详细内容（前10条）

1. ⭐ GSE312209 致癌 KRAS 驱动的分泌组涉及 TNFα，促进胰腺癌发生前的微环境准备 [共培养 scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:onco(logy|logist|gene|genic)、scRNA、KRAS
• 📝 描述：Contributors : Chantal Allgoewer ; Markus Breunig ; Alexander KlegerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Pancreatic ductal adenocarcinomas (PDACs) are highly lethal and aggressive with oncogenic KRAS being the main oncogenic driver of the disease. PDACs have been extensively profiled at advanced stages, and in advanced disease the tumor microenvironment is a major determinant that critically shapes patient outcomes. Since the molecular events occurring prior to invasive growth remain poorly understood, we aimed to investigate changes in the precancerous epithelium and its surrounding niche.Methods: We acquired time-resolved, single-cell transcriptomic (scRNAseq), and accessible-chromatin data from human pluripotent stem cell-derived pancreatic duct-like organoids (PDLO) inducibly expressing KRASG12D and from various niche cells. Results: Analysis of the pure epithelium already revealed key signatures of matrix remodeling and inflammation-related signaling upon few days of KRASG12D expression. Machine learning captured KRASG12D-dependent transcriptomic classifiers with high prediction accuracy and niche preparatory relevance. Various co-culture approaches followed by scRNAseq and functional validation, including T-cell microfluidics, demonstrated that the KRASG12D-induced PDLO-secretome activates pancreatic stellate cells (PaSCs) and protects precancerous organoids from T cell infiltration. Additional, in silico approaches reconstructed a virtual pancreatic (pre)cancerous space to profile cell-cell interactions between PDLOs and niche cells. TNFα emerged as a top-ranked ligand and was functionally validated to mediate T-cell shielding and PaSC activation. Cyst fluid from 80 prospectively sampled Intraductal Papillary Mucinous Neoplasm (IPMNs) –well-known cystic PDAC precursor lesions– showed a stepwise TNFα rise across LGD (low-grade), HGD (high-grade), and IC (invasive cancer).Conclusion: Our study reveals that oncogenic KRAS orchestrates niche-preparatory programs that precede PDAC formation and highlight a T cell exclusion program governed by epithelial-derived TNFα.
• 🔗 查看原文

2. ⭐ GSE284392 致癌 KRAS 驱动的分泌组涉及 TNFα，促进胰腺癌发生前的微环境准备 [时间序列 scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:onco(logy|logist|gene|genic)、scRNA、KRAS
• 📝 描述：Contributors : Chantal Allgoewer ; Markus Breunig ; Alexander KlegerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Pancreatic ductal adenocarcinomas (PDACs) are highly lethal and aggressive with oncogenic KRAS being the main oncogenic driver of the disease. PDACs have been extensively profiled at advanced stages, and in advanced disease the tumor microenvironment is a major determinant that critically shapes patient outcomes. Since the molecular events occurring prior to invasive growth remain poorly understood, we aimed to investigate changes in the precancerous epithelium and its surrounding niche.Methods: We acquired time-resolved, single-cell transcriptomic (scRNAseq), and accessible-chromatin data from human pluripotent stem cell-derived pancreatic duct-like organoids (PDLO) inducibly expressing KRASG12D and from various niche cells. Results: Analysis of the pure epithelium already revealed key signatures of matrix remodeling and inflammation-related signaling upon few days of KRASG12D expression. Machine learning captured KRASG12D-dependent transcriptomic classifiers with high prediction accuracy and niche preparatory relevance. Various co-culture approaches followed by scRNAseq and functional validation, including T-cell microfluidics, demonstrated that the KRASG12D-induced PDLO-secretome activates pancreatic stellate cells (PaSCs) and protects precancerous organoids from T cell infiltration. Additional, in silico approaches reconstructed a virtual pancreatic (pre)cancerous space to profile cell-cell interactions between PDLOs and niche cells. TNFα emerged as a top-ranked ligand and was functionally validated to mediate T-cell shielding and PaSC activation. Cyst fluid from 80 prospectively sampled Intraductal Papillary Mucinous Neoplasm (IPMNs) –well-known cystic PDAC precursor lesions– showed a stepwise TNFα rise across LGD (low-grade), HGD (high-grade), and IC (invasive cancer).Conclusion: Our study reveals that oncogenic KRAS orchestrates niche-preparatory programs that precede PDAC formation and highlight a T cell exclusion program governed by epithelial-derived TNFα.
• 🔗 查看原文

3. ⭐ GSE284390 致癌 KRAS 驱动的分泌组涉及 TNFα，促进胰腺癌发生前的微环境准备 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:onco(logy|logist|gene|genic)、ATAC-seq、KRAS
• 📝 描述：Contributors : Chantal Allgoewer ; Markus Breunig ; Alexander KlegerSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensBackground: Pancreatic ductal adenocarcinomas (PDACs) are highly lethal and aggressive with oncogenic KRAS being the main oncogenic driver of the disease. PDACs have been extensively profiled at advanced stages, and in advanced disease the tumor microenvironment is a major determinant that critically shapes patient outcomes. Since the molecular events occurring prior to invasive growth remain poorly understood, we aimed to investigate changes in the precancerous epithelium and its surrounding niche.Methods: We acquired time-resolved, single-cell transcriptomic (scRNAseq), and accessible-chromatin data from human pluripotent stem cell-derived pancreatic duct-like organoids (PDLO) inducibly expressing KRASG12D and from various niche cells. Results: Analysis of the pure epithelium already revealed key signatures of matrix remodeling and inflammation-related signaling upon few days of KRASG12D expression. Machine learning captured KRASG12D-dependent transcriptomic classifiers with high prediction accuracy and niche preparatory relevance. Various co-culture approaches followed by scRNAseq and functional validation, including T-cell microfluidics, demonstrated that the KRASG12D-induced PDLO-secretome activates pancreatic stellate cells (PaSCs) and protects precancerous organoids from T cell infiltration. Additional, in silico approaches reconstructed a virtual pancreatic (pre)cancerous space to profile cell-cell interactions between PDLOs and niche cells. TNFα emerged as a top-ranked ligand and was functionally validated to mediate T-cell shielding and PaSC activation. Cyst fluid from 80 prospectively sampled Intraductal Papillary Mucinous Neoplasm (IPMNs) –well-known cystic PDAC precursor lesions– showed a stepwise TNFα rise across LGD (low-grade), HGD (high-grade), and IC (invasive cancer).Conclusion: Our study reveals that oncogenic KRAS orchestrates niche-preparatory programs that precede PDAC formation and highlight a T cell exclusion program governed by epithelial-derived TNFα.
• 🔗 查看原文

4. ⭐ GSE304485：来自13种TCGA癌症类型和正常组织的批量RNA-Seq基因表达谱，用于肿瘤分类

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、TCGA、RNA-seq
• 📝 描述：Contributor : Sergii BabichevSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis dataset includes bulk RNA-Seq gene expression profiles of 6310 samples from 13 cancer types and normal tissues, obtained from The Cancer Genome Atlas (TCGA) and processed using a standardized pipeline. The raw count matrix, initially containing 60,660 genes, was filtered to retain only valid ENTREZ gene identifiers matched via the org.Hs.eg.db annotation package. Genes with zero variance across samples were removed. Normalization was performed by transforming expression values into log2 Counts Per Million (CPM) using the edgeR::cpm() function with log transformation. To ensure all values were positive and suitable for downstream modeling, a global shift was applied by adding the absolute minimum value. Subsequently, Gene Ontology (GO) analysis was performed across all three categories (Biological Process, Molecular Function, Cellular Component) using the TopGO package. Significant genes were selected, followed by Benjamini–Hochberg p-value correction, and validated using both Fisher’s and Kolmogorov–Smirnov tests. The resulting expression matrix consists of 18,564 functionally relevant genes across 6310 samples and forms the basis for clustering, classification, and metric evaluation within hybrid modeling frameworks for cancer diagnostics.
• 🔗 查看原文

5. ⭐ GSE319409 利用空间转录组学绘制创伤性脑损伤的继发反应图谱显示，急性 4-氨基吡啶治疗可减轻轴突和分子病理学

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Genevieve M Sullivan ; Kryslaine L Radomski ; Shaoqiu He ; Matthew D Wilkerson ; Clifton L Dalgard ; Camille Alba ; Xiaomei Zi ; Martin L Doughty ; Regina C ArmstrongSeries Type : OtherOrganism : Mus musculusDamage to long myelinated axons of white matter tracts is a hallmark pathology resulting from traumatic brain injury (TBI) forces and secondary injury processes. 4-aminopyridine (4-AP) is an FDA-approved Kv1 potassium channel inhibitor designed to mitigate axon dysfunction. We examined repurposing 4-AP as an acute TBI treatment using clinically-oriented neuropathology of axon damage combined with unbiased genome-wide spatial transcriptomics for comprehensive analysis of secondary injury processes. Adult male and female mice received a non-penetrating impact TBI with 4-AP (i.p., b.i.d) on days 1-7 post-injury. Along corpus callosum (CC) axons, TBI disrupted node of Ranvier domains, exposing the putative 4-AP target of mislocalized Kv1 channels (p < 0.005). Clinically reasonable 4-AP dosing (0.5 mg/kg) reduced nodal Nav1.6 channel loss (p < 0.05) and Caspr heminode formation (p < 0.005) after injury. Quantification of β-amyloid precursor protein immunolabeling showed significantly reduced CC axon damage at 4-AP doses of 0.5 mg/kg and 5 mg/kg (each p < 0.005). 4-AP safety, based on potential seizure risk after TBI, was unaltered with vehicle or 0.5 mg/kg 4-AP, while the 5 mg/kg dose induced seizure behavior in sham and TBI groups (p < 0.0001). Spatial transcriptomics mapped molecular signatures to tissue pathology. TBI increased axonal injury response genes in the CC and in motor and somatosensory cortex sites of CC projection neurons. TBI induced disease-associated glial phenotypes that mapped predominantly within the CC. TBI increased pathway expression for immune and vascular functions, neuron and glial cell signaling, and cellular dyshomeostasis, while reducing expression in myelination-related pathways. Gene expression analysis of 4-AP treatment (0.5 mg/kg) indicated potassium channel target engagement and increased neuroaxonal activity, along with dampened secondary injury responses. Collectively, these findings reveal underlying molecular pathology of the secondary injury response and advance 4-AP translation to reduce axon damage and stimulate activity-dependent repair after acute TBI.
• 🔗 查看原文

6. ⭐ GSE294652 人类 CAR-T 细胞样本的单细胞 RNA 测序数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、sequencing、single-cell
• 📝 描述：Contributors : Yuki Okuhiro ; Yasuhiro Kojima ; Hiroyoshi NishikawaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRaw RNA sequencing data derived from human CAR-T cell samples are deposited in this repository. The datasets include bulk single-cell RNA-seq reads generated for research purposes.
• 🔗 查看原文

7. GSE310017 STAT5B SH2 结构域上的疾病相关突变调节肝脏中的胆固醇和脂质代谢 [RNA-Seq 肝脏]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、RNA-seq
• 📝 描述：Contributor : Hye Kyung LeeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGrowth hormone (GH) signaling through STAT5B is a central regulator of hepatic metabolism, yet the functional consequences of disease-associated STAT5B variants remain poorly understood. Here, we generated mice carrying STAT5BY665F (gain-of-function) and STAT5BY665H (loss-of-function) alleles using CRISPR/Cas9-mediated base editing to dissect their impact on metabolic regulation. STAT5BY665F mutants developed hepatic lipid accumulation, hypercholesterolemia, and enhanced insulin sensitivity, whereas STAT5BY665H mice displayed reduced body weight and impaired insulin responsiveness. Transcriptomic analyses revealed that STAT5BY665F strongly activated lipid, cholesterol, and immune transcriptional programs, while STAT5BY665H failed to induce these pathways. ChIP-seq demonstrated extensive STAT5BY665F enhancer occupancy at metabolic and immune loci, contrasting with the minimal chromatin engagement of STAT5BY665H. Beyond the liver, STAT5BY665F broadly reprogrammed adipose tissue gene expression, activating lipid metabolism and immune regulatory networks, whereas STAT5BY665H exerted more restricted effects. Notably, transcriptional and chromatin remodeling by STAT5B variants displayed sex-dependent differences, with male livers showing more pronounced reprogramming than females. Together, these findings illustrate how alterations in STAT5B activity that alter enhancer activation led to altered metabolic function in liver and adipose tissue.
• 🔗 查看原文

8. GSE309955 STAT5B SH2 结构域上的疾病相关突变调节肝脏中的胆固醇和脂质代谢 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、RNA-seq
• 📝 描述：Contributor : Hye Kyung LeeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGrowth hormone (GH) signaling through STAT5B is a central regulator of hepatic metabolism, yet the functional consequences of disease-associated STAT5B variants remain poorly understood. Here, we generated mice carrying STAT5BY665F (gain-of-function) and STAT5BY665H (loss-of-function) alleles using CRISPR/Cas9-mediated base editing to dissect their impact on metabolic regulation. STAT5BY665F mutants developed hepatic lipid accumulation, hypercholesterolemia, and enhanced insulin sensitivity, whereas STAT5BY665H mice displayed reduced body weight and impaired insulin responsiveness. Transcriptomic analyses revealed that STAT5BY665F strongly activated lipid, cholesterol, and immune transcriptional programs, while STAT5BY665H failed to induce these pathways. ChIP-seq demonstrated extensive STAT5BY665F enhancer occupancy at metabolic and immune loci, contrasting with the minimal chromatin engagement of STAT5BY665H. Beyond the liver, STAT5BY665F broadly reprogrammed adipose tissue gene expression, activating lipid metabolism and immune regulatory networks, whereas STAT5BY665H exerted more restricted effects. Notably, transcriptional and chromatin remodeling by STAT5B variants displayed sex-dependent differences, with male livers showing more pronounced reprogramming than females. Together, these findings illustrate how alterations in STAT5B activity that alter enhancer activation led to altered metabolic function in liver and adipose tissue.
• 🔗 查看原文

9. GSE309954 STAT5B SH2 结构域上的疾病相关突变调节肝脏中的胆固醇和脂质代谢 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ChIP-seq
• 📝 描述：Contributor : Hye Kyung LeeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusGrowth hormone (GH) signaling through STAT5B is a central regulator of hepatic metabolism, yet the functional consequences of disease-associated STAT5B variants remain poorly understood. Here, we generated mice carrying STAT5BY665F (gain-of-function) and STAT5BY665H (loss-of-function) alleles using CRISPR/Cas9-mediated base editing to dissect their impact on metabolic regulation. STAT5BY665F mutants developed hepatic lipid accumulation, hypercholesterolemia, and enhanced insulin sensitivity, whereas STAT5BY665H mice displayed reduced body weight and impaired insulin responsiveness. Transcriptomic analyses revealed that STAT5BY665F strongly activated lipid, cholesterol, and immune transcriptional programs, while STAT5BY665H failed to induce these pathways. ChIP-seq demonstrated extensive STAT5BY665F enhancer occupancy at metabolic and immune loci, contrasting with the minimal chromatin engagement of STAT5BY665H. Beyond the liver, STAT5BY665F broadly reprogrammed adipose tissue gene expression, activating lipid metabolism and immune regulatory networks, whereas STAT5BY665H exerted more restricted effects. Notably, transcriptional and chromatin remodeling by STAT5B variants displayed sex-dependent differences, with male livers showing more pronounced reprogramming than females. Together, these findings illustrate how alterations in STAT5B activity that alter enhancer activation led to altered metabolic function in liver and adipose tissue.
• 🔗 查看原文

10. GSE301206 组蛋白乳酸化介导的血管平滑肌细胞代谢重塑通过促进乳酸积累加剧主动脉瘤和主动脉夹层。

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、histone
• 📝 描述：Contributors : Liwei Liu ; Aijun Sun ; Junbo GeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe phenotypic switch of vascular smooth muscle cells (VSMCs) is a crucial pathogenesis in aortic aneurysm and dissection (AAD), metabolic remodeling from oxidative phosphorylation (OXPHOS) to glycolysis involved in the process. Histone lactylation expression was analyzed in aorta of aortic aneurysm (AA) patients and AAD mice, as well as the AngII(angiotensin II)-treated VSMCs. CUT&Tag was used to explore the downstream target gene for H4K16 lactylation (H4K16la) between AngII-induced VSMCs and Control. The finding was to explore the impact of histone lactylation (H4K16la) on the progress of AAD.
• 🔗 查看原文

💡 该来源还有 48 条内容，详见 文末

详细内容（全部3条）

1. MEBOCOST——利用单细胞RNA测序绘制代谢物介导的细胞间通讯图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、single-cell
• 📝 描述：Using RNA sequencing and metabolic modeling, researchers developed MEBOCOST to map metabolite driven cell communication, revealing new insights into adipose tissue biology…
• 🔗 查看原文

2. 科学家发现一种能够使衰老脑细胞恢复活力的蛋白质

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：A newly identified protein may hold the key to rejuvenating aging brain cells. Researchers found that boosting DMTF1 can restore the ability of neural stem cells to regenerate, even when age-related damage has set in. Without it, these cells struggle to renew and support memory and learning. The findings raise hopes for treatments that could slow or even reverse aspects of brain aging.
• 🔗 查看原文

3. 小行星贝努揭示了生命化学的新途径

• ✍️ 作者：未知作者
• 🏷️ 关键词：pathway
• 📝 描述：Dust from asteroid Bennu is revealing a surprising origin story for life’s building blocks. New research suggests some amino acids formed in frozen ice exposed to radiation, not warm liquid water as scientists long believed. Isotopic clues show Bennu’s chemistry differs sharply from well-studied meteorites, pointing to multiple pathways for creating life’s ingredients.
• 🔗 查看原文

• GSE292907 选择性 CDK7 抑制通过阻断 RNA 聚合酶 II 起始复合物向延伸的转变，使肿瘤对拓扑异构酶 I 抑制剂-抗体药物偶联物敏感 [ChIP-seq]
• GSE292860 选择性 CDK7 抑制通过阻断 RNA 聚合酶 II 起始复合物向延伸的转变，使肿瘤对拓扑异构酶 I 抑制剂-抗体药物偶联物敏感 [RNA-seq]
• GSE312193 DDX53 驱动人类 TCam-2 细胞的转录组变化（RNA-seq 数据）
• GSE309309 中期冷冻保存和转录组分析作为识别用于急性髓系白血病免疫治疗的功能性NK细胞扩增最佳供体的策略
• GSE300791 增强子动力学和空间组织驱动人类脊髓中解剖学上受限的细胞状态 [scRNA-seq]
• GSE300782 增强子动力学和空间组织驱动人类脊髓中解剖学限制的细胞状态 [ATAC-seq]
• GSE282496 研究发现，新生儿幼稚 CD4+ T 细胞表达 CD38，这塑造了它们独特的代谢状态和高调节性 T 细胞潜能。
• GSE319341：整合单细胞转录组学和磷酸化蛋白质组学，解析调控皮质胶质细胞生成的EGFR依赖性网络
• GSE292266 利用 sci-L3-Strand-seq 进行单细胞模板链测序的高通量线性扩增
• GSE318830 LncRNA NAS1 缺陷驱动非小细胞肺癌的顺铂耐药性
• GSE300637 批量 RNA-seq 数据集支持对胸腺细胞和 T 细胞急性淋巴细胞白血病 (T-ALL) 中 MYC–USP10–SOX4 通路的分析。
• GSE289711 组蛋白变体 H2A.Z 对 Epstein-Barr 病毒潜伏的调控 [ChIP-seq]
• GSE319375 肺泡巨噬细胞的训练免疫通过增强 KLF4-MERTK 介导的胞吞作用促进损伤消退 [2]
• GSE319368 皮层祖细胞的多样性指导神经元层形成和区域胶质细胞模式形成
• GSE319345 胆管结扎后肝内胆管上皮细胞的单细胞 RNA 测序。
• GSE317656 Erastin诱导的铁死亡增强自然杀伤细胞的抗肿瘤活性，并有望用于治疗神经母细胞瘤
• GSE315862 靶向非同源末端连接途径使 MDM2 扩增的脂肪肉瘤对阿霉素诱导的衰老和 p53 介导的衰老敏感。
• GSE310018 Disease-associated mutations on the STAT5B SH2 domain regulate cholesterol and lipid metabolism in liver
• GSE301003 重症间日疟原虫疟疾中 vir 基因的比较临床转录组
• GSE300144 对间日疟原虫临床分离株（包括非复杂性疾病和复杂性疾病）中的正义和天然反义转录本 (NAT) 进行全转录组分析。
• GSE292846 选择性 CDK7 抑制通过阻断 RNA 聚合酶 II 起始复合物向延伸的转变，使肿瘤对拓扑异构酶 I 抑制剂-抗体药物偶联物敏感 [fastGRO]
• GSE281817 Dbf4依赖性激酶在染色体复制起点微调INO80功能
• GSE279121 染色质重塑因子 Arp9 调节黄曲霉的耐药性
• GSE261739 二恶英是一种内分泌干扰物，子宫内暴露会对男性 DNA 甲基化产生长期影响。
• GSE318972 β细胞中突触蛋白4的富集可阻止非肥胖糖尿病（NOD）小鼠向自身免疫性糖尿病的转化
• GSE318481 交感神经-成纤维细胞相互作用驱动胰腺癌中的神经损伤、成纤维细胞活化和基质重塑
• GSE312430 衰老关节滑膜巨噬细胞的性别相关变化
• GSE306921 新进化的内源性逆转录病毒启动卵巢储备以进行激活 [RNA-seq]
• GSE306919 新进化的内源性逆转录病毒启动卵巢储备以进行激活 [ATAC-seq]
• GSE304792 SP1在牛和人类胚胎基因组激活及早期胚胎发育中的物种特异性作用
• GSE300809 增强子动力学和空间组织驱动人类脊髓中解剖学限制的细胞状态 [STABseq]
• GSE300798 增强子动力学和空间组织驱动人类脊髓中解剖学上受限的细胞状态 [snRNA-seq]
• GSE300786 增强子动力学和空间组织驱动人类脊髓中解剖学限制的细胞状态 [snATAC-seq]
• GSE296577 临床试验中单次溶瘤病毒治疗后持续的T细胞活化和对胶质母细胞瘤的细胞毒性
• GSE293356 形态创新无需基因共选：果蝇性梳的进化是通过发育节奏和能量代谢的变化实现的
• GSE285755 LMO1 在神经母细胞瘤细胞中的表达重编程肿瘤相关巨噬细胞以促进转移。
• GSE317117 对感染嵌合 EV-A71 毒株的细胞进行 RNA 测序分析，其中 3C 蛋白酶区域与其他 EV-A71 毒株进行了交换。
• GSE312969 以单细胞分辨率绘制绵羊垂体青春期相关调控图谱
• GSE295191 RNA测序数据集来自小鼠CD8阳性T细胞
• GSE292265 脂肪细胞中 RUNX1 或 RUNX2 的基因缺失增强了米色脂肪的形成 [ChIP-Seq; CUT&Tag]
• GSE292124 脂肪细胞中 RUNX1 或 RUNX2 的基因缺失增强了米色脂肪的形成 [ATAC-seq]
• GSE318881 RNA-Seq定量分析慢性粒细胞白血病患者血浆外泌体对慢性粒细胞白血病细胞转录组的调控作用
• GSE318537 通过系统靶向和抑制鉴定骨矿物质密度 GWAS 位点的目标基因和调控网络 [hFOB ATAC-seq]
• GSE315711 从复发性扁桃体炎和 IgA 肾病患者的腭扁桃体中分离的滤泡间 Tfh 细胞的批量 RNA 测序。
• GSE314708 小胶质细胞 TFEB 激活通过增强自噬-溶酶体功能减轻阿尔茨海默病病理
• GSE309901 肌醇六磷酸激酶 (IP6K) 水平降低会损害克氏锥虫在人类心肌细胞内的生命周期转变和细胞内发育
• GSE307982 PTMA 保护线粒体完整性以维持 CD8+ T 细胞的代谢功能和抗肿瘤持久性
• GSE288513 Scap稳定PKM2以促进糖酵解并增强巨噬细胞的抗真菌免疫力