科研日报 2026-04-30

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📅 Daily Report - 2026-04-30

今日筛选出 71 条内容,来自 2 个来源

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🤖 今日AI智能总结

🧬 数据前沿

今日焦点: Kmt2c/Kmt2d基因缺陷对胃癌表观遗传和转录组的影响,以及mediator复合物调控黑色素瘤可塑性和治疗抵抗性的新机制。

主要方向

  • 肿瘤微环境与免疫调控:研究KMT2C/D基因在胃癌中的作用,以及TREM2在肝癌免疫治疗中的影响。
  • 表观遗传与基因调控:探索mediator复合物、ATAC-seq/ChIP-seq在黑色素瘤耐药中的作用,以及组蛋白乙酰化对基因组组织的影响。
  • 单细胞转录组学应用:解析帕金森病中神经元代谢通路失调,以及衰老与复壮对肌源性干/祖细胞的影响。

技术亮点

  • 空间转录组学:应用于杜氏肌营养不良症肌纤维损伤和拟谷精草发育研究。
  • 单细胞RNA测序:用于分析CD8 T细胞对LCMV感染的响应,以及妊娠高血压疾病中的免疫微环境重塑。

🧪 博客更新

今日焦点: Takara Bio推出新型空间转录组学技术Trekker FX,显著提升单细胞分辨率,为癌症研究提供更精细的肿瘤微环境分析工具。

主要方向

  • 癌症治疗新靶点:发现长链非编码RNA (lncRNA) IGF1R-AS1在的前列腺癌进展中起关键作用,提示其作为潜在治疗靶点的可能。
  • 癌症预后预测:开发scSurvival工具,利用单细胞RNA测序数据实现细胞分辨率的生存分析,提高癌症患者风险预测的准确性。

技术亮点

  • 新型空间转录组学技术(Trekker FX)实现单细胞级别的高分辨率细胞相互作用检测。
  • 单细胞RNA测序与生存分析相结合,实现细胞层面的癌症风险评估。

📚 分类浏览

🧬 数据前沿 (66条)

详细内容(前10条)

1.GSE317003 Kmt2c/Kmt2d 缺陷型胃癌的表观遗传和转录改变 [ChIP-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、ChIP-seq、epigenetic
  • 📝 描述:Contributors : Dan Li ; Naitao Wang ; Yu ChenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusKMT2C and KMT2D are two of the most frequently mutated genes in gastric adenocarcinoma, yet their function in cancer initiation remains poorly understood. In this study, we developed mouse models to investigate the molecular mechanism of Kmt2c/d loss in gastric tumorigenesis.
  • 🔗 查看原文

2.GSE316994 Kmt2c/Kmt2d 缺陷型胃癌的表观遗传和转录改变 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、RNA-seq、epigenetic
  • 📝 描述:Contributors : Dan Li ; Naitao Wang ; Yu ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusKMT2C and KMT2D are two of the most frequently mutated genes in gastric adenocarcinoma, yet their function in cancer initiation remains poorly understood. In this study, we developed mouse models to investigate the molecular mechanism of Kmt2c/d loss in gastric tumorigenesis.
  • 🔗 查看原文

3.GSE329359 无菌和SPF小鼠在LCMV Docile感染后16天,从SI-LP和脾脏中分选的gp33四聚体阳性CD8 T细胞的单细胞RNA测序[scRNA-Seq 10x]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:sequencing、scRNA、10x
  • 📝 描述:Contributors : Miriam Kuhlmann ; Gustavo P de Almeida ; Wurmser Christine ; Dietmar ZehnSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusProlonged antigen exposure in chronic viral infections reduces the effector capacity of cytotoxic T cells - a phenomenon known as T cell exhaustion. Development of T cell exhaustion is driven by high viral titers, strong TCR stimulation, and high antigen concentrations associated with strong inflammatory signals. A largely unexplored factor has been the influence of the microbiome in these processes. Here, we report that T cell exhaustion progresses independently of the presence or absence of a microbiome in chronic lymphocytic choriomeningitis virus (LCMV) infections. Virus-specific CD8 T cells in germ-free mice showed high expression of the inhibitory receptor PD-1 and decreased cytokine production. Moreover, their global gene expression patterns, as determined by single-cell sequencing, were similar to those of cells in specific pathogen-free mice. In line with this, we observed similar pathogen loads with and without a microbiome. Thus, our study demonstrates that the microbiome is dispensable for the induction of T cell exhaustion and for the limited virus control seen in chronic LCMV infections.
  • 🔗 查看原文

4.GSE329173 整合单细胞和宏观转录组学以解码与重度子痫前期绒毛外滋养层侵袭停滞相关的转录和免疫微环境重塑

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、single-cell、transcriptomics
  • 📝 描述:Contributors : Qihang Zhao ; Xiao Lin ; Juanmei Gao ; Linzhen WuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPreeclampsia is a pregnancy-specific systemic disorder that poses significant threats to maternal and perinatal health. The core pathological features of this condition involve shallow invasion of extravillous trophoblasts and defective vascular remodeling at the maternal-fetal interface during early pregnancy. Despite its clinical importance, the transcriptional reprogramming and dynamic cell-to-cell communication at single-cell resolution in severe preeclampsia remain insufficiently explored. This study aims to delineate the lineage shifts of extravillous trophoblasts and the associated immune microenvironment crosstalk
  • 🔗 查看原文

5.GSE316132 黑色素瘤表型可塑性和治疗耐药性的表观遗传调控[ATAC-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:resistance、ATAC-seq、epigenetic
  • 📝 描述:Contributors : Hongkuan Wang ; Hongwen Xuan ; Yucong Yu ; Xiaobing ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMelanoma progression and treatment failure are driven in part by the ability of tumor cells to undergo dynamic phenotypic state transitions. Here, we identify the SAGA chromatin-modifying complex as a critical epigenetic regulator that constrains melanoma phenotypic plasticity and preserves therapeutic vulnerability. Loss of SAGA-dependent epigenetic regulation disrupts lineage-associated chromatin states, leading to widespread transcriptional reprogramming and enhanced cellular adaptability. As a consequence, SAGA-deficient melanoma cells exhibit increased phenotypic heterogeneity and acquire resistance to targeted therapy. Mechanistically, SAGA loss impairs histone acetylation–dependent control of gene expression programs linked to differentiation and stress responses, enabling the emergence of drug-tolerant cell states. Together, these findings establish SAGA as an epigenetic safeguard against melanoma cell-state plasticity and reveal how disruption of chromatin regulatory complexes promotes therapeutic resistance.
  • 🔗 查看原文

6.GSE316110 黑色素瘤表型可塑性和治疗耐药性的表观遗传调控[ChIP-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:resistance、ChIP-seq、epigenetic
  • 📝 描述:Contributors : Hongkuan Wang ; Hongwen Xuan ; Yucong Yu ; Xiaobing ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMelanoma progression and treatment failure are driven in part by the ability of tumor cells to undergo dynamic phenotypic state transitions. Here, we identify the SAGA chromatin-modifying complex as a critical epigenetic regulator that constrains melanoma phenotypic plasticity and preserves therapeutic vulnerability. Loss of SAGA-dependent epigenetic regulation disrupts lineage-associated chromatin states, leading to widespread transcriptional reprogramming and enhanced cellular adaptability. As a consequence, SAGA-deficient melanoma cells exhibit increased phenotypic heterogeneity and acquire resistance to targeted therapy. Mechanistically, SAGA loss impairs histone acetylation–dependent control of gene expression programs linked to differentiation and stress responses, enabling the emergence of drug-tolerant cell states. Together, these findings establish SAGA as an epigenetic safeguard against melanoma cell-state plasticity and reveal how disruption of chromatin regulatory complexes promotes therapeutic resistance.
  • 🔗 查看原文

7.GSE311203 空间转录组学和组织病理学分析揭示杜氏肌营养不良症中 2a 型肌纤维的选择性丢失

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Contributors : Clara Martinez Mir ; Paola Pisterzi ; Isabel De Poorter ; Jamilla Beek ; Anna Alemany ; Fanny Sage ; Niels GeijsenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDuchenne muscular dystrophy (DMD) features progressive muscle degeneration with extensive remodeling of fiber type composition and metabolism. To circumvent the lack of regional heterogeneity from bulk or small biopsies studies, we employed spatial transcriptomics, metabolic enzyme profiling, immunohistochemistry, and quantitative fiber-type analysis to map the tibialis anterior (TA) in dystrophic (hDMDdel52/mdx) and control mice. DMD muscles exhibited disrupted metabolic compartmentalization, with reduced central oxidative regions and lower oxidative gene expression. Histology confirmed decreased oxidative enzyme activity and MYH2 expression, the most oxidative type 2 fiber. Analysis across TA, extensor digitorum longus, and soleus muscles revealed consistent MYH2 fiber loss within a mosaic of localized pathological states. Modeling interactions between anatomy and disease highlighted spatially restricted transcriptional programs involving extracellular matrix remodeling, cytoskeletal disruption, and immune infiltration, indicating compartment-specific pathology. This multi-modal, spatially resolved framework advances understanding of muscle remodeling and guides biomarker discovery and therapeutic strategies that account for regional heterogeneity.
  • 🔗 查看原文

8. GSE329327 Queuosine促进海洋细菌冰川希瓦氏菌(Shewanella glacialimarina)中wecB依赖性噬菌体抗性和生物膜形成

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:regex:bacter(ia|ial|ium)、resistance
  • 📝 描述:Contributors : Pavlina Gregorova ; Minna-Maria K Heinonen ; Nina Sipari ; Peter SarinSeries Type : Expression profiling by high throughput sequencingOrganism : Shewanella glacialimarinaTransfer RNA (tRNA) modifications critically fine-tune translational accuracy and efficiency, influencing bacterial adaptation to environmental challenges. Among these, the queuosine (Q) modification has recently emerged as a regulator of biofilm formation, yet its role during phage infection remains unknown. Here, we investigate how Q modification links host translational control to phage infection. We show that phage infection activates the Q biosynthetic pathway, leading to elevated Q levels and enhanced translation of NAT-biased genes. This shift drives two interconnected outcomes, namely increased biofilm formation and enhanced mutagenesis mediated by translesion synthesis polymerases. We further identify conserved, slippage-prone regions within surface-related genes that act as hotspots for adaptive variation. Together, our findings uncover a novel mechanistic link between tRNA modification and phage-driven bacterial diversification.
  • 🔗 查看原文

9. GSE329316 在不同硬度基质上培养的海绵体成纤维细胞的转录组测序。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:sequencing、transcriptome
  • 📝 描述:Contributors : Biao Liu ; Yuzhuo ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensFibrotic diseases involve increased mechanical stress due to extracellular matrix deposition, significantly altering cellular metabolism. However, a systematic understanding of how mechanical force regulates lipid metabolism across different molecular layers remains limited. We employed an integrated multi-omics approach, including transcriptomics, Ribo-seq, proteomics, and lipidomics, to comprehensively assess the effects of mechanical stretch on lipid metabolism in human cavernous fibroblasts. Our analysis revealed that while mechanical force elicits complex multi-layered responses, post-translational regulation predominantly drives this lipid metabolic reprogramming. Lipidomics identified a significant reduction in fatty acids and an upregulation of ganglioside. Key genes central to this mechanosensitive metabolic shift were pinpointed. This study demonstrates that mechanical force hierarchically reprograms lipid metabolism. The shift from fatty acids to ganglioside underscores a key metabolic adaptation in fibroblasts. Targeting the identified critical genes may offer a promising therapeutic strategy for fibrosis-related diseases.
  • 🔗 查看原文

10. GSE328107 PI3K 调控野生型 RAS 信号通路以赋予其对 KRAS 抑制剂的耐药性

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:resistance、KRAS
  • 📝 描述:Contributors : Xiangyu Ge ; Jaffarguriqbal Singh ; Wenxue Li ; Cassandra S Markham ; Christian F Ruiz ; Stites C Edward ; Moitrayee Bhattacharyya ; Yansheng Liu ; Mandar D MuzumdarSeries Type : OtherOrganism : Homo sapiensDespite the availability of RAS inhibitors and the dependence of >90% of pancreatic ductal adenocarcinomas (PDAC) on oncogenic KRAS mutations, resistance to KRAS inhibition remains a serious obstacle. We showed here that PI3K plays a major role in this resistance through upstream activation of wild-type RAS signaling – beyond its known KRAS effector function. The combination of proximity labeling, CRISPR screening, live-cell imaging, and functional assays revealed that PI3K orchestrates phosphoinositide-mediated GAB1 recruitment to the plasma membrane, nucleating assembly of RAS signaling complexes that activate MAPK in an EGFR/SHP2/SOS1-dependent manner. Inhibiting PI3K enhanced sensitivity to mutant-specific KRAS inhibitors in PDAC cells, including in cells with clinically identified PIK3CA mutations. These findings refine RAS-PI3K signaling paradigms, reveal that PI3K-driven wild-type RAS activation drives resistance to KRAS inhibition, and illuminate avenues for augmenting KRAS-targeted therapies in PDAC.
  • 🔗 查看原文

💡 该来源还有 56 条内容,详见 文末

🧪 博客更新 (5条)

详细内容(全部5条)

1.Takara Bio USA, Inc. 通过癌症研究基准研究验证了新型空间转录组学技术

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Takara Bio’s Trekker FX spatial transcriptomics improves single-cell resolution and detects more cell interactions, enhancing analysis of tumor microenvironments in cancer samples…
  • 🔗 查看原文

2. scSurvival——基于细胞分辨率的临床癌症队列数据的单细胞生存分析

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、single-cell
  • 📝 描述:RNA sequencing combined with single-cell analysis enables scSurvival to link specific tumor cell populations to patient risk, improving survival prediction and revealing drivers of cancer progression…
  • 🔗 查看原文

3. 长链非编码RNA可能是一种有前景的癌症治疗靶点。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:RNA sequencing reveals how lncRNA IGF1R-AS1 drives MYC activation through chromatin looping, promoting tumor progression and highlighting a potential therapeutic target in prostate cancer…
  • 🔗 查看原文

4. 维生素D可使乳腺癌治疗成功率提高79%。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:A daily vitamin D supplement may quietly supercharge chemotherapy. In a small study, women who took low doses alongside treatment were far more likely to see their cancer vanish than those who didn’t. Since vitamin D also supports immune function—and many patients are deficient—it could be playing a bigger role than expected. Scientists say this affordable approach deserves much deeper investigation.
  • 🔗 查看原文

5. 麻省理工学院研究发现,儿童更容易受到水中致癌化学物质的影响。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:A troubling new study from MIT reveals that a common environmental contaminant, NDMA—found in polluted water, certain medications, and even processed foods—may pose a far greater cancer risk to children than adults. In experiments with mice, young animals exposed to the chemical developed significantly more DNA damage and cancer, despite experiencing the same initial exposure as adults. The key difference lies in how rapidly children’s cells divide, which turns early DNA damage into dangerous mutations much more easily.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
RNA-seq16
resistance11
cancer9
epigenetic7
single-cell6
ChIP-seq6
regex:intestin(eal)
spatial4
sequencing4
transcriptomics3
transcriptome3
carcinoma3
ATAC-seq3
spatial transcriptomics2
Neuronal2
regex:bacter(iaial
immunity2
scRNA2
immune2
T cell2

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🧬 数据前沿 其他内容 (56条)

📅 报告生成时间:2026-04-29 22:15
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