详细内容（前10条）

1. ⭐ 健康成年人免疫老化全景图；空间多组学智能整合与调控网络推断、单细胞批次整合、单细胞可变剪切、发育潜能预测等工具上新 |单细胞视角

• ✍️ 作者：单细胞天地
• 🏷️ 关键词：免疫、单细胞、空间组学
• 🔗 查看原文

2. ⭐ 9.4分非肿瘤生信，衰老+机器学习+分型+免疫浸润+表达验证。这我也能做呀！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、免疫、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

3. ⭐ 非肿瘤纯生信，基于机器学习，无监督聚类等研究细胞衰老在疾病中的特征。衰老热点经久不衰！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、生信、聚类
• 📝 描述：点击查看详情
• 🔗 查看原文

4. ⭐ 最新8.1分非肿瘤生信，针对PANoptosis热点进行机器学习+单细胞筛选+简单验证，全文只有4个Figure！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

5. ⭐ 复旦大学发 Nat Cancer |临床试验+单细胞测序，看看他们是怎么做的

• ✍️ 作者：生信钱同学
• 🏷️ 关键词：cancer、测序、单细胞
• 📝 描述：临床实验配合单细胞测序
• 🔗 查看原文

6. ⭐ 文献分享|Nature Communications: 四大空间转录组平台性能大比拼：谁在肿瘤研究中更胜一筹？

• ✍️ 作者：王永成Lab
• 🏷️ 关键词：肿瘤、空间转录组、转录组
• 📝 描述：Nature Communications近年来，空间转录组学技术在分辨率与通量方面取得显著突破，但现有技术评
• 🔗 查看原文

7. 最新5.7分生信，单细胞泛癌+空转泛癌+百种机器学习研究CAF的衰老表型，投稿到接收仅48天，可谓是水刊中的天花板！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

8. 5月最新10+生信，基于细胞死亡和衰老的肿瘤分型及模型构建，分析不难，实验只有半个figure，值得学习！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、生信
• 🔗 查看原文

9. 15.7分纯生信，基于单细胞构建细胞衰老的细胞类型特异性图谱。自定义算法鉴定出新的衰老基因集！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

10. 蛋白质组转录组分析两三事：KEGG已经不是以前的KEGG了

• ✍️ 作者：Dr.X的基因空间
• 🏷️ 关键词：转录组、蛋白质组
• 📝 描述：旧代码需要定期检查运行稳定性，特别是代码中依赖到第三方数据库和网站时，需要警惕外部变化为内部分析带来不可忽视的影响
• 🔗 查看原文

💡 该来源还有 16 条内容，详见 文末

详细内容（前10条）

1. ⭐ GSE217286 缺血性心力衰竭预后指标真核翻译起始因子 3m 的 RNA 结合模式揭示其在心肌缺血再灌注后硝化损伤调控中的独特作用 [ClIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、leukemia、immune、immunity、immunology、TME、cardiac、glioma、kinase、resistance、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、Hi-C、single.cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、bioinformatics、R package、Bioconductor、Seurat、epigenetic、epigenome、histone、enrichment、clustering
• 📝 描述：Contributors : Zilun Wei ; Yongchao Zhao ; Aijun Sun ; Junbo GeSeries Type : OtherOrganism : Homo sapiens ; Rattus norvegicusRNA undergoes various modifications in a manner similar to DNA, thereby opening up the research field of epitranscriptomics. Regulators of mRNA modifications play a role in many molecular processes, biological functions, and disease prognosis. Differential expression profile of RNA modification regulators from HFrEF patients’ hearts remains deficient at present, let alone their affections on the prognosis. A risk score model based on two modifications-related modulators (eIF3m and Nudt12) was built and screened out with a LASSO regression analysis. Translation dysregulation upon eIF3m knock down in cardiomyocytes was examined by combined high-throughput methods of transcriptome sequencing, ribosome profiling, proteome research, and Clip analyses. Metabolic assays and flux analysis were used to characterize the effects of eIF3m and its downstream mediator in metabolic reprogramming with high-level exogenous TNF-α to mimic a highly oxidative inflammatory injury. eIF3m deficiency leads to decoupling of the major steps in translation initiation and elongation. It stabilizes eIF3m-f-h subcomplex through proteasome dependent-polyubiquitination, and controls translational response of specific mRNAs. eIF3m directly binds to Mt2 5’ leader to upregulate its translation in NRCMs and H9c2 cells. eIF3m knockdown induced expression of genes involved in proinflammatory and oxidative stress, resulting in 3-NT modification to a key glycolysis enzyme Pfkfb3 when co-cultured with exogenous TNF-α. CM-specific eIF3m deletion deteriorates cardiac function and increases infarction size after I/R operation, whereas CM-specific eIF3m overexpression reverses the phenotype. Additionally, eIF3m overexpression inhibits whereas RNAi-mediated Mt2 knockdown activates NF-κB signaling and aggravates nitrative damage. Metabolic analyses highlighted the role for eIF3m in promoting glycolysis and biosynthesis required for functional recovery of the myocardium. Our study demonstrates that the prognosis indicator eIF3m alleviates oxidative inflammatory injury and promotes glycolytic reprograming mainly by binding to Mt2 mRNA. Therapeutic strategies enhancing eIF3m level may possess therapeutic potential against I/R injury.
• 🔗 查看原文

2. ⭐ GSE217295 缺血性心力衰竭预后指标真核翻译起始因子 3m 的 RNA 结合模式揭示其在心肌缺血再灌注后硝化损伤调节中的独特作用 [Ribo-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、leukemia、immune、immunity、immunology、TME、cardiac、glioma、kinase、resistance、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、single.cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、bioinformatics、R package、Bioconductor、Seurat、epigenetic、epigenome、histone、enrichment、clustering
• 📝 描述：Contributors : Zilun Wei ; Yongchao Zhao ; Aijun Sun ; Junbo GeSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Rattus norvegicusRNA undergoes various modifications in a manner similar to DNA, thereby opening up the research field of epitranscriptomics. Regulators of mRNA modifications play a role in many molecular processes, biological functions, and disease prognosis. Differential expression profile of RNA modification regulators from HFrEF patients’ hearts remains deficient at present, let alone their affections on the prognosis. A risk score model based on two modifications-related modulators (eIF3m and Nudt12) was built and screened out with a LASSO regression analysis. Translation dysregulation upon eIF3m knock down in cardiomyocytes was examined by combined high-throughput methods of transcriptome sequencing, ribosome profiling, proteome research, and Clip analyses. Metabolic assays and flux analysis were used to characterize the effects of eIF3m and its downstream mediator in metabolic reprogramming with high-level exogenous TNF-α to mimic a highly oxidative inflammatory injury. eIF3m deficiency leads to decoupling of the major steps in translation initiation and elongation. It stabilizes eIF3m-f-h subcomplex through proteasome dependent-polyubiquitination, and controls translational response of specific mRNAs. eIF3m directly binds to Mt2 5’ leader to upregulate its translation in NRCMs and H9c2 cells. eIF3m knockdown induced expression of genes involved in proinflammatory and oxidative stress, resulting in 3-NT modification to a key glycolysis enzyme Pfkfb3 when co-cultured with exogenous TNF-α. CM-specific eIF3m deletion deteriorates cardiac function and increases infarction size after I/R operation, whereas CM-specific eIF3m overexpression reverses the phenotype. Additionally, eIF3m overexpression inhibits whereas RNAi-mediated Mt2 knockdown activates NF-κB signaling and aggravates nitrative damage. Metabolic analyses highlighted the role for eIF3m in promoting glycolysis and biosynthesis required for functional recovery of the myocardium. Our study demonstrates that the prognosis indicator eIF3m alleviates oxidative inflammatory injury and promotes glycolytic reprograming mainly by binding to Mt2 mRNA. Therapeutic strategies enhancing eIF3m level may possess therapeutic potential against I/R injury.
• 🔗 查看原文

3. ⭐ GSE217293 缺血性心力衰竭预后指标真核翻译起始因子 3m 的 RNA 结合模式揭示其在心肌缺血再灌注后硝化损伤调控中的独特作用 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、leukemia、immune、immunity、immunology、TME、cardiac、glioma、kinase、resistance、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、single.cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、bioinformatics、R package、Bioconductor、Seurat、epigenetic、epigenome、histone、enrichment、clustering
• 📝 描述：Contributors : Zilun Wei ; Yongchao Zhao ; Aijun Sun ; Junbo GeSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusRNA undergoes various modifications in a manner similar to DNA, thereby opening up the research field of epitranscriptomics. Regulators of mRNA modifications play a role in many molecular processes, biological functions, and disease prognosis. Differential expression profile of RNA modification regulators from HFrEF patients’ hearts remains deficient at present, let alone their affections on the prognosis. A risk score model based on two modifications-related modulators (eIF3m and Nudt12) was built and screened out with a LASSO regression analysis. Translation dysregulation upon eIF3m knock down in cardiomyocytes was examined by combined high-throughput methods of transcriptome sequencing, ribosome profiling, proteome research, and Clip analyses. Metabolic assays and flux analysis were used to characterize the effects of eIF3m and its downstream mediator in metabolic reprogramming with high-level exogenous TNF-α to mimic a highly oxidative inflammatory injury. eIF3m deficiency leads to decoupling of the major steps in translation initiation and elongation. It stabilizes eIF3m-f-h subcomplex through proteasome dependent-polyubiquitination, and controls translational response of specific mRNAs. eIF3m directly binds to Mt2 5’ leader to upregulate its translation in NRCMs and H9c2 cells. eIF3m knockdown induced expression of genes involved in proinflammatory and oxidative stress, resulting in 3-NT modification to a key glycolysis enzyme Pfkfb3 when co-cultured with exogenous TNF-α. CM-specific eIF3m deletion deteriorates cardiac function and increases infarction size after I/R operation, whereas CM-specific eIF3m overexpression reverses the phenotype. Additionally, eIF3m overexpression inhibits whereas RNAi-mediated Mt2 knockdown activates NF-κB signaling and aggravates nitrative damage. Metabolic analyses highlighted the role for eIF3m in promoting glycolysis and biosynthesis required for functional recovery of the myocardium. Our study demonstrates that the prognosis indicator eIF3m alleviates oxidative inflammatory injury and promotes glycolytic reprograming mainly by binding to Mt2 mRNA. Therapeutic strategies enhancing eIF3m level may possess therapeutic potential against I/R injury.
• 🔗 查看原文

4. ⭐ GSE217285 缺血性心力衰竭预后指标真核翻译起始因子 3m 的 RNA 结合模式揭示其在心肌缺血再灌注后硝化损伤调控中的独特作用 [Mt2RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、leukemia、immune、immunity、immunology、TME、cardiac、glioma、kinase、resistance、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、single.cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、bioinformatics、R package、Bioconductor、Seurat、epigenetic、epigenome、histone、enrichment、clustering
• 📝 描述：Contributors : Zilun Wei ; Yongchao Zhao ; Aijun Sun ; Junbo GeSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusRNA undergoes various modifications in a manner similar to DNA, thereby opening up the research field of epitranscriptomics. Regulators of mRNA modifications play a role in many molecular processes, biological functions, and disease prognosis. Differential expression profile of RNA modification regulators from HFrEF patients’ hearts remains deficient at present, let alone their affections on the prognosis. A risk score model based on two modifications-related modulators (eIF3m and Nudt12) was built and screened out with a LASSO regression analysis. Translation dysregulation upon eIF3m knock down in cardiomyocytes was examined by combined high-throughput methods of transcriptome sequencing, ribosome profiling, proteome research, and Clip analyses. Metabolic assays and flux analysis were used to characterize the effects of eIF3m and its downstream mediator in metabolic reprogramming with high-level exogenous TNF-α to mimic a highly oxidative inflammatory injury. eIF3m deficiency leads to decoupling of the major steps in translation initiation and elongation. It stabilizes eIF3m-f-h subcomplex through proteasome dependent-polyubiquitination, and controls translational response of specific mRNAs. eIF3m directly binds to Mt2 5’ leader to upregulate its translation in NRCMs and H9c2 cells. eIF3m knockdown induced expression of genes involved in proinflammatory and oxidative stress, resulting in 3-NT modification to a key glycolysis enzyme Pfkfb3 when co-cultured with exogenous TNF-α. CM-specific eIF3m deletion deteriorates cardiac function and increases infarction size after I/R operation, whereas CM-specific eIF3m overexpression reverses the phenotype. Additionally, eIF3m overexpression inhibits whereas RNAi-mediated Mt2 knockdown activates NF-κB signaling and aggravates nitrative damage. Metabolic analyses highlighted the role for eIF3m in promoting glycolysis and biosynthesis required for functional recovery of the myocardium. Our study demonstrates that the prognosis indicator eIF3m alleviates oxidative inflammatory injury and promotes glycolytic reprograming mainly by binding to Mt2 mRNA. Therapeutic strategies enhancing eIF3m level may possess therapeutic potential against I/R injury.
• 🔗 查看原文

5. ⭐ GSE217296 RNA 结合模式揭示了缺血性心力衰竭预后指标真核翻译起始因子 3m 在心肌缺血再灌注后硝化损伤调控中的独特作用，提示其在心肌缺血再灌注损伤调控中发挥重要作用。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、leukemia、immune、immunity、immunology、TME、cardiac、glioma、kinase、resistance、TCGA、DepMap、depmap、RNAseq、single.cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、bioinformatics、R package、Bioconductor、Seurat、epigenetic、epigenome、histone、enrichment、clustering
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiens ; Rattus norvegicusThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

6. ⭐ GSE281368 THOC5 依赖性转录后控制维持血管平滑肌细胞稳态，对抗慢性肾脏病相关血管钙化 [RIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、immune、TME、cardiac、glioma、kinase、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、scRNA、scDNA、scATAC、spatial、spatially、genome、genomics、transcriptome、transcriptomics、proteome、proteomics、Seurat、Scanpy、methylation、histone、enrichment
• 📝 描述：Series Type : OtherOrganism : Mus musculusBackground: Despite transcriptional control mechanisms of VSMC osteogenic transition having been extensively studied, posttranscriptional regulation is still awaiting elucidation. In the present study, we explore the mechanism of THOC5-dependent VSMCs osteochondrogenic switching. Methods: Von Kossa staining and immunohistochemistry staining were used to detect calcification and expression of THOC5 respectively. Thoc5 shRNA and Thoc5 overexpression lentivirus were used to modulate the expression of Thoc5. RNA-Seq combined with RIP-Seq was used to explore the target mRNAs that directly bind to THOC5, and FISH was used to confirm its subcellular localization. Results: Immunohistochemical staining showed significantly increased THOC5 expression in the calcified artery of CKD patients. Besides, calcification-induced increase of THOC5 expression was found in both in vivo and in vitro calcification models. The overexpression of Thoc5 relieves the calcification and osteogenic differentiation of VSMCs significantly in vitro, which is mainly manifested by the reduction of calcium ion deposition and the decreased expression of osteogenic markers. Furthermore, RNA-Seq revealed that THOC5 overexpression in osteogenic-induced VSMCs closely resembled the gene expression changes induced on TGF-β treatments in cultured VSMCs. In addition, overexpression of THOC5 alleviates the exacerbation of calcification in vivo. Our previous studies found that THOC5 displayed limited binding to VSMCs genomic DNA, so RIP-Seq was selected to detect target genes of THOC5. It was found that THOC5 directly interacts with Guanylate exchange factors (GEFs) mRNAs, and is required for their export. Thereby THOC5 maintaining RhoA GTPase activation contributes to increasing the expression of VSMCs contraction marker, which maintains the contraction phenotype of VSMCs. ROCK (Rho-kinase) inhibitor Y-27632 reversed the protective role of THOC5 on osteoblastic transdifferentiation and calcification, as well as the maintenance of the spindle morphology of VSMCs. Conclusions: Our data introduce the binding of THOC5 to GEFs as a novel mechanism contributing to maintaining VSMCs homeostasis and imply THOC5 as a potential intervention node for vascular calcification diseases.
• 🔗 查看原文

7. ⭐ GSE309106 单细胞 RNA 测序揭示了芳烃受体激活通过涉及肺部免疫细胞和上皮细胞的多条通路减轻急性呼吸窘迫综合征

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、immunity、TME、cardiac、glioma、resistance、TCGA、sequencing、RNAseq、single.cell、single-cell、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、transcriptome、proteome、Seurat、Scanpy、epigenetic、epigenome、methylation、histone、pathway、clustering
• 📝 描述：Contributor : Mitzi NagarkattiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute Respiratory Distress Syndrome (ARDS) is a severe inflammatory lung disorder triggered by pneumonia, sepsis, trauma, and COVID-19, leading to high mortality. In this study, we investigated the effect of Aryl Hydrocarbon Receptor (AhR) activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent ligand, on LPS-induced ARDS in mice using single-cell RNA sequencing (scRNA-seq). scRNA-seq revealed sixteen transcriptionally distinct cell clusters in the lungs. AhR activation reversed the decreased pulmonary functions caused by LPS, and significantly reduced pulmonary infiltration of monocytes, neutrophils, and macrophages. Interestingly, AhR activation during ARDS led to increased proportions of alveolar macrophages, and angiogenic and quiescent endothelial cells (AECs and QECs, respectively). Among the downregulated pathways, prostaglandin signaling was the most broadly suppressed across many cell types in the LPS+TCDD group. AhR activation suppressed the neutrophil chemotaxis pathway involving Cxcl2, Cxcl3, and Cxcl10. The damage to endothelial and epithelial cells induced during ARDS was also blocked by AhR activation. This was associated with decreased expression of S100a8 and S100a9. Notably, multiple pathways related to cellular junction organization were enriched following AhR activation. Additionally, Scgb1a1, also called Club cell protein 16 (CC16), primarily secreted by Club cells in the respiratory epithelium, was highly upregulated following AhR activation accounting for lung homeostasis. Together, these findings demonstrate that AhR activation mitigates key inflammatory and barrier-disruptive processes involving multiple cell types in LPS-induced ARDS. These data identify AhR as a central regulator of pulmonary inflammation and epithelial–endothelial integrity and support the future evaluation of AhR-targeted therapeutics as potential treatment for ARDS.
• 🔗 查看原文

8. ⭐ GSE281115 THOC5 依赖性转录后控制维持血管平滑肌细胞稳态，抵抗慢性肾脏病相关血管钙化 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、carcinoma、immune、TME、cardiac、glioma、kinase、TCGA、RNA-seq、RNAseq、DNA-seq、ATAC-seq、scRNA、scDNA、scATAC、spatial、spatially、genome、genomics、transcriptome、transcriptomics、proteome、proteomics、Seurat、Scanpy、methylation、histone、enrichment
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Despite transcriptional control mechanisms of VSMC osteogenic transition having been extensively studied, posttranscriptional regulation is still awaiting elucidation. In the present study, we explore the mechanism of THOC5-dependent VSMCs osteochondrogenic switching. Methods: Von Kossa staining and immunohistochemistry staining were used to detect calcification and expression of THOC5 respectively. Thoc5 shRNA and Thoc5 overexpression lentivirus were used to modulate the expression of Thoc5. RNA-Seq combined with RIP-Seq was used to explore the target mRNAs that directly bind to THOC5, and FISH was used to confirm its subcellular localization. Results: Immunohistochemical staining showed significantly increased THOC5 expression in the calcified artery of CKD patients. Besides, calcification-induced increase of THOC5 expression was found in both in vivo and in vitro calcification models. The overexpression of Thoc5 relieves the calcification and osteogenic differentiation of VSMCs significantly in vitro, which is mainly manifested by the reduction of calcium ion deposition and the decreased expression of osteogenic markers. Furthermore, RNA-Seq revealed that THOC5 overexpression in osteogenic-induced VSMCs closely resembled the gene expression changes induced on TGF-β treatments in cultured VSMCs. In addition, overexpression of THOC5 alleviates the exacerbation of calcification in vivo. Our previous studies found that THOC5 displayed limited binding to VSMCs genomic DNA, so RIP-Seq was selected to detect target genes of THOC5. It was found that THOC5 directly interacts with Guanylate exchange factors (GEFs) mRNAs, and is required for their export. Thereby THOC5 maintaining RhoA GTPase activation contributes to increasing the expression of VSMCs contraction marker, which maintains the contraction phenotype of VSMCs. ROCK (Rho-kinase) inhibitor Y-27632 reversed the protective role of THOC5 on osteoblastic transdifferentiation and calcification, as well as the maintenance of the spindle morphology of VSMCs. Conclusions: Our data introduce the binding of THOC5 to GEFs as a novel mechanism contributing to maintaining VSMCs homeostasis and imply THOC5 as a potential intervention node for vascular calcification diseases.
• 🔗 查看原文

9. ⭐ GSE300680 人类单核细胞衍生巨噬细胞的生成和多组学分析的简化和综合方案 [bulk RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、oncology、immune、TME、glioma、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ChIP-seq、ATAC-seq、Hi-C、scRNA、scDNA、scATAC、spatial、spatially、Visium、genome、genomics、proteome、proteomics、epigenetic、epigenome、histone
• 📝 描述：Contributors : Olivia G Palmer ; Laurent Perreard ; Fred W Kolling IV ; Patricia A Pioli ; Brittany A GoodsSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMacrophages are versatile immune cells with phenotypes ranging from inflammatory (M1-like) to anti-inflammatory (M2-like), shaped by diverse differentiation and polarization conditions. We present a standardized protocol to generate and characterize human macrophages from frozen PBMC-derived monocytes using cytokine profiling, transcriptomics, and snRNA-seq, including depolarization studies. This streamlined approach facilitates reproducible macrophage studies from biobanked samples, advancing both research and therapeutic applications.
• 🔗 查看原文

10. ⭐ GSE293108 SKIDA1 在新生儿期短暂维持 MLL::ENL 表达的造血祖细胞，并促进 B 细胞谱系启动 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymphoma、immune、TME、glioma、kinase、resistance、TCGA、DepMap、depmap、RNA-seq、RNAseq、DNA-seq、ATAC-seq、Hi-C、scRNA、scDNA、scATAC、10x、spatial、genome、genomics、proteome、proteomics、Seurat、epigenetic、epigenome、histone
• 📝 描述：Contributors : Jonny Mendoza-Castrejon ; Jeffrey A MageeSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusTo assess changes in transcriptional responses to Skida1 deletion in the context of MLL::ENL, we performed CITE-seq on Tet-Off-ME mice.
• 🔗 查看原文

💡 该来源还有 44 条内容，详见 文末

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1. 人造甜味剂在癌症免疫治疗中的苦涩回味

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、免疫
• 📝 描述：Secret hovertext: 摘要：Morder、Nguyen、Wilfahrt 及其同事报告说，非营养性甜味剂通过涉及微生物群和代谢物调节的机制损害抗 PD-1 治疗的疗效。他们的研究结果强调了多种癌症类型长期生活方式干预的临床相关性，例如限制非营养性甜味剂的每日摄入量。参见 Morder 等人的相关文章，第 2278 页
• 🔗 查看原文

2. 人类癌症危机：柳叶刀肿瘤学委员会

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、癌症
• 📝 描述：Secret hovertext: 在肿瘤学领域前所未有的科学进步中，越来越多的证据表明，人类癌症护理经历中存在着平行而深刻的危机。尽管总体生存结果有所改善，但旨在提供护理的系统在解决癌症的情感、关系和生存方面越来越不足。尽管在每种环境中都可以找到富有同情心和细心护理的例子，但全球范围内的患者和家属仍然报告说，由于优先考虑技术精确性而不是人类存在的护理结构，他们没有被倾听、没有支持，有时甚至受到积极伤害。本《 柳叶刀肿瘤学委员会》提出，人类癌症危机不是由病理学、死亡率或原因定义的，而是由癌症经历中意义、联系和同情心的侵蚀来定义的。这场危机是由存在和不存在的东西决定的：支离破碎、昂贵和缺乏个人化的系统的存在，以及人际联系、心理安全和关系关怀的缺失。这是一场涵盖分娩、心理健康、姑息治疗、研究和教育的危机——这场危机不是肿瘤学进步的边缘，而是其失败的核心。那些已经因不平等、歧视和经济不稳定而变得脆弱的人感受到了这场危机的影响最为强
• 🔗 查看原文

3. 利用前列腺癌中的 AR 协同代谢脆弱性

• ✍️ 作者：未知作者
• 🏷️ 关键词：代谢
• 📝 描述：Secret hovertext: 对雄激素剥夺疗法的耐药性仍然是前列腺癌的主要临床挑战，需要替代治疗策略。雄激素受体 （AR） 通过增强 AR 信号传导、DNA 修复和自噬等机制在驱动耐药性方面发挥核心作用。在本期《癌症研究》中，Cordova 及其同事发现了 AR 蛋白合成中的代谢脆弱性，表明隔日禁食 （ADF） 通过诱导 AR mRNA 上的核糖体碰撞来损害 AR 翻译。这种应激反应激活激酶，例如 p38 MAPK，并选择性地降低 AR 蛋白水平，与转录或蛋白质稳定性无关。值得注意的是，ADF 增强了恩杂鲁胺在多种前列腺癌模型中的疗效。与传统的 AR 靶向方法不同，ADF 揭示了营养胁迫下 AR 表达的转录后依赖性，同时保留了大多数其他蛋白质。这些发现凸显了前列腺癌中一种新的转化脆弱性，并支持将饮食干预与 AR 靶向疗法相结合，以克服耐药性并改善患者的预后。参见 Cordova 等人的相关文章，第 4182 页
• 🔗 查看原文

4. GLP-1 激动剂会削弱肥胖与癌症之间的联系吗？

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 摘要：胰高血糖素样肽1受体激动剂在逆转肥胖症患者的一些癌症风险方面有很大的希望，到目前为止，新兴的临床试验支持这一点。然而，一些临床前工作和人体研究的警告强调，需要更多的工作来了解抗肥胖药物在癌症中的机制和全部潜力。
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5. 从创新到影响力：共同推进癌症研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 摘要：癌症研究已进入一个变革时代，其特点是免疫疗法、早期检测、精准肿瘤学和人工智能的快速进步正在重塑预防、治疗和生存率。为了保持势头，全球癌症界必须围绕投资、合作和公平团结起来，以确保每位患者都能从这些突破中受益。
• 🔗 查看原文

6. 肺内皮 PEAR1 诱导肿瘤细胞休眠

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 在许多癌症患者中，远处转移是在多年的休眠后发展起来的。了解通常在微血管系统附近发现的播散性肿瘤细胞 （DTC） 如何保持休眠状态以及调节其重新激活的因素是肿瘤生物学的主要挑战之一。在筛选能够调节肿瘤细胞休眠的内皮分泌蛋白和质膜蛋白时，我们鉴定了跨膜蛋白血小板和内皮聚集受体 1 （PEAR1）。缺乏 PEAR1 的人和小鼠内皮细胞失去了促进不同肿瘤细胞休眠的能力，PEAR1 的细胞外部分能够挽救这种作用。同样，在内皮细胞中缺乏 PEAR1 的小鼠中，肺部肿瘤细胞休眠减少，肿瘤转移增加。我们发现 PEAR1 通过结合赖氨酰氧化酶样 2（LOXL2）和组织蛋白酶 D（CTSD）来诱导肿瘤细胞休眠，这既能抑制肿瘤细胞休眠，又能促进肿瘤生长和转移。CTSD 表达受到抑制的肿瘤细胞在体内表现出休眠增加和转移潜力降低。我们的数据确定了肿瘤细胞休眠的潜在机制，并建议将 CTSD 和 LOXL2 作为促进休眠的方法的靶点。
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7. 抗体-药物偶联物在癌症治疗中的应用：现状、挑战和未来方向

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 抗体-药物偶联物 （ADC） 已成为肿瘤学中的一种变革性模式，它将抗体的靶标特异性与多种细胞毒性有效载荷的高效相结合。本综述提供了从分子设计到临床转化的 ADC 的综合概述。我们剖析了结构成分、抗体、接头和有效载荷，并阐明了它们对药代动力学、肿瘤选择性和治疗指数的影响。强调了包括抗原识别、受体介导的内化、有效载荷释放和免疫原性细胞死亡 （ICD） 在内的机制途径，为 ADC 功能提供背景信息。在临床上，ADC 已证明对血液系统和实体恶性肿瘤具有疗效，已获得 15 项美国食品和药物管理局 （FDA） 批准，并不断扩大研究管道。然而，挑战依然存在，包括抗原异质性、耐药机制、全身毒性和制造复杂性。双特异性 ADC、免疫刺激有效载荷、人工智能引导设计和纳米技术增强递送等新兴创新正在重塑 ADC 格局。最后，我们强调了诊断精度和合理组合策略的必要性，同时强调了共同塑造下一代 ADC 疗法未来方向的新兴创新。
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详细内容（全部2条）

1. R Shiny 中的行为驱动开发：使用给定步骤设置测试前提条件

• ✍️ 作者：未知作者
• 🏷️ 关键词：Hi-C、histone
• 📝 描述：Learn how to set up test preconditions in Shiny BDD using Given steps. Master dependency injection, test doubles, and composable setup patterns for reliable R testing. Continue reading: Behavior-Driven Development in R Shiny: Setting Up Test Preconditions with Given Steps
• 🔗 查看原文

2. Maestro 0.7.0 引入了条件管道

• ✍️ 作者：未知作者
• 🏷️ 关键词：scDNA
• 📝 描述：The 0.7.0 release of maestro is out, and with it is the ability to conditionally run pipelines. In a nutshell, this is especially useful when you have DAG pipelines and you want to branch or only execute parts of a DAG when the output meets a pa… Continue reading: maestro 0.7.0 introduces conditional pipelines
• 🔗 查看原文

详细内容（全部3条）

1. ⭐ 利用单细胞RNA测序解码肾癌中的干扰素信号通路

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、kinase、TCGA、sequencing、RNA-seq、RNAseq、DNA-seq、Hi-C、single.cell、single-cell、scRNA、scATAC
• 📝 描述：Single-cell RNA sequencing reveals how interferon signaling in macrophages drives resistance to immunotherapy in renal cell carcinoma, offering new insights for biomarker discovery and treatment strategies…
• 🔗 查看原文

2. ⭐ isoLASER长读长RNA测序可区分顺式和反式定向的RNA选择性剪接

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、cardiac、resistance、RNA-seq、RNAseq、DNA-seq、scRNA、scDNA、scATAC
• 📝 描述：RNA sequencing using long-read technology reveals how cis- and trans-acting elements control splicing in disease-related genes including MAPT and BIN1…
• 🔗 查看原文

3. ⭐ 从实验室到生物信息学：构建下一代基因测序网络

• ✍️ 作者：未知作者
• 🏷️ 关键词：TME、kinase、TCGA、sequencing、RNAseq、bioinformatics、histone
• 📝 描述：RNA sequencing advances are empowering veterinary diagnosticians to detect emerging pathogens faster and improve animal health surveillance through hands-on training in next-generation sequencing and bioinformatics…
• 🔗 查看原文

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• GSE305252 乳酰-HDAC1介导的表观遗传门控通过代谢重编程调控血管生成转录[ChIP-seq]
• GSE299661 ORB2 RNA结合蛋白通过其功能保守的锌结合“ZZ”结构域，在果蝇母体向合子转变过程中抑制其靶转录本的翻译。
• GSE299140 果蝇母源向合子转变过程中，ORB2 RNA结合蛋白通过其功能保守的锌结合“ZZ”结构域抑制靶转录本的翻译。
• GSE299109 果蝇母源向合子转变过程中，ORB2 RNA结合蛋白通过其功能保守的锌结合“ZZ”结构域抑制靶转录本的翻译。
• GSE305251 乳酰-HDAC1介导的表观遗传门控通过代谢重编程调控血管生成转录[RNA-seq]
• GSE293173 HIV 对 Mtb/SIV 共感染恒河猴模型中潜伏性结核感染影响的单细胞转录组学研究 [scRNA-seq cART+3HP]
• GSE268719 先锋转录因子之间的分子和上位性相互作用塑造核小体动力学和细胞分化
• GSE291137 转录组学揭示了蜱虫 Ixodes ricinus 中肠蛋白金属蛋白酶和抗原 p23 的功能作用
• GSE300681 人类单核细胞衍生巨噬细胞的生成和多组学分析的简化和综合方案
• GSE293107 SKIDA1 在新生儿期短暂维持 MLL::ENL 表达的造血祖细胞，并促进 B 细胞谱系启动 [RNA-Seq]
• GSE309745 利用小鼠模型和人肺组织的单细胞和单核转录组分析研究肺纤维化
• GSE309471 博来霉素诱导和强力霉素诱导的TGF-β转基因小鼠肺纤维化模型肺细胞的单细胞RNA测序
• GSE303777 痣源性黑素细胞及其匹配的病灶周围皮肤黑素细胞的单细胞RNA测序
• GSE281161 一项 CDK9 抑制剂 voruciclib 治疗复发/难治性急性髓系白血病和 B 细胞恶性肿瘤的 1 期研究
• GSE291941 缺氧条件下盘基网柄菌基因表达变化的全局特征
• GSE302849 前粒蛋白通过作用于星形胶质细胞促进海马神经元的树突生长
• GSE302070 Treg 对白细胞介素-2 反应的异质性和同质性 [RNAseq2：IL2 免疫细胞因子对免疫细胞类型的差异性激活]
• GSE309373 正常人肺组织离体精确切割肺切片的单核RNA测序
• GSE217257 葡萄糖代谢通过CCN1影响骨细胞对机械刺激的适应性反应
• GSE277340转录组分析揭示了Hedgehog信号通路作为生物标志物在梅内特里尔病发病机制中的作用
• GSE296838 多西他赛治疗通过激活花生四烯酸通路上调三阴性乳腺癌细胞中雌激素受体的表达
• GSE299316 Treg 对白细胞介素-2 反应的异质性和同质性 [scATAC-seq1: IL2 2h 和 PBS Ctl]
• GSE268543 一项比较转录组分析为香蕉鱼蛇的生态适应性提供了新的见解
• GSE272769 全血转录组分析鉴定出脓毒症死亡率的表达特征
• GSE301342 Treg 对白细胞介素-2 反应的异质性和同质性 [scRNA-seq: IL2/JES6-1 时间序列]
• GSE299361 Treg 对白细胞介素-2 反应的异质性和同质性 [scATAC-seq2: IL2/JES6-1 时间进程]
• GSE297939 绘制 ER 阳性乳腺癌对帕博西尼的多层次分子反应图谱
• GSE73606 低剂量抗雄激素物质对Wistar大鼠睾丸的影响[转录组分析]
• GSE279769 利用配体功能化的 CRISPR-Cas9 对单个 G-四链体进行靶向，揭示了转录依赖性功能反应。
• GSE292707 UGT2B17的非经典功能促进去势抵抗性前列腺癌的进展
• GSE303687 ChAT-eGFP+脂肪基质血管细胞的单细胞RNA测序
• GSE217623 斑马鱼适用蛋白质数据库构建的蛋白质基因组学策略比较
• GSE217269 野生型 (WT) 和 Mettl3-/- (KO) BMDM（骨髓来源巨噬细胞）转录组的 RNA-seq 分析
• GSE296893 研究发现，接受抗逆转录病毒治疗的 HIV 感染者中，持续存在的肺炎球菌定植与鼻腔炎症相关。
• GSE296240 Treg 对白细胞介素-2 反应的异质性和同质性 [RNAseq1: IL2/JES6-1 时间序列]
• GSE306285 不同的白血病突变在核相分离凝聚体中汇聚
• GSE307517 ClinASO：间隙反义寡核苷酸快速药物发现指南
• GSE73605 低剂量抗雄激素物质对Wistar大鼠睾丸的影响[miRNome分析]
• GSE292424 EGF激活POMC基因转录是通过STAT3介导的。
• GSE281062甲基化芯片信号无需亚硫酸氢盐转化即可预测实际年龄
• GSE73607 低剂量抗雄激素物质对Wistar大鼠睾丸的影响
• GSE217338 人类心脏组织和人类iPSCs的RNA测序
• GSE297025 Treg细胞对白细胞介素-2反应的异质性和同质性
• GSE287252 RNA-seq 分析 WT 和 shTRIP6 RKO 细胞之间差异表达基因。