详细内容（前10条）

1. ⭐ Nature重磅｜空间转录组+单细胞揭秘肠道TRM细胞命运：代码全公开，可复现

• ✍️ 作者：生信小博士
• 🏷️ 关键词：T细胞、单细胞、空间转录组、转录组、肠道
• 📝 描述：https://pmc.ncbi.nlm.nih.gov/articles/PMC11903307/研究背景组
• 🔗 查看原文

2. ⭐ 44.5分顶刊发文，单细胞鉴定出乏氧巨噬细胞进行后续研究。前有衰老CD8T，现有乏氧巨噬。识别某种表型的XX细胞可发高分文章！

• ✍️ 作者：东晓生物
• 🏷️ 关键词：衰老、T细胞、巨噬细胞、单细胞
• 🔗 查看原文

3. ⭐ 7+单基因生信，2026年单基因如何发文？大量空间转录组分析必不可少！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：空间转录组、基因组、转录组、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

4. ⭐ Nat Commun丨樊嘉/杨欣荣/朱棣/胡博团队：从新靶点BCL9到先导药hsBCL9Z96，“加热”冷肿瘤攻克肝癌免疫耐药

• ✍️ 作者：人体蛋白质组导航计划
• 🏷️ 关键词：肿瘤、免疫、耐药
• 🔗 查看原文

5. ⭐ 单细胞+空转+代谢组，公开数据集找出亮点就能发1区12分

• ✍️ 作者：生信人
• 🏷️ 关键词：代谢、代谢组、单细胞
• 🔗 查看原文

6. ⭐ Cancer Cell重磅：肿瘤竟被自己人背刺！突变引爆免疫治疗

• ✍️ 作者：生信人
• 🏷️ 关键词：肿瘤、cancer、免疫
• 📝 描述：10月16日，Cancer Cell发表了德州大学MD安德森癌症中心Padmanee Sharma教授团队的重
• 🔗 查看原文

7. ⭐ 效果明显！北京医院马洁/赵云博/肖飞团队NK细胞联合治疗晚期胰腺癌肿瘤显着缩小，首次绘制治疗过程中免疫系统动态变化图谱

• ✍️ 作者：转化医学网
• 🏷️ 关键词：肿瘤、免疫、NK细胞
• 📝 描述：首次绘制了NK细胞治疗过程中免疫系统的动态变化图谱，揭示了响应治疗的患者体内特定的NK细胞和T细胞亚群的变化规律。
• 🔗 查看原文

8. 话进六 ｜现在我们该如何学单细胞分析工具：Seurat？

• ✍️ 作者：单细胞天地
• 🏷️ 关键词：单细胞、Seurat
• 📝 描述：塞尔，你好。这是运来哥生信家书的第七十六封。内含代码
• 🔗 查看原文

9. 聚焦神经调控肿瘤？上交大这篇 27 分综述帮你一次读懂关键机制！

• ✍️ 作者：同医济云Medfocus
• 🏷️ 关键词：肿瘤、神经
• 📝 描述：文章系统梳理了神经系统如何通过不同信号分子直接或间接影响肿瘤的生长、扩散及其微环境，并指出神经活动同样会左右治疗效果，为未来围绕神经—肿瘤调控轴的新型治疗策略提供了方向。
• 🔗 查看原文

10. 《自然》：被忽视的抗癌免疫真相！科学家证实，异型细胞簇中的CD8阳性T细胞可分离、可扩增，且具备超强癌细胞杀伤活性

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：免疫、T细胞
• 📝 描述：把和洗澡水一起倒掉的孩子捡回来。
• 🔗 查看原文

💡 该来源还有 19 条内容，详见 文末

详细内容（前10条）

1. ⭐ GSE300819 小鼠皮内感染结核分枝杆菌后颈部淋巴结的单细胞RNA测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、RNA-seq、single-cell
• 📝 描述：Contributors : Johannes Nemeth ; Katharina Kusejko ; Cédric Dollé ; Edoardo Sarti ; Dat Mai ; Ana N Jahn ; Dong Liu ; Gregory S Olson ; Alan H DiercksSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIn mice, establishment of a contained and persistent yet non-pathogenic infection with Mtb (“contained Mtb infection”, CMTB) rapidly and durably reduces tuberculosis disease burden after re-exposure through aerosol challenge. The bacteria are introduced by intradermal inoculation into the ear and are contained in the corresponsing cervical lymph node. Protection is associated with elevated activation of alveolar macrophages, the first cells that respond to inhaled Mtb, and accelerated recruitment of Mtb-specific T cells to the lung parenchyma. This study used single-cell RNA-seq to compare the cellularity and transcriptional profiles of innate immune cells in the cervical lymph node of naive mice and mice with CMTB.
• 🔗 查看原文

2. ⭐ GSE310786 葡萄球菌肠毒素A影响单核细胞转录和巨噬细胞极化：对感染和炎症中免疫反应的意义

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、macrophage、monocyte、inflammation
• 📝 描述：Contributors : Claudia Arasa ; Khaleda Rahman Qasi ; David Brodin ; Manuel Mata Forsberg ; Eva Sverremark-EkströmSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensStaphylococcal enterotoxins (SE) crosslink the MHC-II on antigen-presenting cells (APC) with the T-cell receptor, inducing a polyclonal T-cell response. Although APCs are the initial targets of SE and are critical in shaping subsequent T-cell activation, the effects of SE on APC function remain poorly understood. This study investigates the immunomodulatory effects of staphylococcal enterotoxin A (SEA) on monocytes and their differentiation into monocyte-derived dendritic cells (moDC) or macrophages (MDM). Transcriptomic analyses of human monocytes via RNA sequencing revealed SEA-induced enrichment of gene pathways associated with inflammation, infection and dermatitis, effects that were amplified in the presence of T-cells. Phenotypic and functional characterization showed that SEA-primed monocytes differentiated into MDM with an altered polarization, deviating from classical M1/M2 pathways. SEA-primed MDM exhibited downregulayion of key markers including HLA-DR, CD80, CD86 and PD-L1. Functional assays demonstrated that SEA-primed MDM pushed hyperinflammatory T-cell responses, with significantly enhanced proliferation and IFN-γ secretion. In contrast, moDC retained robust antigen-presenting capabilities even upon SEA-priming. These findings provide mechanistic insights into SEA-mediated immune modulation, illustrating how SEA reprograms MDM functions and amplify proinflammatory T-cell responses. This advances our understanding of superantigen-driven immune interactions, offering a foundation for developing therapeutic strategies to mitigate superantigen-mediated immune conditions.
• 🔗 查看原文

3. ⭐ GSE248347 利用空间转录组学解析实验性自身免疫性心肌炎中心脏成纤维细胞的分子特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Monika Stefanska ; Katarzyna Sarad ; Marta Kot ; Martyna Strzelec ; Daria KrzysztofikSeries Type : OtherOrganism : Mus musculusMyocarditis is a severe inflammatory cardiac disease that can progress to dilated cardiomyopathy and heart failure. Experimental autoimmune myocarditis (EAM) represents an animal model of acute myocarditis, which is followed by the development of post-inflammatory cardiac fibrosis and systolic dysfunction. In this model, cardiac inflammation is characterized by the massive influx of myeloid infiltrates and is paralleled by the activation of extracellular matrix-producing cardiac fibroblasts. 6–8-week-old BALB/c mice were immunized with αMyHC peptide together with Complete Freunds’ Adjuvant to induce EAM. Heart tissues were isolated, embedded in OTC, sectioned into 10 µm-thick fragments, and placed on a 10x Genomics Visium Gene Expression Slide. Single-cell spatial libraries were prepared using 10x Genomics Visium protocols, and the sequencing was performed using Illumina Chemistry. Single-cell RNA sequencing data was analyzed using RStudio software. In our analysis, we included three biological time points: a healthy heart (d0), acute myocarditis (d19). Following sequencing, we analyzed 3789 spots under the tissue. We identified the main cell populations present in the mouse heart, including fibroblasts, immune cells, endothelial cells, smooth muscle cells, and cardiomyocytes. Subset analysis on cardiac fibroblasts resulted in the presence of four different subsets (FB1–FB6). Subset FB3 has a myofibroblastic signature defined by the expression of, among others, Acta2, Postn, Vim, Col1a1 and Col3a1. This subset is transiently present at d19 of EAM. Spatial analysis of infiltrating immune cells characterized by the expression of, e.g., Ly6c1 and Lyz2 resulted in the presence of five subsets (INF1–INF5). The INF4 subset is present only at acute myocarditis phase (d19) and is spatiotemporally colocalized with the myofibroblastic subset(FB3). Our data indicate that myofibroblasts and infiltrating immune cells colocalize within the tissue during acute phase of myocarditis. This may indicate active molecular interplay between inflammatory cells and cardiac fibroblasts.
• 🔗 查看原文

4. ⭐ GSE305108 大麻二酚对慢性粒细胞白血病细胞系影响的生物信息学差异表达分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、bioinformatics、differential expression
• 📝 描述：Contributor : Petar P DonchevSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChronic myeloid leukemia (CML) is the first clonal myeloproliferative disorder of the pluripotent stem cell to be associated with a specific genetic abnormality, the Philadelphia chromosome, bearing the BCR-ABL1 fusion oncogene. First treatment option for control of the chronic phase of CML are the tyrosine kinase inhibitors (TKIs), though alternative treatments are necessary for resistant cases. Cannabidiol (CBD), one of the major constituents of hemp oil exerts a broad range of pharmacological effects in various malignancies, yet its molecular mechanisms in leukemia remain unclear. In the present study, Imatinib-sensitive K-562S cells were subjected to CBD treatment (IC50: 17.69 μM) for 4 and 12 hours, followed by RNA sequencing to identify differentially expressed genes (DEGs). The consecutive transcriptomic profiling revealed 3518 DEGs at 12 hours and 3433 DEGs at 4 hours of treatment, showing significant modulation of metallothionein-regulated oxidative stress responses (MT1, MT2, SLC30A2), p53-mediated apoptosis (TP53TG3, DDIT4, BBC3, CHAC1, NOXA1, DAPK2), alteration in immune signaling pathways, including type I interferon activation, PI3K-Akt-mTOR and Toll-like receptor signaling, crucial in leukemia progression, as well as shifts in lipid metabolism and mitochondrial homeostasis. The results presented in this study invigorate the considerable potential of CBD to induce broad transcriptional and signaling alterations, related to immune modulation, apoptosis, and metabolic processes in K-562S cells. These findings provide new insights in the therapeutic potential of CBD and lay the groundwork for further investigation into its precision applications in hematological malignancies.
• 🔗 查看原文

5. ⭐ GSE298701 衰老微环境是胰腺癌免疫排斥和转移命运的决定因素

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、aging
• 📝 描述：Contributors : Priyanka Gupta ; Cosimo CommissoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAging is a critical yet understudied determinant in pancreatic ductal adenocarcinoma (PDAC). Despite a strong epidemiological association with age, conventional PDAC preclinical models fail to capture the histopathological and stromal complexities that emerge in older organisms. Using an age-relevant syngeneic orthotopic model, we demonstrate that organismal aging accelerates PDAC progression and metastasis. Through transcriptomic profiling, we identify a conserved extracellular matrix gene signature enriched in cancer-associated fibroblasts (CAFs) from aged tumors, consistent with an augmented fibrotic landscape that supports immunosuppression, metastatic tropism, and poor prognosis. To directly test the functional impact of stromal aging, we employed heterochronic co-implantation models, revealing that revitalizing the aged tumor stroma with young CAFs restores immune infiltration and attenuates metastasis in older hosts. Conversely, aged CAFs, while immunosuppressive, fail to enhance metastasis in young hosts, suggesting that a youthful microenvironment exerts dominant regulatory control over disease progression. These findings demonstrate that stromal age is a critical modulator of both immune exclusion and metastatic behavior in PDAC. Importantly, our work establishes a new conceptual framework for understanding how aging shapes the tumor microenvironment in PDAC and opens a fertile avenue of investigation into age-specific stromal regulation. Moreover, this work raises compelling questions about the underlying molecular mechanisms—questions now accessible through our models—and lays the foundation for future efforts to therapeutically target stromal aging in PDAC.
• 🔗 查看原文

6. ⭐ GSE307506 致癌 KRAS/ERK/JUNB 信号通路抑制胰腺癌中的分化调节因子 GATA6

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:onco(logy|logist|gene|genic)、KRAS
• 📝 描述：Contributors : Zheng Zhong ; David VirshupSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensGATA6 is a master regulator of differentiation in the pancreas and its expression levels determine the two main molecular subtypes of pancreatic cancer. High GATA6 contributes to the “classical” pancreatic cancer subtype, which is associated with a higher degree of tumor differentiation and better disease prognosis. However, why GATA6 expression varies across pancreatic cancers and what regulate GATA6 expression remain elusive. Here we report that the oncogenic KRAS-activated ERK signaling suppresses GATA6 transcription in pancreatic cancers. GATA6 mRNA levels inversely correlated with KRAS/ERK activity in pancreatic tumors. A genome-wide CRISPR screen in a GATA6-EGFP reporter knockin cell line identified JUNB as the ERK-regulated transcriptional repressor for GATA6. Active ERK stabilizes JUNB protein while KRAS/ERK inhibition led to ubiquitin-independent proteasomal degradation of JUNB and increased transcription of GATA6. Up-regulation of GATA6 enhanced chemosensitivity of pancreatic cancer cells and KRAS/ERK inhibitors synergized with chemotherapy in a GATA6-dependent manner. Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.
• 🔗 查看原文

7. GSE308504 SAM合成酶对代谢和线粒体的特异性影响是秀丽隐杆线虫耐热应激的基础

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、resistance
• 📝 描述：Contributors : Athena L Munden ; Dominique S Lui ; Daniel P Higgins ; Matthew P Fanelli ; Thien-Kim Ngyuen ; Maria Ericsson ; Adwait A Godbole ; Jessica B Spinelli ; John Haley ; Caroline Lewis ; Daniel Promislow ; Benjamin Harrison ; Daniel Raftery ; Danijel Djukovic ; Dana L Miller ; Amy K WalkerSeries Type : Expression profiling by high throughput sequencingOrganism : Caenorhabditis elegansS-adenosylmethionine (SAM), produced by SAM synthases, is critical for various cellular regulatory pathways and the synthesis of diverse metabolites. Studies have often equated the effects of knocking down one synthase with broader SAM-dependent outcomes such as histone methylation or phosphatidylcholine (PC) production. However, many organisms express multiple synthase genes including humans and Caenorhabditis elegans. Evidence in C. elegans, which possesses an expanded family of SAM synthases, suggest that the enzymatic source of SAM impacts its function. For instance, loss of sams-1 leads to enhanced heat shock survival and increased lifespan, whereas reducing sams-4 adversely affects heat stress survival. Here, we reveal that loss of sams-1 exerts age-dependent effects on nuclear-encoded mitochondrial gene expression, mitochondrial metabolites, and mitophagy. Notably, we find that that SAMS-1 exerts synthase-specific effects on PC production. We propose a mechanistic framework wherein the reduced SAM from SAMS-1 acts through PC to impact mitochondrial fission and mitophagy, thereby enhancing survival during heat stress. This study highlights multifaceted roles of SAM across metabolic pathways and synthase-specific SAM functions.
• 🔗 查看原文

8. GSE272489 BXD重组近交系小鼠肠道微生物群与胆汁酸相互作用的遗传和饮食决定因素

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Johan Auwerx ; Kristina Schoonjans ; Xiaoxu Li ; Alessia Perino ; Hao LiSeries Type : Expression profiling by arrayOrganism : Mus musculusTranscriptome data measured by microarray in proximal colon of the BXD mouse genetic diversity model under a standard chow or a high fat diet at a postprandial state.
• 🔗 查看原文

9. GSE310783 对灌胃给予水或β-羟基丁酸酯的小鼠体内循环41BBzeta CART19细胞进行单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Shan Liu ; Puneeth Guruprasad ; Maayan Levy ; Marco RuellaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSingle-cell gene expression of circulating 41BBzeta CART19 cells isolated from lymphoma-bearing NSG mice treated with daily oral gavage of water or beta-hydroxybutyrate. Cells were captured and processed using 10X 3’ GEX Reagent Kit v2
• 🔗 查看原文

10. GSE280382 GLP-1R激动剂的功能性和多组学抗衰老研究[批量RNA测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、RNA-seq
• 📝 描述：Contributors : Andrew J. Kwok ; Junzhe Huang ; Ho KoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIdentifying readily implementable methods that can effectively counteract aging is urgently needed for tackling age-related degenerative disorders. Here, we conducted functional assessments and deep molecular phenotyping in the aging mouse to demonstrate that glucagon-like peptide-1 receptor agonist (GLP-1RA) treatment attenuates body-wide age-related changes. In male mice treated with a GLP-1RA from 11 months of age for 30 weeks, we observed improvements in physical and cognitive performance, alongside age-counteracting effects that are prominently evident at multiple omic levels. These span the transcriptomes and DNA methylomes of various tissues, organs and circulating white blood cells, as well as the plasma metabolome. Importantly, the beneficial effects are specific to the aging mice, not young adults, and are achieved with a relatively low dosage of GLP-1RA which has a negligible impact on food consumption and body weight. In older mice treated with a GLP-1RA from 18 months of age for 13 weeks, the molecular rejuvenation effects are even more prominent and generally dependent on hypothalamic GLP-1R, pointing to a brain-body axis of aging modulation. We benchmarked the GLP-1RA age-counteracting effects against those of mTOR inhibition, a well-established anti-aging intervention, observing a strong resemblance across the two strategies. Our findings have broad implications for understanding the mechanistic basis of the clinically observed pleiotropic effects of GLP-1RAs, the design of intervention trials for age-related diseases, and the development of anti-aging-based therapeutics.
• 🔗 查看原文

💡 该来源还有 44 条内容，详见 文末

详细内容（全部6条）

1. ⭐ 新冠疫苗能否提升癌症免疫疗法的疗效？

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、免疫、疫苗
• 📝 描述：Secret hovertext:
• 🔗 查看原文

2. 卡硫桑尼联合尼伏单抗用于晚期胰外神经内分泌肿瘤（epNET）的二期临床试验

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、神经
• 📝 描述：Secret hovertext: 背景：卡波替尼是一种多激酶抑制剂，能改善晚期胰外神经内脏内特（epNET）患者的无进展生存期（PFS）。卡替替尼通过减少调控 T 细胞和 CD14+单核细胞的存在，使肿瘤微环境对免疫细胞更为友好。本试验探讨了卡替尼与尼沃利单抗联合使用在 epNET 晚期患者的疗效和安全性。方法：开放标签单臂 II 期试验，招募了晚期 epNET 患者。患者在第 1 天和第 15 天静脉注射 240 毫克尼沃利单抗，28 天周期内每日口服 40 毫克卡苯替尼。主要终点为 RECIST v1.1 的客观反应率（ORR）。采用西蒙斯两阶段设计，第一阶段招募了 19 名患者。次要目标包括免疫相关反应标准（irRECIST）、PFS 和安全性。探索性目标包括免疫与血管生成蛋白质组谱之间的相关性及临床结局。结果：19 名纳入患者中有 18 例对缓解有效。最佳反应为部分反应 1（5%）、稳定疾病 16（90%）和进展性疾病
• 🔗 查看原文

3. ZNF526 通过增强 TNBC 中 SHMT1 依赖性的丝氨酸代谢和抗氧化能力，促进肿瘤生长

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、代谢
• 📝 描述：Secret hovertext: 三阴性乳腺癌（TNBC）是一种侵袭性恶性肿瘤，治疗选择有限且预后较差。尽管 ZNF526 中的单核苷酸多态性 rs3810151（p.Val94Ala）已被确定为乳腺癌易感位点，但 ZNF526 在 TNBC 中的功能作用和机制基础仍不清楚。本研究中，我们观察到 ZNF526 在 TNBC 中表达较高，其升高的表达与较差的临床结局相关。功能性检测显示，ZNF526 的过表达促进 TNBC 细胞生长，而其敲低作用则抑制肿瘤生长。机制上，我们发现 ZNF526 激活 SHMT1 表达，进而增强丝氨酸-甘氨酸-一碳（SGOC）代谢通路的通量。这种代谢激活增加了谷胱甘肽（GSH）的产生，降低活性氧（ROS）水平，并增强细胞抗氧化防御，从而促进 TNBC 的进展。我们的发现表明，ZNF526 是通过 SHMT1 介导的代谢调控，能够调节 TNBC 氧化还原平衡，使其成为 TNBC 潜在的治疗靶点。
• 🔗 查看原文

4. 凋亡细胞分泌的精明通过调节骨肉瘤中的β链环蛋白活性，增强化疗耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：耐药
• 📝 描述：Secret hovertext: 目的：化疗耐药性仍是骨肉瘤（OS）治疗中的关键障碍。本研究旨在阐明精明酮（SPD）在骨肉瘤化学耐药中的作用及其潜在机制。实验设计：利用 OS 细胞系和异种移植，我们结合流式细胞术、西方印迹法、蛋白质组质谱和 RNA 测序，以表征 SPD 驱动的细胞通路和耐药特征变化。我们测试了单用或联合标准化疗药物抑制 SPD 生物合成是否能改善体内治疗反应。结果：经过化疗，无论是顺铂（CDP）还是多柔比星（DOX），凋亡的 OS 细胞表现出鸟氨酸脱羧酶 1（ODC1）和精脚合酶（SRM）上调，这两种酶是 SPD 合成的关键酶，导致该多胺水平升高。SPD 降低了 CDP 和 DOX 在 OS 细胞中的治疗效果，无论是体外还是体内。从机制上看，SPD 增强β-链蛋白活性，进而上调与癌症干细胞和 ATP 结合盒（ABC）转运蛋白相关的基因，这两者都与药物耐药性有关。此外，使用 DFMO 药理抑制 SPD 合成显著提高了
• 🔗 查看原文

5. DNMT3A R882H 在原发性人类急性髓白血病中并非疾病维持必需，但与白血病干细胞频率增加相关

• ✍️ 作者：未知作者
• 🏷️ 关键词：T细胞
• 📝 描述：Secret hovertext: 人类癌症中的遗传突变正在被全面绘制，但癌症生物学中的一个根本问题是，这些突变是否在癌症启动、既有癌症维持或两者兼具的功能性需求中存在。在这里，我们将在人类急性骨髓性白血病（AML）的背景下研究这个问题，其中 DNMT3AR882 错义突变常在白血病前的克隆造血中早期出现，并破坏 DNA 甲基化景观以启动白血病。我们开发了基于 CRISPR 的方法，直接纠正患者白血病细胞中的 DNMT3AR882 突变。令人惊讶的是，DNMT3AR882 突变在疾病维持中大多可替代。用野生型 DNMT3A 替代 DNMT3AR882 突变体并未削弱 AML 细胞体内移植能力，且 DNA 甲基化仅有微小改变。综合来看，DNMT3AR882 突变最初是 AML 启动的必要条件，但在疾病维护中基本可替代。启动癌基因与维持癌症基因的不同这一观点对癌症进化和治疗具有重要意义。
• 🔗 查看原文

6. 长非编码 RNA AFAP1-AS1 通过促进 SRSF 相分离，促进 AXIN2 的替代剪接，从而诱导肺腺癌中的耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：耐药
• 📝 描述：Secret hovertext: 肺癌目前在全球恶性肿瘤中发病率和死亡率最高，其中肺腺癌是最常见且致命的亚型。化疗和靶向治疗仍是肺腺癌的标准治疗，但肿瘤耐药性仍是临床上的重要挑战。本研究发现，肺腺癌中表达较高的长非编码 RNA 肌动蛋白丝状蛋白 1 反义 RNA 1（AFAP1-AS1）通过招募丝氨酸和精氨酸富集拼接因子 1 和 3（SRSF1 和 SRSF3）调控 RNA 替代剪接，促进其液相分离。在受影响的剪接事件中，关键调控基因 AXIN2 的 7 外显子跳跃，该基因参与 Wnt/β-catenin 信号通路，最显著地受 AFAP1-AS1 调控，导致截断 AXIN2 异构体（AXIN2-S）的翻译。该异构体促进细胞核内β-catenin 的积累，并持续激活 Wnt/β-catenin 信号通路，最终促进肺腺癌的药物耐药性。我们的研究揭示了 AFAP1-AS1 通过调节剪接因子相分离调节 RNA 替代剪接的新功能。该机制凸显了
• 🔗 查看原文

详细内容（全部2条）

1. 利用单细胞技术深入了解甘蓝型油菜叶片的发育过程

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：Single cell RNA sequencing reveals how Brassica rapa leaf vascular cells develop and differentiate, uncovering key regulatory genes shaping xylem, phloem, and overall leaf morphogenesis…
• 🔗 查看原文

2. 阻断单个蛋白质即可迫使癌细胞自我毁灭

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers uncovered a powerful weakness in lung cancer by shutting down a protein that helps tumors survive stress. When this protein, FSP1, was blocked, lung tumors in mice shrank dramatically, with many cancer cells essentially triggering their own self-destruct mode. The work points to a fresh strategy for targeting stubborn lung cancers.
• 🔗 查看原文

• 这次真的是Y叔的锅了吗：为什么KEGG通路富集结果中的分类有NA呢？
• Nature Aging：刘光慧等发现缓解前列腺衰老新策略
• 顶刊里程碑突破！哈佛团队绘 170 万 T 细胞图谱，生信注释有了 “黄金标尺”
• 单细胞测序和深度学习系列三：细胞类型分类器
• 人体淋巴循环系统（建议收藏）
• 新一期单细胞学习小组即将发车
• 气泡图-如何优雅的绘制多组富集结果进行类比
• 谁说单基因没前途，结合单细胞，空转和实验验证，照样发8分1区文章！
• Cell Reports Medcine：谭兰/郁金泰团队揭示癫痫发作相关的血浆蛋白质组
• Cancer Cell！胶质瘤逃逸新靶点
• 肿瘤CRISPR Screen在线平台！重磅推荐！
• 独家干货 | 基于R语言的单细胞多组学分析教程，零基础也能搞定！
• Nature：scWGS+scRNA解密全基因组倍增的演化动态
• 别傻了！多组学只做关联和通路？这波血亏！
• 腾讯登26.6分Nature子刊，只有你想不到的蛋白质！没有这个模型预测不了的
• 新免疫抑制回路！南开大学发文：可改善胰腺癌患者治疗效果的新策略
• 原位肿瘤模型构建回归专场即将启动！
• 语言模型 | Nat.Genet. | 基因组语言模型的核苷酸依赖性分析可检测功能元件
• 西安交大最新Nature Cancer论文：新型AI病理模型，实现大规模肿瘤筛查及细粒度量化诊断

• GSE290305 阿尔茨海默病小鼠模型海马体中表观基因组和转录组改变先于淀粉样变性[RNA-seq]
• GSE303144 IL-9信号通路将CAR T细胞的命运导向CD8+记忆和CD4+增殖状态，从而增强抗肿瘤疗效
• GSE287512 MP0317（一种FAPxCD40 DARPin）通过肿瘤局部CD40激动作用重塑肿瘤微环境——一项I期单药治疗研究的结果
• GSE281094 中华绒螯蟹蜕皮间期肌肉的ATAC-seq和RNA-seq分析
• GSE310641 FluPRINT 研究：LAIV 免疫和转录反应的特征分析
• GSE308595 细胞焦亡调节靶向治疗黑色素瘤中的多种免疫细胞群
• GSE304438 异染色质表观突变导致线粒体功能障碍，从而赋予抗真菌耐药性
• GSE304360 运动发酵单胞菌氧化应激转录组学
• GSE294147 阻断受损线粒体从癌细胞向RGS5+ MYL9+ CAFs的转移可降低EGFR突变型肺癌对TKIs的持续耐受性
• GSE269350 Erg 的动态表达控制造血系统从胎儿到成体的成熟 [ChIP-seq]
• GSE269184 Erg 的动态表达控制造血系统从胎儿到成体的成熟 [RNA-seq]
• GSE310817 使用 Infinium 小鼠甲基化微珠芯片构建小鼠 DNA 甲基化图谱 [EPIC 阵列分析]
• GSE310713 ClpC1靶向肽天然产物差异性地扰乱结核分枝杆菌的蛋白质组。
• GSE310667 幼年神经系统的基因表达图谱。
• GSE310303 鉴定出 UVB 诱导的 TREM-1 阳性耐受性树突状细胞，并将 TREM-1 信号通路作为预防 UVB 诱导的免疫抑制和皮肤癌变的靶点。
• GSE310223 精细化的细胞活性表达特征为量化单细胞数据中肿瘤内表型异质性提供了一个靶向框架 IV
• GSE310222 精细化的细胞活性表达特征为量化单细胞数据中肿瘤内表型异质性提供了一个靶向框架 III
• GSE310220 精细化的细胞活性表达特征为量化单细胞数据中肿瘤内表型异质性提供了一个靶向框架 II
• GSE310219 精细化的细胞活性表达特征为量化单细胞数据中肿瘤内表型异质性提供了一个靶向框架 I
• GSE310041 头颈部鳞状细胞癌的批量 RNA 测序
• GSE303376 靶向编辑组蛋白 H3K27 三甲基化阐明其在光周期调控开花中的重要性
• GSE298655 Arpc5 对肠道巨噬细胞基因表达的贡献
• GSE295144 糖尿病通过激活树突状细胞和γδ T细胞中的CD137L-CD137轴加剧破坏性炎症
• GSE293402 协同基因家族进化塑造了二态生物的基因组
• GSE290132 HIV诱导的感染细胞上的唾液酸聚糖促进免疫逃逸，逃避髓系细胞介导的杀伤作用
• GSE289702 PABPN1-C5轴通过NF-κB激活促进肝细胞癌进展
• GSE283061 核外泌体靶向复合物在全基因组范围内调控三维染色质相互作用
• GSE279437 GLP-1R激动剂的功能性和多组学抗衰老作用
• GSE211986 将人类神经胶质祖细胞移植到成年亨廷顿病小鼠体内可挽救神经元结构和某些行为特征
• GSE154099 PAXT/NEXT 靶向 RNA 外泌体通过黏连蛋白介导的长程接触调节反义转录本 [RNA-seq]
• GSE154083 PAXT/NEXT 靶向 RNA 外泌体通过黏连蛋白介导的长程接触调节反义转录本 [ChIP-seq]
• GSE310289 PLK3抑制剂治疗对静息CD4+ T细胞整体转录组的影响
• GSE310288 PLK3抑制剂治疗对静息CD4+ T细胞整体转录组的影响
• GSE309497 用户自定义肽库实现癌症抗原的灵敏直接检测
• GSE290397 阿尔茨海默病小鼠模型海马体中表观基因组和转录组改变先于淀粉样变性 [BiSulfite-seq]
• GSE290154 表观基因组和转录组改变先于阿尔茨海默病小鼠模型海马中的淀粉样变性
• GSE310831 利美替罗在代谢功能障碍相关性脂肪性肝炎（MASH）中的细胞和分子机制：一项转录组分析研究
• GSE310290 早期生命微生物群影响骨髓造血前体细胞的长期基因表达和表观基因组
• GSE310020 TGFα是衰老过程中毛囊功能所必需的，其缺失会导致进行性脱发。
• GSE303648 Rb1 缺陷与 ATR 和 PKMYT1 共抑制在乳腺癌中诱导合成致死
• GSE295626 去泛素化酶OTUD1通过破坏RAD23B/XPC的稳定性来调控非小细胞肺癌对顺铂化疗的敏感性
• GSE282471 日本黑色素瘤的基因组和转录组分析揭示了免疫检查点抑制剂反应者的候选生物标志物。
• GSE280706 RNA-seq 时间序列分析 Nudt21 KO 和 Nudt21 低表达型食管基底细胞
• GSE218499 涡虫再生神经内分泌控制（RNAi scRNA-seq）