科研日报 2026-02-22
📅 Daily Report - 2026-02-22
今日筛选出 36 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 研究揭示Hippo通路在癌相关成纤维细胞中调控PD-L1免疫治疗抗性,并发现ARID1A缺陷型胃癌存在嘧啶代谢脆弱性。
主要方向:
- 急性髓系白血病中CoREST、p300与视黄酸信号的相互作用。
- 细胞外囊泡介导的人菌跨界通讯机制。
- 癌症(胃癌、乳腺癌、B-ALL)的分子机制与生物标志物探索。
- 神经元、β细胞、心肌细胞等特定细胞功能与代谢调控。
- 免疫应答与病原体相互作用。
技术亮点:
- 多组学联合分析(RNA-seq, ATAC-seq, ChIP-seq, smallRNA-seq)深入解析基因调控网络。
- 单细胞分辨率转录组分析。
🧪 博客更新
今日焦点: 新型STING激动剂疗法有望激活脑膜瘤免疫应答;常见肺炎细菌或与阿尔茨海默病发生相关。
主要方向:
- 探索STING通路在脑膜瘤免疫治疗中的作用。
- 研究肺炎衣原体在阿尔茨海默病发病机制中的角色。
- 评估空气污染对老年人群阿尔茨海默病风险的影响。
- 揭示运动如何通过修复脑部保护机制延缓阿尔茨海默病。
技术亮点:
- 单细胞RNA测序技术揭示STING通路在脑膜瘤中的激活。
- 结合多项大规模流行病学研究,评估环境因素与疾病风险关联。
📚 分类浏览
🧬 数据前沿 (32条)
详细内容(前10条)
1. ⭐ GSE313827 研究发现,癌症相关成纤维细胞中 Hippo 通路的失调与抗 PD-L1 抗体阿特珠单抗耐药相关。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、resistance、pathway
- 📝 描述:Contributors : Juliette Roels ; Hamid Ghaedi ; Soren Muller ; Akshay T Krishnamurty ; Ramya Ganesan ; Priyanka BabuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe use of immunotherapy in solid tumors has significantly improved the outcomes and quality of life for cancer patients. However, a substantial fraction of patients remain unresponsive, highlighting the urgent need to identify novel mechanisms of resistance to enhance immune-centric, chemo-free treatment regimens. In this study, we investigate associations with immunotherapy resistance by integrating RNAseq data from 2800 bladder cancer patients enrolled in the IMvigor trials, focusing on resistance to the anti-PD-L1 therapy atezolizumab, along with single-cell data from 200 patient samples and healthy donors. To expand the analysis to a massive collection of over 100M cells from hundreds of diverse single cell studies, we present Firmament, a newly developed method to efficiently identify cell populations that show enrichment for expression of gene signatures. Through these analyses, we identify the Hippo pathway as critically associated with immunotherapy resistance in bladder cancer and other solid tumors. Our findings indicate that Hippo dysregulation in stromal cells, rather than cancer cells, drives the high YAP/TAZ signal in these tumors. We specifically identify dysregulated Hippo signaling in cancer-associated fibroblasts compared to healthy donor fibroblasts. These insights will be important for developing novel therapeutic combinations to improve outcomes for patients with solid tumors treated with immune checkpoint inhibitors.
- 🔗 查看原文
2. GSE300988 急性髓系白血病中 CoREST、p300 和视黄酸信号通路之间的相互作用 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:leukemia、RNA-seq
- 📝 描述:Contributors : Mina M. Tayari ; Helena Gomes Dos Santos ; Sadat Dokaneheifard ; Monica Valencia ; Felipe Beckedorff ; Arigela Harikumar ; Justin M. Watts ; Philip A. Cole ; Ramin ShiekhattarSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe histone demethylase KDM1A (LSD1), a component of the CoREST corepressor complex, is highly expressed in hematologic malignancies and regulates hematopoietic differentiation. Despite its essential developmental role, LSD1 inhibition has emerged as a promising strategy to enhance retinoic acid (RA)-responsive gene expression in subsets of acute myeloid leukemia (AML). Here, we show that LSD1 physically interacts with RAR/RXR heterodimers at specific genomic loci, restricting chromatin accessibility and transcriptional activation of differentiation programs. Single-agent inhibition of LSD1 or HDACs promotes only partial differentiation. In contrast, Corin, a dual LSD1/CoREST inhibitor, synergizes with all-trans retinoic acid (ATRA) to induce robust myeloid differentiation and apoptosis. Corin treatment increases H3K4me3 and H3K27ac at promoters of ATRA-responsive genes and disrupts CoREST–RAR/RXR complexes, enabling recruitment of the coactivator p300. This epigenetic switch facilitates transcriptional reprogramming essential for terminal differentiation. Our findings identify the functional antagonism between CoREST and p300 as a regulatory axis of RA signaling in AML. Targeting this mechanism with Corin and ATRA re-sensitizes non-APL AML cells to RA-induced differentiation, suggesting a broader therapeutic approach for overcoming resistance in ATRA-refractory leukemias.
- 🔗 查看原文
3. GSE300987 急性髓系白血病中 CoREST、p300 和视黄酸信号传导的相互作用 [ATAC-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:leukemia、ATAC-seq
- 📝 描述:Contributors : Mina M. Tayari ; Helena Gomes Dos Santos ; Sadat Dokaneheifard ; Monica Valencia ; Felipe Beckedorff ; Arigela Harikumar ; Justin M. Watts ; Philip A. Cole ; Ramin ShiekhattarSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe histone demethylase KDM1A (LSD1), a component of the CoREST corepressor complex, is highly expressed in hematologic malignancies and regulates hematopoietic differentiation. Despite its essential developmental role, LSD1 inhibition has emerged as a promising strategy to enhance retinoic acid (RA)-responsive gene expression in subsets of acute myeloid leukemia (AML). Here, we show that LSD1 physically interacts with RAR/RXR heterodimers at specific genomic loci, restricting chromatin accessibility and transcriptional activation of differentiation programs. Single-agent inhibition of LSD1 or HDACs promotes only partial differentiation. In contrast, Corin, a dual LSD1/CoREST inhibitor, synergizes with all-trans retinoic acid (ATRA) to induce robust myeloid differentiation and apoptosis. Corin treatment increases H3K4me3 and H3K27ac at promoters of ATRA-responsive genes and disrupts CoREST–RAR/RXR complexes, enabling recruitment of the coactivator p300. This epigenetic switch facilitates transcriptional reprogramming essential for terminal differentiation. Our findings identify the functional antagonism between CoREST and p300 as a regulatory axis of RA signaling in AML. Targeting this mechanism with Corin and ATRA re-sensitizes non-APL AML cells to RA-induced differentiation, suggesting a broader therapeutic approach for overcoming resistance in ATRA-refractory leukemias.
- 🔗 查看原文
4. GSE300986 急性髓系白血病中 CoREST、p300 和视黄酸信号通路之间的相互作用 [ChIP-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:leukemia、ChIP-seq
- 📝 描述:Contributors : Mina M. Tayari ; Helena Gomes Dos Santos ; Sadat Dokaneheifard ; Monica Valencia ; Felipe Beckedorff ; Arigela Harikumar ; Justin M. Watts ; Philip A. Cole ; Ramin ShiekhattarSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe histone demethylase KDM1A (LSD1), a component of the CoREST corepressor complex, is highly expressed in hematologic malignancies and regulates hematopoietic differentiation. Despite its essential developmental role, LSD1 inhibition has emerged as a promising strategy to enhance retinoic acid (RA)-responsive gene expression in subsets of acute myeloid leukemia (AML). Here, we show that LSD1 physically interacts with RAR/RXR heterodimers at specific genomic loci, restricting chromatin accessibility and transcriptional activation of differentiation programs. Single-agent inhibition of LSD1 or HDACs promotes only partial differentiation. In contrast, Corin, a dual LSD1/CoREST inhibitor, synergizes with all-trans retinoic acid (ATRA) to induce robust myeloid differentiation and apoptosis. Corin treatment increases H3K4me3 and H3K27ac at promoters of ATRA-responsive genes and disrupts CoREST–RAR/RXR complexes, enabling recruitment of the coactivator p300. This epigenetic switch facilitates transcriptional reprogramming essential for terminal differentiation. Our findings identify the functional antagonism between CoREST and p300 as a regulatory axis of RA signaling in AML. Targeting this mechanism with Corin and ATRA re-sensitizes non-APL AML cells to RA-induced differentiation, suggesting a broader therapeutic approach for overcoming resistance in ATRA-refractory leukemias.
- 🔗 查看原文
5. GSE297395 细胞外囊泡及其 RNA 货物促进人类细胞和细菌细胞之间的双向跨界通讯 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:regex:bacter(ia|ial|ium)、RNA-seq
- 📝 描述:Contributors : Laura Gröger ; Shusruto Rishik ; Nicole Ludwig ; Amila Beganovic ; Marcus Koch ; Stefanie Rheinheimer ; Martin Hart ; Petra König ; Tabea Trampert ; Pascal Paul ; Annette Boese ; Claus-Michael Lehr ; Sören L. Becker ; Gregor Fuhrmann ; Andreas Keller ; Eckart MeeseSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensExtracellular vesicles (EVs), released by both eukaryotic and prokaryotic cells, have emerged as key mediators of cell-to-cell communication. Recent advances highlight their crucial role in cross-kingdom communication, bridging the microbial world with human biology. Here, we investigated the molecular mechanisms underlying EV-mediated bidirectional communication within the gastrointestinal ecosystem. Using a model that includes human colon cells and both Gram-positive and Gram-negative gut bacteria, we reveal an intricate exchange of information between these kingdoms. Our analysis uncovered highly specific responses of host cells to bacterial EVs (BEVs) and BEV-RNA cargo, including uptake rates by human cells, impact on human cell viability, and alterations in their transcriptomic landscape. In parallel, we discovered that host-derived EVs and miR-192-5p are internalized by gut bacteria, leading to changes in their growth pattern. These findings highlight the precision with which EVs and their RNA cargo mediate interkingdom communication. Our results underscore the importance of tailored, context-specific analyses for understanding the scope of EV-mediated interactions in complex biological systems.
- 🔗 查看原文
6. GSE319750 ARID1A缺陷在弥漫型胃癌中促进嘧啶代谢脆弱性
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、metabolic
- 📝 描述:Contributor : Hideaki OgiwaraSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensLoss-of-function mutations in ARID1A define an aggressive subtype of diffuse gastric cancer (DGC) that is often resistant to standard chemotherapy. Here, we uncover a precise metabolic vulnerability in ARID1A-deficient DGC driven by a specific transporter defect. Through integrated metabolomic and transcriptomic analyses, we demonstrate that ARID1A loss transcriptionally represses the high-affinity nucleoside transporter SLC28A3. Our profiling revealed a critical lack of redundancy in the concentrative transporter family (CNT) in DGC, establishing a strict reliance on SLC28A3 for maintaining intracellular deoxycytidine (dC) pools. Consequently, ARID1A deficiency creates a severe “low-dCTP” metabolic bottleneck. We show that the dC analog Gemcitabine exploits this state through a distinct functional dichotomy: it enters via intact equilibrative transporters (ENTs) to target cells that have lost their competitive dC barrier. Mechanistically, Gemcitabine exerts a “dual-hit” effect by outcompeting the scarce dC pool for DNA incorporation while simultaneously inhibiting ribonucleotide reductase, thereby blocking de novo nucleotide synthesis. This synergistic collapse of pyrimidine metabolism was validated in patient-derived ex vivo cultures and in vivo peritoneal dissemination models. Our findings provide a robust mechanistic basis for repurposing Gemcitabine as a precision therapy for ARID1A-deficient DGC, offering a potent strategy for this intractable malignancy.
- 🔗 查看原文
7. GSE241255 神经-2a (N2a) 细胞中 Zmiz1 的染色质免疫沉淀 DNA 测序 (ChIP-seq)
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、ChIP-seq
- 📝 描述:Contributors : K C Rajan ; Stryder Meadows ; Maria J GalazoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusPurpose: Zinc Finger MIZ-Type Containing 1 (Zmiz1) is a member of the PIAS family of protein and function as a transcriptional coactivator of Notch, Androgen Receptor (AR), p53, Estrogen Receptor (ER), and Smad3/4 . Here, we use Neuro-2a cell line to perform ChIP sequencing on Zmiz1 bound, direct or indirect to profile Zmiz1 associated genomic regulation.Methods: Neuro-2a (N2a) (ATCC, CCL-131) were cultured in DMEM-high glucose (Cytiva, SH30022) supplemented with 5 % FBS (Cytiva, SH3008803) and 50 U/ml Penicillin-Streptomycin (Thermo Fisher Scientific, 15070063) at 37 °C and 5% CO2. Zmiz1-HA was overexpressed in N2a cells and subsequently, ChIP DNA samples were obtained by using ChIP-IT Express Enzymatic Kit (Active Motif, 53009) and processed according to manufacturer specifications. Anti-HA-Tag Antibody (Cell Signaling, 3724S) was used for immunoprecipitation. Pull down DNA quantity was measured using Qubit DNA HS kit (Thermo Fisher Scientific, Q32851). The sequencing library was prepared using TruSeq ChIP Library Preparation Kit (Illumina, IP-202–1012). Ten nanograms of starting material were used for library preparation. Library quality and quantity were assessed using Agilent DNA 1000 chip (Agilent 5067-1504) and Qubit DNA HS kit respectively. Libraries were sequenced using the NextSeq1000/2000 P2 Reagents (200 Cycles) v3 (Illumina, 20046812) on a Nextseq1000/2000 system. Sequencing analysis was done using the ChIPSeq App from BaseSpace Labs (Illumina), which uses MACS2 for region enrichment and HOMER for motif analysis.Results: ChIP-seq peaks analysis identified thousands of peaks which are mostly located in intergenic regions followed by introns.Conclusions: We identify Zmiz1 bound DNA (direclty or indireclty) in Neuro-2a cells thus providing genomic regulation in neurodevelopmental events.
- 🔗 查看原文
8. GSE320031 通过RT-qPCR验证MCC-Spain研究中与乳腺癌亚型相关的循环miRNA
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:Contributors : Inés Gómez-Acebo ; Sara Valero-Domínguez ; Javier Llorca ; Jessica Alonso-Molero ; Thalía Belmonte ; Gemma Castaño-Vinyals ; Víctor Moreno ; Aina Romaguera ; Pilar Amiano ; Juan Alguacil ; Vicente Martín ; Beatriz Pérez-Gómez ; Rosana Burgui ; Ana Molina-Barceló ; Paz Rodríguez-Cundín ; Manolis Kongevinas ; Marina Pollán ; Trinidad Dierssen-SotosSeries Type : Expression profiling by RT-PCROrganism : Homo sapiensThis study represents the validation phase of circulating microRNAs associated with breast cancer detection within the MCC-Spain study. A total of 444 participants (127 cancer-free controls and 317 breast cancer cases) were included. Cases were stratified into molecular subtypes (Luminal A, Luminal B, HER2-positive, and Basal-like) according to St. Gallen criteria. A panel of 46 candidate miRNAs was quantified in serum samples using RT-qPCR (miRCURY LNA technology). Two endogenous miRNAs (let-7d-5p and let-7i-5p) were used for normalization. Differential expression and predictive modeling were performed using normalized and log₂-transformed expression values. This dataset supports subtype-specific and overall breast cancer detection models integrating molecular and epidemiological factors.
- 🔗 查看原文
9. GSE319901 将循环 microRNA 与流行病学因素相结合可提高乳腺癌亚型的检出率:筛查阶段 [miRNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:Contributors : Inés Gómez-Acebo ; Sara Valero-Domínguez ; Javier Llorca ; Jessica Alonso-Molero ; Thalía Belmonte ; Gemma Castaño-Vinyals ; Víctor Moreno ; Aina Romaguera ; Pilar Amiano ; Juan Alguacil ; Vicente Martín ; Beatriz Pérez-Gómez ; Rosana Burgui ; Ana Molina-Barceló ; Paz Rodríguez-Cundín ; Manolis Kongevinas ; Marina Pollán ; Trinidad Dierssen-SotosSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensExploratory small RNA sequencing analysis of circulating miRNAs in serum samples from 40 women (30 breast cancer cases and 10 controls) recruited within the MCC-Spain study.
- 🔗 查看原文
10. GSE310958 IKAROS 重新表达调节 IKZF1 突变 Ph+ B-ALL 中的转录网络 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq
- 📝 描述:Contributors : Seth Frietze ; Boyd JosephSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWith the goal to investigate tumor suppressor mechanisms regulated by IKAROS (IKZF1) in PH chromosome–positive B-cell acute lymphoblastic leukemia (B-ALL) harboring IKZF1 mutations. This dataset includes bulk RNA-seq profiles from human MXP5 and PDX2 cell lines, which were engineered to express doxycycline-inducible wild-type IKAROS (IK1) or an empty vector control. RNA was collected 24 hours post-induction to capture early transcriptional responses to IK1 re-expression. These data are part of a larger multi-omics study integrating RNA-seq, ChIP-seq, CUT&RUN, ATAC-seq, and HiChIP to define IKAROS-regulated transcriptional and chromatin networks in IKZF1-deficient Ph⁺ B-ALL.
- 🔗 查看原文
💡 该来源还有 22 条内容,详见 文末
🧪 博客更新 (4条)
详细内容(全部4条)
1. RNA测序揭示脑膜瘤中STING驱动的免疫治疗靶点
- ✍️ 作者:未知作者
- 🏷️ 关键词:regex:immuno(logy|therapy|suppression)、sequencing
- 📝 描述:Single-cell RNA sequencing revealed STING pathway activation in meningioma tumor and immune cells, and RNA sequencing showed inflammatory cell death mechanisms following STING agonist treatment, supporting a…
- 🔗 查看原文
2. 常见肺炎细菌可能加剧阿尔茨海默病
- ✍️ 作者:未知作者
- 🏷️ 关键词:regex:bacter(ia|ial|ium)、Alzheimer
- 📝 描述:A common bacterium best known for causing pneumonia and sinus infections may also play a surprising role in Alzheimer’s disease. Researchers found that Chlamydia pneumoniae can invade the retina and brain, where it sparks inflammation, nerve cell death, and the buildup of amyloid-beta—the hallmark protein linked to Alzheimer’s. Higher levels of the bacterium were found in people with Alzheimer’s, especially those carrying the high-risk APOE4 gene, and were tied to more severe cognitive decline.
- 🔗 查看原文
3. 空气污染与2800万美国老年人患阿尔茨海默病风险增加有关
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Breathing polluted air may do more than harm your lungs — it could also increase your risk of Alzheimer’s disease. In a sweeping study of nearly 28 million older Americans, researchers found that long term exposure to fine particle air pollution was linked to a higher likelihood of developing Alzheimer’s. The connection appeared to stem largely from pollution’s direct effects on the brain, rather than through related health conditions like hypertension or depression.
- 🔗 查看原文
4. 科学家揭示运动如何保护大脑免受阿尔茨海默病侵害
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Exercise may sharpen the mind by repairing the brain’s protective shield. Researchers found that physical activity prompts the liver to release an enzyme that removes a harmful protein causing the blood-brain barrier to become leaky with age. In older mice, dialing down this protein reduced inflammation and improved memory. The discovery points to a surprising body-to-brain pathway that could inspire new Alzheimer’s therapies.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| RNA-seq | 7 |
| sequencing | 4 |
| cancer | 4 |
| ATAC-seq | 4 |
| leukemia | 4 |
| ChIP-seq | 3 |
| transcriptome | 3 |
| Alzheimer | 3 |
| immune | 3 |
| regex:bacter(ia | ial |
| metabolic | 2 |
| pathway | 2 |
| regex:immuno(logy | therapy |
| resistance | 1 |
| regex:intestin(e | al) |
| scRNA | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (22条)
- GSE310890 IKAROS 重新表达调节 IKZF1 突变 Ph+ B-ALL 中的转录网络 [ChIP-Seq]
- GSE310887 IKAROS 重新表达调节 IKZF1 突变 Ph+ B-ALL 中的转录网络 [ATAC-seq]
- GSE308564 CHD3 和 CHD4 协调基因表达程序以维持体内 β 细胞的功能和特性 [RNA-seq]
- GSE308381 CHD3 和 CHD4 协调基因表达程序以维持体内 β 细胞的功能和特性 [ATAC-seq]
- GSE307669 琥珀酸-GPR91信号通路促进心肌细胞代谢重编程和NAD⁺生成,从而缓解HFpEF。
- GSE300989 急性髓系白血病中 CoREST、p300 和视黄酸信号传导的相互作用 [CUT&Run]
- GSE283280 Kitl/kit信号通路调控小鼠雌性性腺的减数分裂
- GSE279666 小鼠缺血性中风从急性期到慢性期的转录组分析[2]
- GSE279665 小鼠缺血性卒中从急性期到慢性期的转录组分析
- GSE314067 泛素连接酶 CBL 和 Fas 相关因子 2 协同调节对结核分枝杆菌的先天免疫反应
- GSE311695 ARHGEF2 亚型转换将肠道上皮屏障功能与对病原体的自噬反应联系起来
- GSE297396 细胞外囊泡及其 RNA 货物促进人类细胞和细菌细胞之间的双向跨界通讯 [smallRNA-Seq]
- GSE297088 安氏革蜱唾液腺的单细胞分辨率转录组
- GSE290648 肩胛硬蜱唾液腺 RNA 测序 [bulkRNA-dissociated-SG]
- GSE290647 肩胛硬蜱唾液腺的 RNA-seq [bulkRNA-intact-SG]
- GSE275695 双功能兼职 RNA 协调通路以调控人类胚胎发育 [scRNA-seq]
- GSE275691 双功能兼职 RNA 协调通路以调节人类胚胎发育 [ATAC-seq]
- GSE275690 双功能兼职 RNA 协调通路以调控人类胚胎发育 [RNA-seq]
- GSE241140 对野生型和 Zmiz1-KO 皮层中 P1 和 P14 富集神经元进行 RNA 测序
- GSE225333 RNA测序,分析野生型和Zmiz1-KO皮层中分离的E15.5祖细胞
- GSE285852 胆固醇使结核肉芽肿中的先天性-适应性免疫轴脱钩[小鼠]
- GSE285046 胆固醇使结核肉芽肿中的先天性-适应性免疫轴脱钩[人类]
📅 报告生成时间:2026-02-21 21:42
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