michael A Koldobskiy ; Andrew P FeinbergSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensEpigenetic regulators are frequently mutated in acute myeloid leukemia (AML). We investigated DNA methylation stochasticity in genetic subtypes of AML using WGBS data and publicly-available ERRBS data, and identified transcriptional dysregulation and altered chromatin accessibility related to methylation entropy using single-cell RNA-seq and single-cell ATAC-seq data.
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详细内容（全部2条）

1. ⭐ 单细胞RNA测序和空间转录组学揭示乳腺癌淋巴结转移中细胞、代谢和免疫之间复杂的相互作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immunity、lymph、regex:lymph(o|atic)?、metabolism、sequencing、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：RNA sequencing combined with spatial transcriptomics maps gene activity across breast cancer lymph node metastases…
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2. 细胞核内发现的隐蔽代谢

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism
• 📝 描述：Researchers have found hundreds of metabolic enzymes attached to human DNA inside the cell nucleus. Different tissues and cancers show unique patterns of these enzymes, forming a “nuclear metabolic fingerprint.” Some of the enzymes gather around damaged DNA to assist with repair. The discovery reveals an unexpected link between metabolism and gene regulation that could influence how cancers grow and respond to treatment.
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• GSE314922 免疫-微生物组协调定义了健康人类的干扰素设定点 [批量 RNA-seq]
• GSE314194 m6A 甲基化通过抑制 Alu 重复序列的双链 RNA 积累来抑制结直肠癌中的抗肿瘤免疫反应 [RNAseq2]
• GSE289982 m6A甲基化通过抑制Alu重复序列双链RNA的积累来抑制结直肠癌中的抗肿瘤免疫反应
• GSE289971 m6A 甲基化通过抑制 Alu 重复序列的双链 RNA 积累来抑制结直肠癌中的抗肿瘤免疫反应 [RNA-Seq1]
• GSE289970 m6A 甲基化通过抑制 Alu 重复序列双链 RNA 的积累来抑制结直肠癌中的抗肿瘤免疫反应 [MeRIP]
• GSE289969 m6A 甲基化通过抑制 Alu 重复序列的双链 RNA 积累来抑制结直肠癌中的抗肿瘤免疫反应 [MDA5]
• GSE289968 m6A 甲基化通过抑制 Alu 重复序列双链 RNA 的积累来抑制结直肠癌中的抗肿瘤免疫反应 [CUT&Run]
• GSE286060 内在无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [ATAC-seq]
• GSE281087 DNA甲基化随机性与转录变异性相关，并识别出AML基因定义的亚型中趋同的表观遗传破坏[scRNAseq]
• GSE239608 tRNA m1A修饰通过促进关键干扰素相关基因的翻译来增强巨噬细胞的抗肿瘤免疫力
• GSE288463 AMBRA1 作为髓母细胞瘤中 SHH 通路的新型正调控因子 [scRNA-seq]
• GSE288462 AMBRA1 作为髓母细胞瘤中 SHH 通路的新型正调控因子 [RNA-Seq]
• GSE323366 全基因组分析揭示了 EGFR 抑制后细胞死亡的遗传依赖性 [RNA-Seq]
• GSE300751 CDK16 和 CDK18 抑制可抑制核孔介导的 DNA 修复和肝细胞癌 [肝肿瘤]
• GSE291596 联合靶向 CDK2 和 CDK9 可抑制 MYC 致癌程序，并在 CIC 重排肉瘤中发挥抗肿瘤作用
• GSE286901 鼻病毒通过差异性激活上皮固有免疫信号通路引发不同的宿主反应 [scRNA-Seq]
• GSE286616 鼻病毒通过差异性地激活上皮固有免疫信号通路引发不同的宿主反应 [RNA-Seq]
• GSE248025 阵发性睡眠性血红蛋白尿患者骨髓细胞的单细胞 RNA 测序。
• GSE324142 揭示 p53 变体 p53psi 的发育和肿瘤抑制作用
• GSE318419 神经元 GPCR 修饰神经肽信号传导以抑制远端组织中的蛋白质稳态 [AM140]
• GSE317361：全基因组范围内的编码，用于定义细胞类型特异性的CTCF结合和染色质组织
• GSE314923 免疫-微生物组协调决定健康人类的干扰素设定点
• GSE314416 免疫-微生物组协调决定健康人类的干扰素设定点 [CITE-seq]
• GSE310860 核斑点能够加工来自富含 GC 等位基因的 RNA [RNA-Seq]
• GSE310803 核斑点能够加工来自富含 GC 的等位基因的 RNA [Df1 RNA-Seq]
• GSE310736 Wnt 物质维持人类骨骼干细胞中的 H3K14 乙酰化，用于组织工程和骨修复 [RNA-Seq]
• GSE310733 Wnt 物质维持人类骨骼干细胞中的 H3K14 乙酰化，用于组织工程和骨修复 [ATAC-Seq]
• GSE309663 Wnt抑制通过减轻内源性逆转录病毒的表观遗传抑制来激活干扰素刺激基因表达
• GSE305606 固有无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向作用 [附加数据]
• GSE305471 女性特异性 Cx3cr1 驱动的 tau 蛋白病中 ALS 和阿尔茨海默病风险基因的调控
• GSE301805 串联重复序列内转录因子基序簇的抑制是免疫稳态所必需的
• GSE300320 序列特异性 RNA 识别驱动限制子介导的基因外转录终止 [HeLa__4sU-RNAseq]
• GSE300319 序列特异性 RNA 识别驱动限制子介导的基因外转录终止 [HCT116_4sU-RNAseq]
• GSE300318 序列特异性 RNA 识别驱动限制子介导的基因外转录终止 [ChIP-Seq]
• GSE296339 神经元 GPCR 修饰神经肽信号传导以抑制远端组织中的蛋白质稳态
• GSE287065 固有无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [组蛋白 LCD]
• GSE286066 固有无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [YY1]
• GSE286065 固有无序区限制了哺乳动物和植物中 RNA 和组蛋白去甲基酶的基因组靶向 [m6a]
• GSE286064 内在无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [Histone_LCD_RNA]
• GSE286063 固有无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [Histone_ALKBH]
• GSE286062 内在无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [CLIP-seq]
• GSE286061 内在无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [caRNA m6A]
• GSE286059 固有无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [欧盟]
• GSE285802 内在无序区抑制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [MeRIP-seq]
• GSE285801 内在无序区限制哺乳动物和植物中 RNA 和组蛋白去甲基化酶的基因组靶向 [基因组占位]
• GSE228318 髓腔扩张是由胎儿骨骼发育过程中不同的细胞群介导的[scRNA-seq]
• GSE228317 髓腔扩张是由胎儿骨骼发育过程中不同的细胞群介导的[批量RNA测序]
• GSE205248 H3K27me3 扩散组织典型的 PRC1 染色质结构以调节发育程序 [scRNA-seq]
• GSE205246 H3K27me3 扩散组织典型的 PRC1 染色质结构以调节发育程序 [RNA-seq]
• GSE205245 H3K27me3 扩散组织典型的 PRC1 染色质结构以调节发育程序 [ChIP-seq]
• GSE205224 H3K27me3 扩散组织典型的 PRC1 染色质结构以调节发育程序 [Hi-C ]
• GSE324301 线粒体DNA异质性驱动携带常见m.3243A>G突变的人类类器官皮层神经元紊乱
• GSE290707 墨西哥患者的乳腺癌样本
• GSE324361 人类中枢和周围神经系统中大tau蛋白亚型的分布
• GSE324000 噬菌体编码的 CasPRs 转录沉默多种 CRISPR-Cas 系统 [RNA-Seq]
• GSE323365 全基因组分析揭示了 EGFR 抑制后细胞死亡的遗传依赖性
• GSE300754 CDK16 和 CDK18 抑制可抑制核孔介导的 DNA 修复和肝细胞癌
• GSE300032 肌球蛋白VB对肠道祖细胞功能至关重要
• GSE292828 人类子宫移植后抑制 NFAT 会促进组织驻留 NK 细胞的丢失和相关的妊娠并发症 [scRNA-Seq]
• GSE291754 利用体内单细胞 CRISPR 筛选微蛋白，鉴定出一种关键的核糖体组分
• GSE286903 鼻病毒通过差异性激活上皮固有免疫信号通路引发不同的宿主反应
• GSE227992 Kdm6a ChIP-seq 用 MTX 处理 Sv129 小鼠胚胎干细胞
• GSE227083 CDK16 和 CDK18 抑制可抑制核孔介导的 DNA 修复和肝细胞癌 [Huh7]