科研日报 2026-07-01

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📅 Daily Report - 2026-07-01

今日筛选出 195 条内容,来自 2 个来源

Powered by 科研普拉斯 & Claude

🤖 今日AI智能总结

🧬 数据前沿

今日焦点: 利用空间转录组学揭示卒中驱动胶质瘤进展的微环境重塑,并发现CD99是弥漫性中线胶质瘤的新型免疫治疗靶点。

主要方向

  • 肿瘤微环境调控与疾病进展(如卒中驱动胶质瘤、胰腺癌巨噬细胞反应)
  • 表观遗传学机制在细胞功能调控中的作用(如组蛋白甲基化影响肠道干细胞代谢,CARM1抑制树突状细胞功能)
  • 肠道上皮与免疫细胞互作及其在稳态维持中的作用
  • 免疫细胞(NK细胞、巨噬细胞)的功能重塑与疾病治疗潜力

技术亮点

  • 空间转录组学(Spatial Transcriptomics)和单细胞RNA测序(scRNA-seq)等高通量测序技术在解析复杂生物系统中的应用。

🧪 博客更新

今日焦点: 科学家发现一种新型机制,有望实现胰腺癌细胞的自毁,并揭示了阿尔茨海默病在脑部扩散的潜在途径。

主要方向

  • 靶向抑制胰腺癌细胞迁移,实现其自毁。
  • 阻断携带 tau 蛋白的有害蛋白包,阻止阿尔茨海默病在脑部扩散。
  • 利用 RNA 测序技术对月经液进行时间分辨分析,以诊断女性健康问题。

技术亮点

  • 发现实验性 PCAI 化合物对胰腺癌细胞具有强大的抗癌作用,可阻断超过90%的癌细胞迁移。
  • 识别出一种常见的脑蛋白可能作为载体,将 tau 蛋白从受损神经元传播到健康神经元。

📚 分类浏览

🧬 数据前沿 (192条)

详细内容(前10条)

1.GSE325817 中风通过重塑肿瘤微环境驱动胶质瘤进展 [空间转录组学]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、tumor microenvironment、glioma、spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Contributors : Qi Ye ; Hari Krishna Yalamanchili ; Hyun Kyoung LeeSeries Type : OtherOrganism : Mus musculusEpidemiological studies suggest increased brain tumor risk in patients with prior stroke. Comparative transcriptomic analyses reveal enrichment of stroke-associated gene signatures in high-grade gliomas; nevertheless, the mechanisms that unify these conditions remains unclear. Here we show that stroke promotes tumor infiltration towards the site of stroke injury in human and mouse glioma models, accompanied by reduced overall survival. Stroke induces remodeling of the tumor microenvironment (TME), including the emergence of a unique population of tumor-associated astrocytes (TAAs) that exhibit reduced Ca2+ activity at the infiltrative edge, and enrichment of tumor-associated microglia and macrophages (TAMs). Chemogenetic stimulation of Ca2+ signaling in TAAs or depletion of TAMs reverses stroke-induced glioma progression. We further identify the sodium–bicarbonate cotransporter Slc4a4 as a key regulator of Ca2+ activity in TAAs and associated TAM recruitment. Collectively, our findings demonstrate that stroke accelerates glioma progression through remodeling of astrocytic and immune compartments of the TME.
  • 🔗 查看原文

2.GSE283729 组蛋白 3 赖氨酸 36 甲基化塑造肠道干细胞的表观遗传景观,从而调控脂质代谢并防止细胞衰老 [ATAC-seq 2]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、ATAC-seq、epigenetic、methylation、histone、regex:intestin(e|al)
  • 📝 描述:Contributors : Yue Xu ; Ziyi WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity and differentiation potential of intestinal stem cells (ISCs) decline with age, leading to a loss of homeostasis and increased susceptibility to intestinal diseases. Despite the established importance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms linking these processes to aging-associated ISC dysfunction remain elusive. Here, we demonstrate that H3K36 methylation, caused by NSD2 or SETD2, is critical to ISC fate. We found that the deficiency of H3K36 methylation results in reduced ISC proliferation and differentiation, disturbs fatty acid metabolism, and induces ISC senescence. This loss leads to increased chromatin accessibility and enhancer activation, impairing the function of the SWI/SNF chromatin remodeling complex and affecting genes expression. Importantly, we find that metabolic intervention can rescue the decline in ISC numbers due to H3K36 methylation deficiency. Our findings reveal a critical role for H3K36 methylation in maintaining epigenetic landscape to orchestrate lipid metabolism and determine intestinal stem cell fate.
  • 🔗 查看原文

3.GSE283728 组蛋白 3 赖氨酸 36 甲基化塑造肠道干细胞的表观遗传景观,从而调控脂质代谢并防止细胞衰老 [ATAC-seq 1]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、ATAC-seq、epigenetic、methylation、histone、regex:intestin(e|al)
  • 📝 描述:Contributors : Yue Xu ; Ziyi WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity and differentiation potential of intestinal stem cells (ISCs) decline with age, leading to a loss of homeostasis and increased susceptibility to intestinal diseases. Despite the established importance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms linking these processes to aging-associated ISC dysfunction remain elusive. Here, we demonstrate that H3K36 methylation, caused by NSD2 or SETD2, is critical to ISC fate. We found that the deficiency of H3K36 methylation results in reduced ISC proliferation and differentiation, disturbs fatty acid metabolism, and induces ISC senescence. This loss leads to increased chromatin accessibility and enhancer activation, impairing the function of the SWI/SNF chromatin remodeling complex and affecting genes expression. Importantly, we find that metabolic intervention can rescue the decline in ISC numbers due to H3K36 methylation deficiency. Our findings reveal a critical role for H3K36 methylation in maintaining epigenetic landscape to orchestrate lipid metabolism and determine intestinal stem cell fate.
  • 🔗 查看原文

4.GSE280531 通过派氏淋巴集结中的肠上皮免疫动力学塑造肠道免疫。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、immunity、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
  • 📝 描述:Contributors : M Zeeshan Chaudhry ; Wang Cao ; Gabrielle BelzSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMicrofold (M) cells are specialized antigen-sampling cells that transcytose luminal antigens to underlying immune cells to initiate mucosal immunity. How they are programmed in different intestinal tissues and their role during enteric infections has not been resolved. Here, we demonstrate that M cells are critical for B cell activation and IgA production that shapes the intestinal microbiome and maintains steady-state intestinal epithelial integrity. Tuft cells and M cells share expression of SPI-B. Molecular mapping revealed that M cells exhibit significant heterogeneity including tissue-specific and pathogen-specific tailored programs. These include key pathways regulating fatty acid uptake and metabolism in the intestinal epithelium. Confocal imaging demonstrated that Peyer’s patch SPI-B+ M cells act to retain group 3 innate lymphoid cells and IL-22 production within the Peyer’s patch epithelium. By identifying interconnected cellular and molecular programs, we uncover novel spatially organized immune-epithelial regulatory networks essential for immune protection.
  • 🔗 查看原文

5.GSE336978 单细胞RNA和空间转录组学分析毛里求斯猕猴和印度猕猴外周血单核细胞和组织中等位基因特异性MHC表达

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:MHC、scRNA、spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Macaca fascicularis ; Macaca mulattaThis SuperSeries is composed of the SubSeries listed below.
  • 🔗 查看原文

6.GSE336518 人类胰腺癌中的多核巨细胞是经历 DNA 损伤反应的独特巨噬细胞群,与侵袭性肿瘤微环境相关 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、cancer、tumor microenvironment、macrophage、RNA-seq
  • 📝 描述:Contributors : AR Putignano ; M Viatore ; R Polidori ; F Marchesi ; A MantovaniSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMacrophages constitute a dominant and functionally diverse immune population within the microenvironment of pancreatic ductal adenocarcinoma (PDAC), yet how this heterogeneity contributes to the tumor remains poorly defined. In an institutional cohort of 145 PDAC specimens, we identified a population of multinucleated giant cells (MGCs) of macrophage origin, an entity previously described in chronic inflammation but rarely in cancer. CD68⁺ MGCs were present in 28% of tumors, enriched in squamous, non-glandular regions, and more frequent after neoadjuvant chemotherapy. By integrating spatial transcriptomics and quantitative imaging, we defined the features of these cells, which, compared with MGCs in non-neoplastic inflammatory lesions, lacked canonical polarization markers (HLA-DR, CD163) and displayed a distinctive transcriptional program characterized by upregulation of POLR2K, TUBA8, COX5B, and VDAC1 genes, involved in DNA repair, oxidative stress, and MYC signaling. Spatial analyses revealed activation of hypoxia and extracellular matrix–remodeling pathways in MGC-associated niches, and experimental hypoxia promoted MGC formation in vitro. Consistently, a macrophage MGC gene signature was enriched in the squamous PDAC subtype and correlated with poorer overall survival in TCGA (p = 0.018). Morphometric and immunofluorescence analyses further showed increased 53BP1⁺/Ki67⁺ nuclei and nuclear atypia in MGCs, indicating ongoing proliferation despite DNA damage. Together, these data identify multinucleated macrophages as a previously unrecognized immune cell state shaped by hypoxia and stress signaling, associated with aggressive tumor phenotypes, and potentially exploitable as an immune classifier in pancreatic cancer.
  • 🔗 查看原文

7.GSE300017 CARM1 表观遗传酶抑制癌症免疫中的交叉呈递树突状细胞功能 [scRNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、immunity、dendritic cell、scRNA、epigenetic
  • 📝 描述:Contributors : Xixi Zhang ; Yuyang HanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe cancer-immunity cycle requires cross-presenting dendritic cells (cDC1) that induce T cell-mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are inadequate. We discovered the epigenetic enzyme Carm1 as a selective negative regulator of cancer antigen presentation by cDC1s, but not cDC2s. Carm1 inactivation promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors; and a Carm1 inhibitor enhanced cDC1-mediated priming of T cells by a cancer vaccine. Carm1 inhibition increased chromatin accessibility at BATF3-JUN and RELA sites critical for cDC1 function and activation. Carm1 expression was regulated by TGF-beta, explaining why Carm1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify Carm1 as a therapeutic target for enhancing the anti-tumor function of murine and human cDC1.
  • 🔗 查看原文

8.GSE300014 CARM1 表观遗传酶抑制癌症免疫中的交叉呈递树突状细胞功能 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、immunity、dendritic cell、RNA-seq、epigenetic
  • 📝 描述:Contributor : Xixi ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe cancer-immunity cycle requires cross-presenting dendritic cells (cDC1) that induce T cell-mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are inadequate. We discovered the epigenetic enzyme Carm1 as a selective negative regulator of cancer antigen presentation by cDC1s, but not cDC2s. Carm1 inactivation promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors; and a Carm1 inhibitor enhanced cDC1-mediated priming of T cells by a cancer vaccine. Carm1 inhibition increased chromatin accessibility at BATF3-JUN and RELA sites critical for cDC1 function and activation. Carm1 expression was regulated by TGF-beta, explaining why Carm1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify Carm1 as a therapeutic target for enhancing the anti-tumor function of murine and human cDC1.
  • 🔗 查看原文

9.GSE300010 CARM1 表观遗传酶抑制癌症免疫中的交叉呈递树突状细胞功能 [ATAC-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、immunity、dendritic cell、ATAC-seq、epigenetic
  • 📝 描述:Contributors : Xixi Zhang ; Wen WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe cancer-immunity cycle requires cross-presenting dendritic cells (cDC1) that induce T cell-mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are inadequate. We discovered the epigenetic enzyme Carm1 as a selective negative regulator of cancer antigen presentation by cDC1s, but not cDC2s. Carm1 inactivation promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors; and a Carm1 inhibitor enhanced cDC1-mediated priming of T cells by a cancer vaccine. Carm1 inhibition increased chromatin accessibility at BATF3-JUN and RELA sites critical for cDC1 function and activation. Carm1 expression was regulated by TGF-beta, explaining why Carm1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify Carm1 as a therapeutic target for enhancing the anti-tumor function of murine and human cDC1.
  • 🔗 查看原文

10.GSE283733 组蛋白3赖氨酸36甲基化塑造肠道干细胞的表观遗传图谱,从而调控脂质代谢并防止细胞衰老

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、epigenetic、methylation、histone、regex:intestin(e|al)
  • 📝 描述:Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
  • 🔗 查看原文

💡 该来源还有 182 条内容,详见 文末

🧪 博客更新 (3条)

详细内容(全部3条)

1. 即将举办的RNA测序网络研讨会——量化月经液中的炎症消退

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNA-seq
  • 📝 描述:RNA sequencing of menstrual fluid enables time-resolved analysis of inflammation, tissue repair, and the microbiome, supporting new approaches for women’s health diagnostics… The post Upcoming RNA-Seq Webinar – Quantifying Inflammatory Resolution in Menstrual Fluid appeared first on RNA-Seq Blog.
  • 🔗 查看原文

2. 科学家发现一种意想不到的方法,使胰腺癌细胞自毁

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:Researchers tested experimental PCAI compounds against pancreatic cancer cells and found they had powerful anticancer effects. One leading compound blocked more than 90% of cancer cell migration, suggesting it could help prevent the spread of tumors. Rather than suppressing cancer signaling, the treatment hyperactivated key pathways until the cells essentially self-destructed.
  • 🔗 查看原文

3. Scientists may have finally found how Alzheimer’s spreads through the brain

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:Alzheimer
  • 📝 描述:A common brain protein may be giving Alzheimer’s disease an unexpected way to spread, carrying toxic Tau proteins from damaged neurons into healthy ones. By blocking these harmful protein packages before they reach new cells, researchers believe it may one day be possible to slow the disease’s relentless progression.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
cancer49
RNA-seq30
epigenetic14
regex:intestin(eal)
tumor12
transcriptome11
immune11
scRNA11
sequencing10
macrophage9
methylation9
spatial8
immunity8
genome8
T cell8
metabolism8
pathway7
Alzheimer6
kinase6
ATAC-seq6

📎 更多内容

🧬 数据前沿 其他内容 (182条)

📅 报告生成时间:2026-06-30 22:46
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