详细内容（前10条）

1. ⭐ GSE327404 体内工程改造肿瘤细胞，使其成为具有全抗原谱的通用“一体化”癌症疫苗 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、vaccine、antigen、scRNA
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusCancer vaccines offer a promising strategy to initiate de novo T cell responses or enhance existing ones, either functioning independently or synergizing with T cell-modulating therapeutics to reduce tumor burden. The clinical development of cancer vaccines faces challenges such as limited antigen coverage, insufficient antigen presentation, immune suppressive microenvironment, and the availability of personalized vaccines. In this study, we developed a Universal ‘all-in-one’ Cancer cell-derived Vaccine (UniCVac) with comprehensive antigen spectrum coverage by programming tumor cells into antigen-presenting cells (APCs) through the co-delivery of CIITA, NLRC5, CD80, and IL-2. This reprogramming mimics the professional APC phenotype, providing simultaneous HLA-I and HLA-II antigen presentation, co-stimulation, and T cell proliferation signals. These tumor-derived UniCVac can directly activate both CD4+ and CD8+ T cells in vitro, independent of APCs. Additionally, their co-stimulation and T cell growth-stimulating capabilities result in superior CD4+ and CD8+ T cell activation and proliferation comparable to traditional APCs, with enhanced PI3K-AKT pathways activation. Single cell transcriptome analysis confirmed the similarity in cellular subtypes between UniCVac and traditional APCs activated T cells. In mouse models, the UniCVac vaccination reprogramed the tumor microenvironment from immunosuppressive to immune-permissive, induced robust CD4+ and CD8+ T cell expansion in both preventive and therapeutic tumor models and achieved complete tumor regression in vivo. Our approach provides a platform for the development of universal cancer vaccines with full antigen spectrum coverage and the ability to directly activate both CD4+ and CD8+ T cells, offering potential combinatorial opportunities with existing T cell-based immunotherapies against cancer.
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2. ⭐ GSE327399：体内工程改造肿瘤细胞，使其成为具有全抗原谱的通用“一体化”癌症疫苗

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、vaccine、antigen
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCancer vaccines offer a promising strategy to initiate de novo T cell responses or enhance existing ones, either functioning independently or synergizing with T cell-modulating therapeutics to reduce tumor burden. The clinical development of cancer vaccines faces challenges such as limited antigen coverage, insufficient antigen presentation, immune suppressive microenvironment, and the availability of personalized vaccines. In this study, we developed a Universal ‘all-in-one’ Cancer cell-derived Vaccine (UniCVac) with comprehensive antigen spectrum coverage by programming tumor cells into antigen-presenting cells (APCs) through the co-delivery of CIITA, NLRC5, CD80, and IL-2. This reprogramming mimics the professional APC phenotype, providing simultaneous HLA-I and HLA-II antigen presentation, co-stimulation, and T cell proliferation signals. These tumor-derived UniCVac can directly activate both CD4+ and CD8+ T cells in vitro, independent of APCs. Additionally, their co-stimulation and T cell growth-stimulating capabilities result in superior CD4+ and CD8+ T cell activation and proliferation comparable to traditional APCs, with enhanced PI3K-AKT pathways activation. Single cell transcriptome analysis confirmed the similarity in cellular subtypes between UniCVac and traditional APCs activated T cells. In mouse models, the UniCVac vaccination reprogramed the tumor microenvironment from immunosuppressive to immune-permissive, induced robust CD4+ and CD8+ T cell expansion in both preventive and therapeutic tumor models and achieved complete tumor regression in vivo. Our approach provides a platform for the development of universal cancer vaccines with full antigen spectrum coverage and the ability to directly activate both CD4+ and CD8+ T cells, offering potential combinatorial opportunities with existing T cell-based immunotherapies against cancer.
• 🔗 查看原文

3. ⭐ GSE319703 YTHDF1 作为一种非经典的核检查点，将 R 环稳态与癌症中的先天免疫抑制和适应性免疫抵抗联系起来（RNA-seq II）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、resistance、RNA-seq
• 📝 描述：Contributors : Xiaofeng Zhu ; Shan GaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensInnate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling
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4. ⭐ GSE319690 YTHDF1 作为一种非经典的核检查点，将 R 环稳态与癌症中的先天免疫抑制和适应性免疫抵抗联系起来（RNA-seq i）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、resistance、RNA-seq
• 📝 描述：Contributors : Xiaofeng Zhu ; Shan GaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensInnate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling
• 🔗 查看原文

5. ⭐ GSE319911 YTHDF1 作为一种非经典的核检查点，将 R 环稳态与癌症中的先天免疫抑制和适应性免疫抵抗联系起来（CUT&Tag）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、resistance
• 📝 描述：Contributors : Xiaofeng Zhu ; Shan GaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensInnate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling
• 🔗 查看原文

6. ⭐ GSE319910 YTHDF1 作为一种非经典的核检查点，将 R 环稳态与癌症中的先天免疫抑制和适应性免疫抵抗联系起来（R 环 CUT&Tag）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、resistance
• 📝 描述：Contributors : Xiaofeng Zhu ; Shan GaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensInnate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling
• 🔗 查看原文

7. ⭐ GSE318635 肠道菌群相关色氨酸代谢产物可预防代谢功能障碍相关的脂肪肝疾病

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Tingting Wang ; Shuping Qiao ; Shuangya Fan ; Juan Xu ; Zhen Xu ; Chen Peng ; Junxing QuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAccumulating evidence suggests that the intestinal microbiota participates in the development of metabolic dysfunction-associated steatotic liver disease (MASLD) through metabolite-host interaction. However, the beneficial role of commensal mycobiota in MASLD progression remains poorly understood. Comparing the gut microbiome differences, we demonstrated that the deficiency of Caspase Recruitment Domain-containing protein 9 (CARD9), an adaptor protein for a microbiota recognition receptor, exacerbated HFD-induced MASLD in a gut fungi-dependent manner. CARD9 deficiency reduced the abundance of Saccharomyces cerevisiae (S. cerevisiae), which was a probiotic alleviating MASLD progression. S.cerevisiae promoted a significantly greater abundance of 5-hydroxyindoleacetic acid (5-HIAA) in intestine through TLR1, which then alleviated MASLD phenotypes via “gut-liver” axis. Particularly, 5-HIAA directly bond to aryl-hydrocarbon receptor (AhR) and stimulated its nuclear translocation, subsequently inducing fatty acid oxidation via carnitine palmitoyl transferase 1A (CPT1A) and acyl-CoA oxidase 1 (ACOX1) transactivation. MASLD patients exhibited decreased levels of S. cerevisiae and 5-HIAA, and S.cerevisiae effectively ameliorated hepatic steatosis and improved glucose homeostasis in patients with MASLD. In summary, our findings identified a novel pathway of fungi-S. cerevisiae stimulating intestinal 5-HIAA production and indicated that S. cerevisiae and 5-HIAA might alleviate MASLD progression, highlighting that mycobiota-dependent gut-liver axis was a promising target for the prevention of MASLD.
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8. ⭐ GSE308411 超级增强子介导的 SMAD3–NR2F2–ID3 转录复合物调控非小细胞肺癌中的奥希替尼耐药性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、ChIP-seq
• 📝 描述：Contributors : Aochu Liu ; Zhenguo Liu ; Lizhen Jiang ; Andong Huang ; Bingyuan Liu ; Xinqing Lin ; Shiwen Hu ; Junjun Huang ; Liyuan Yin ; Yueyuan Zheng ; Xianping ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensOsimertinib resistance remains a major challenge in the treatment of non–small cell lung cancer (NSCLC). Here, we identify an unconventional super-enhancer–driven transcriptional module, composed of SMAD3, NR2F2, and ID3, in which ID3 functions as a transcriptional co-factor to sustain resistance. Mechanistically, ID3 directly interacts with SMAD3 and NR2F2, inducing conformational rearrangements that enhance their DNA-binding affinity to enhancer regions, thereby increasing transcriptional activity. This ID3-SMAD3/NR2F2 complex selectively activates EPAS1, which in turn promotes neuroendocrine differentiation and suppresses ferroptosis, thereby maintaining the resistant phenotype. Disruption of this complex abrogates EPAS1 expression and restores Osimertinib sensitivity in preclinical models. Our findings uncover a previously unrecognized role of ID3 as a transcriptional co-factor and highlight the super-enhancer–driven SMAD3–NR2F2–ID3–EPAS1 axis as a promising therapeutic target to overcome Osimertinib resistance in NSCLC.
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9. ⭐ GSE306009 ACLY驱动的代谢重编程促进慢性肾脏病中的组蛋白乙酰化和炎症相关纤维化

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、metabolic、histone
• 📝 描述：Contributors : Chunxiu Du ; Dhanunjay Mukhi ; Katalin SusztakSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusConducted chromatin accessibility by ATAC-seq in tubule-specific Acly knockout and WT mice. The dataset includes raw sequencing files.
• 🔗 查看原文

10. ⭐ GSE305504 研究发现，在 BRCA1 缺陷型乳腺癌中，PARP 抑制剂触发的肿瘤细胞固有 dsRNA 先天免疫反应因 IRF3 的抑制而受损。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune
• 📝 描述：Contributors : Chu-Xia Deng ; Cuiting Zhang ; Jing-Bo ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPoly (ADP-ribose) polymerase 1 (PARP1) inhibition represents promising targeted therapy for BRCA deficient cancer patients based on synthetic lethality theory. Recent evidence shows that efficacy of DNA damage drugs depends on two aspects, DNA repair signaling and immune response. Applying a functional proteomics approach, we find that the function of spliceosome is perturbed by PARP inhibitors via enhancing interaction between PARP1 and SF3B1, a key factor of spliceosome. We demonstrate that differential alternative spliced mRNA and accumulation of double strand RNA (dsRNA) are induced by perturbation of spliceosome upon PARP inhibitors treatment, resulting in triggering dsRNA antiviral mimicry innate immune response. Moreover, we identify a novel function of BRCA1, through which BRCA1 regulates innate immune response leading to compromising of the innate immune signaling by downregulation of IRF3 in BRCA1 deficient breast cancer cells, which reduces the sensitivity to PARP inhibitors and causes intrinsic resistance. Polyinosinic-polycytidylic acid (poly(I:C)) is a dsRNA synthetic analog sensitizing PARP inhibitors through further triggering dsRNA signaling. Finally, we show that the combination of PARP inhibitors and poly(I:C) enhances antitumor efficiency in vivo. Overall, our study reveals BRCA1 deficiency impedes tumor cell intrinsic innate immune response, inducing intrinsic resistance to PARP inhibitors that can be overcome when poly(I:C) is combined.
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1. 火山爆发：发布新的 R 包 VolcanoPlotR

• ✍️ 作者：未知作者
• 🏷️ 关键词：R package
• 📝 描述：This is a short post to announce the release of an R package, VolcanoPlotR. Background Using proteomics, we often want to compare two experimental groups. A popular way to visualise this comparison this is via a volcano plot, where the enrichment of proteins in one condition is towards the right … Continue reading: Eruption: announcing new R package VolcanoPlotR
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详细内容（全部4条）

1. ⭐ 科学家最终揭开了常见肠道细菌如何引发结肠癌的谜团。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Researchers solved a long-standing mystery behind how a bacterial toxin associated with colorectal cancer damages the colon. The toxin first binds to a receptor called claudin-4, giving it access to attack the cells’ protective barrier. After identifying this weak point, the team designed a decoy protein that successfully blocked the toxin in mice. The discovery could pave the way for new therapies to prevent inflammation and colon tumors.
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2. STGBench——用于基因组改变的多模态和虚拟细胞基准测试的测序级空间DNA-RNA模拟

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、spatial
• 📝 描述：STGBench generates realistic paired DNA and RNA sequencing datasets with known genetic alterations, enabling accurate benchmarking of spatial genomics and transcriptomics analysis…
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3. 脑细胞内隐藏的骨骼“守门人”可能有助于对抗阿尔茨海默病

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have discovered that a microscopic skeleton inside neurons does much more than hold cells together. It acts as a gatekeeper that controls what brain cells absorb and when they absorb it. When this protective structure weakens, neurons rapidly take in harmful proteins associated with Alzheimer’s disease, suggesting that stabilizing it could become a promising new strategy for preventing brain cell damage.
• 🔗 查看原文

4. 这种宠物壁虎或许能帮助科学家揭开癌症的秘密。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：An unusual leopard gecko that naturally develops aggressive tumors may become an important new model for cancer research. Scientists found its tumors share key genetic changes with human cancers, offering a rare opportunity to study the disease as it develops naturally.
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• GSE301306 人类妊娠早期蜕膜的空间转录组学
• GSE337521 奥拉替尼联合奥妥珠单抗治疗边缘区淋巴瘤的疗效、安全性和空间转录组学原理
• GSE331391 单细胞基因组学将靶向功能操作与抗肿瘤T细胞的疗效相关转录特征联系起来
• GSE330140 P3FI-90 激活三阴性乳腺癌中的先天免疫反应。
• GSE329718 小鼠岛叶皮层组织、投射和功能的空间分辨单细胞解剖
• GSE329706 小鼠海马在保留神经损伤（SNI）模型后的单细胞RNA测序
• GSE328486 HNRNPU 乳酸化通过重编程丝氨酸代谢驱动宫颈癌生长
• GSE326007：红藻氨酸诱导癫痫模型中组蛋白H3K18乳酸化的全基因组分析
• GSE324125 非小细胞肺癌 KRAS G12C 突变细胞依赖于 MUC1-C 对 RAS(ON) 抑制剂产生耐药性
• GSE322907 单细菌 RNA-seq 方案揭示拟杆菌属（Bacteroides thetaiotaomicron）中编码基因和非编码基因的异质性表达
• GSE320158 NCOR2抑制MHC I类分子表达以驱动乳腺癌转移进展
• GSE320109 流感诱导的簇状细胞扩增改变了ILC介导的炎症[免疫]
• GSE317520 线粒体DNA突变驱动乳头状甲状腺癌的肿瘤异质性
• GSE315052 非小细胞肺癌 KRAS G12C 突变细胞依赖于 MUC1-C 对 KRAS 抑制剂产生耐药性
• GSE312885 抑制纤毛形成可通过 PI3K-AKT 通路减缓牙龈成纤维细胞衰老和牙龈老化
• GSE311744：人脐静脉内皮细胞与源自GLS1敲低头颈癌细胞的外泌体共培养后转录组变化的RNA测序分析
• GSE308413 超级增强子介导的SMAD3–NR2F2–ID3转录复合物调控非小细胞肺癌中的奥希替尼耐药性
• GSE308412 超级增强子介导的 SMAD3–NR2F2–ID3 转录复合物调控非小细胞肺癌中的奥希替尼耐药性 [CUT&Tag]
• GSE295864 AATF 沉默通过重编程肝细胞癌的微环境抑制肿瘤进展
• GSE328216 NSD2 降解修复 t(4;14) 多发性骨髓瘤中的致癌 cistrome [RNA-seq]
• GSE328215 NSD2 降解修复 t(4;14) 多发性骨髓瘤中的致癌顺式作用 [ATAC-seq]
• GSE315482：小鼠肝脏免疫微环境的单细胞多组学分析揭示了手术应激后中性粒细胞-库普弗细胞通过血小板反应蛋白-1/CD36介导的相互作用
• GSE338785 识别泛素化组蛋白H2A是RSF1驱动的卵巢癌的治疗靶点
• GSE338455 野生型 COS7 细胞和 ATL2/3 双敲除 COS7 细胞的转录组测序。
• GSE338354 PRMT1介导的精氨酸甲基化重定向胰腺癌中SMAD4的促转移转录输出
• GSE334778 RXRα抑制驱动脓毒症中的肝脏代谢和免疫功能障碍：脓毒症犬和非脓毒症犬的差异基因表达
• GSE307964 miR-342 抑制 E2F 信号网络限制三阴性乳腺癌的转移性生长 [RNA-Seq]
• GSE337805 单细胞分析揭示 USH1C 视网膜类器官中 Müller 胶质细胞介导的细胞间通讯受损和光感受器病理
• GSE337595 小鼠青春期后期器官特异性转录和代谢重塑
• GSE336399 非吸烟者鼻上皮癌相关损伤场的特征分析
• GSE334364 空间转录组图谱揭示 FOXO3 介导的线粒体动力学失衡驱动小鼠卵巢早衰
• GSE333995 内皮细胞衍生的IGFBP5通过激活ITGB3/PI3K/AKT轴驱动结直肠癌的血管侵袭和肝转移
• GSE333276 人类诱导多能干细胞和人类肝脏类器官的批量RNA测序分析
• GSE331197 选择性束周损伤的炎症性肌病的空间和细胞类型特异性分子遗传学研究 [RNA]
• GSE330891 选择性束周损伤的炎症性肌病的空间和细胞类型特异性分子遗传学研究。
• GSE329777 KDM3B 抑制通过调节 Shp1 启动子的表观遗传图谱来抑制 SHP1 表达。
• GSE329419 胶质母细胞瘤细胞利用进化适应的细胞代谢来促进其恶性增殖。
• GSE328872 TRI-LC21 和 BEAS-2B 细胞的比较转录组分析，以研究 SMARCA4 缺陷型未分化肿瘤
• GSE328541 大鼠周围神经成纤维细胞来源的细胞外囊泡的 miRNA 测序
• GSE326541 CDO1 是一种可用于区分侵袭性前列腺癌的新型生物标志物
• GSE325427 对人类和小鼠前额叶皮层的整合单核多组学、CUT&Tag 和批量 RNA-seq 分析揭示了皮层发育和 Meis2 功能的基因调控机制
• GSE325077 Glo1通过调节胶质瘤干细胞样细胞中的Sox2转录网络促进胶质瘤进展
• GSE320111 流感诱导的簇状细胞扩增改变了ILC介导的炎症[非免疫]
• GSE316252 重建中枢神经系统微环境信号可部分恢复培养的小鼠原代小胶质细胞的稳态特性
• GSE316250 重建中枢神经系统微环境信号可部分恢复培养的小鼠原代小胶质细胞的稳态特性。
• GSE314891 野生型和Rbm25缺陷型腹膜巨噬细胞感染水疱性口炎病毒（VSV）的RNA测序
• GSE313852 白血病干细胞通过PIEZO1-HIF1A-SLC7A11轴控制胱氨酸摄取来抵抗铁死亡
• GSE313542 PARN 驱动的替代多聚腺苷酸化调节抗体分泌细胞中的免疫球蛋白稳态 [PARN ISO-seq]
• GSE313464 PARN 驱动的替代多聚腺苷酸化调节抗体分泌细胞中的免疫球蛋白稳态 [CRIC-seq]
• GSE313463 PARN 驱动的替代多聚腺苷酸化调节抗体分泌细胞中的免疫球蛋白稳态 [CLIP-seq]
• GSE313461 PARN 驱动的替代多聚腺苷酸化调节抗体分泌细胞中的免疫球蛋白稳态 [2P-seq]
• GSE312680 PARN驱动的替代性多聚腺苷酸化调节抗体分泌细胞中的免疫球蛋白稳态
• GSE310893 颅骨培养的 ctrl 和 TgAPPsweOCN-Cre 成骨细胞的 RNA 测序
• GSE310801 研究通过体外扩增的IL1RAP CAR修饰的TGFβ印迹NK细胞联合IL-15激动剂和抗GD2抗体靶向治疗尤文氏肉瘤
• GSE310452 持续的 A2AR 表达和缺失反而会促进 CD8+ T 细胞耗竭
• GSE309816 受精后7天（dpf）Tg(gnrh3:EGFP)斑马鱼促性腺激素释放激素3（GnRH3）神经元的单核RNA测序
• GSE307245 了解水稻对细菌性穗枯病和夜间高温共同作用的响应
• GSE305841 RNA-seq 检测敲低 RPLP2 和外源补充的原代神经干细胞
• GSE303318 肺癌中细胞外囊泡和其他颗粒的纳米串分析
• GSE302189 一种用于监测药物代谢相关基因表达的液体活检-RNA测序方法：在胆汁淤积性疾病中的概念验证应用
• GSE302138 血浆细胞外囊泡在肺癌转移前微环境形成中的作用
• GSE299706 普通变异型免疫缺陷患者T细胞和单核细胞的转录组调控
• GSE291336 增强肝动脉血流可改善肝移植术后肝细胞簇状硒氨基酸代谢并减轻胆道损伤（130 个字符）
• GSE249850 USP10介导的PFKFB4去泛素化通过激活富马酸/Rad51轴诱导肺癌放射抗性
• GSE230784 CENP-A 在活动诱导的神经元可塑性中的协同作用
• GSE338471 RAD51邻近映射揭示了DNA双链断裂修复过程中同源性搜索的空间限制
• GSE328217 NSD2降解修复t(4;14)多发性骨髓瘤中的致癌顺式作用
• GSE305940 果蝇视觉系统中神经元分化的调控逻辑
• GSE304074 RAD51邻近映射揭示了DNA双链断裂修复过程中同源性搜索的空间限制
• GSE303129 RAD51邻近映射揭示了DNA双链断裂修复过程中同源性搜索的空间限制
• GSE303128 RAD51邻近映射揭示了DNA双链断裂修复过程中同源性搜索的空间限制
• GSE338465 SPOP突变对前列腺癌基因表达的影响
• GSE338388 TGF-β 和 K-975 对 HOVX 人声带成纤维细胞的影响 [RNA-seq]
• [GSE338387 TGF-β 对 HOVX 人声带成纤维细胞中 SMAD2/3 和 YAP/TAZ 的影响 {ChIP-seq]](http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338387)
• GSE319489 组织驻留巨噬细胞对衰老中性粒细胞的清除能力恢复可限制器官衰老
• GSE299376 癫痫发作后 Rrm2 和 Timp3 对神经发生和神经元迁移的调控
• GSE315071 利用大肠杆菌中 CsdA 或 PNPase 交联免疫沉淀法分离 RNA 的高通量测序
• GSE307965 miR-342抑制E2F信号网络限制三阴性乳腺癌的转移性生长
• GSE307720 miR-342 抑制 E2F 信号网络限制三阴性乳腺癌的转移性生长 [HITSCLIP]
• GSE302906 套细胞淋巴瘤中 SOX11 和 SMARCA4 的 CUT&RUN 分析
• GSE278796 果蝇TET过表达导致眼部发育异常，影响视网膜决定和通路调控