详细内容（前10条）

1. ⭐ GSE282203 空间转录组学揭示阿尔茨海默病小鼠模型中大脑节律基因表达的区域性紊乱

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Alon Gelber ; Haylie Romero ; Dominic R Burrows ; Daniel Carlin ; Eran A Mukamel ; Paula A DesplatsSeries Type : OtherOrganism : Mus musculusAlzheimer’s disease (AD) is a progressive neurodegenerative disorder that impairs memory, cognitive function, and the ability to perform everyday activities. In addition to cognitive decline, behavioral disturbances in the sleep-wake cycle such as progressive fragmentation of sleep, decreased total sleep time, and increased confusion or restlessness in the evening (sundowning) are a hallmark of AD. Emerging evidence suggests that these disruptions in sleep and behavior may be underpinned by molecular dysregulation of the circadian clock. Here, we utilize Visium spatial transcriptomics to characterize diurnal transcriptional rhythms across various brain regions in APP23 transgenic mice, a model of AD, and their non-transgenic littermates in 7- and 14-month old mice. We reveal significant alterations in rhythmic gene expression in APP23-TG mice, particularly in the hippocampus and cortex. These changes were evident in 7-month-old animals, coinciding with early amyloid deposition and persisted with advancing pathology. This study offers novel insights into the large-scale dysregulation of rhythmic gene expression in AD, highlighting molecular pathways connected to circadian disruption at various stages of the disease. It underscores the potential role of these disruptions in AD progression and opens new avenues for diagnosis, treatment, and management.
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2. ⭐ GSE317623 AADAT驱动的苹果酸和辅酶Q₁₀代谢调控影响三阴性乳腺癌的免疫逃逸

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、metabolic
• 📝 描述：Contributors : Megha Chatterjee ; Arun SreekumarSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCompared to other subtypes of breast cancer, triple-negative breast cancers (TNBC) have fewer treatment options and exhibit a worse prognosis. Through integrated transcriptomic, metabolomic, immunohistochemical, spatial, and clinical analyses, we identify the mitochondrial enzyme, α-aminoadipate aminotransferase (AADAT) as a previously unrecognized metabolic immune checkpoint in TNBC. AADAT mRNA and protein were significantly upregulated in human TNBC, and high AADAT expression was associated with reduced intra-tumoral CD8⁺ T-cell density and inferior survival. Genetic silencing of AADAT in orthotopic murine TNBC models curtailed primary tumor growth and distant metastasis in a CD8⁺ T-cell–dependent manner, enhanced effector T-cell activation, and sensitized tumors to dual PD-1/CTLA-4 blockade. Mechanistically, unbiased metabolomics showed increased malate levels after AADAT knockdown. Additionally, 4-hydroxyphenylpyruvate, an essential precursor for coenzyme Q₁₀ (CoQ₁₀) biosynthesis, decreased following AADAT knockdown, suggesting an impaired mitochondrial electron transport chain. CoQ₁₀ supplementation restored metabolic balance and reversed malate accumulation caused by AADAT knockdown, indicating that AADAT helps maintain CoQ₁₀-supported redox homeostasis, thereby preventing malate buildup and export. Notably, malate addition directly boosted CD8⁺ T-cell oxidative metabolism, increased the NAD⁺/NADH ratio and reactive oxygen species, and augmented TNF-α and IFN-γ production. In vivo, malate supplementation in drinking water phenocopied AADAT knockdown, restored the response to paclitaxel plus anti–PD-1 therapy in multiple independent syngeneic TNBC models with de novo or acquired resistance to immunotherapy, reduced tumor burden, and prolonged survival. In patient cohorts, higher spatially clustered intra-tumoral malate is associated with co-localization of functional CD8⁺ T cells, decreased exhausted T-cell neighborhoods, and superior post-chemotherapy outcomes. These data position AADAT as a central metabolic orchestrator of immune escape in TNBC and nominate oral malate as a readily translatable adjuvant to reverse chemo-immunotherapy resistance in TNBC.
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3. ⭐ GSE312420 空间转录组学平台性能差异揭示人类炎症性肠病中的 Treg 生物学 [Xenium]

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Yiming Li ; Wenjing Yang ; Hai Wang ; Alan Robinson ; Tianming Yu ; Jenny Y Ding ; Cenfu Wei ; Stephen B Hanauer ; Emanuelle Bellaguarda ; Laura Yun ; Ronen Sumagin ; Guang-Yu Yang ; James D Lewis ; Deyu Fang ; Yingzi Cong ; Yuan Luo ; Parambir S DulaiSeries Type : OtherOrganism : Homo sapiensSpatial transcriptomics is a rapidly growing field with the potential to enhance our ability to uncover novel biology, support drug development, and guide biomarker discovery. However, a biologically validated comparison of leading single-cell-level spatial transcriptomics platforms to guide scientists is lacking in the field. Using intestinal biopsies (n = 40) from patients with inflammatory bowel disease (IBD) of varying disease states and disease locations and non-diseased controls, we systematically compared two imaging based spatial transcriptomics platforms (CosMx and Xenium) to guide translational work for two NIDDK supported IBD consortiums and the Crohn’s and Colitis Foundation Plexus Biorepository. In vitro experiments were conducted to validate key biologic findings. We present a comprehensive data resource of over 1.5 million spatially profiled intestinal cells from healthy and IBD samples. We observed CosMx to have overall better data quality than Xenium in both ulcerative colitis and Crohn’s disease across the full spectrum of commercially available panels. The performance of Xenium, but not CosMx, was significantly influenced by block quality and panel size, with a decline in data quality as the panel size increased. We demonstrate operational feasibility for CosMx in multi-center studies, and CosMx uniquely identified Treg-associated biology in both ulcerative colitis and Crohn’s disease which was validated by in vitro experiments. This study highlights the performance differences between CosMx and Xenium, demonstrating the strengths of CosMx for biology discovery in IBD research. Further studies are needed to explore the broader applicability of CosMx in other gastrointestinal conditions.
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4. ⭐ GSE312415 空间转录组学平台性能差异揭示人类炎症性肠病中的 Treg 生物学 [CosMx]

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Yiming Li ; Wenjing Yang ; Hai Wang ; Alan Robinson ; Tianming Yu ; Jenny Y Ding ; Cenfu Wei ; Stephen B Hanauer ; Emanuelle Bellaguarda ; Laura Yun ; Ronen Sumagin ; Guang-Yu Yang ; James D Lewis ; Deyu Fang ; Yingzi Cong ; Yuan Luo ; Parambir S DulaiSeries Type : OtherOrganism : Homo sapiensSpatial transcriptomics is a rapidly growing field with the potential to enhance our ability to uncover novel biology, support drug development, and guide biomarker discovery. However, a biologically validated comparison of leading single-cell-level spatial transcriptomics platforms to guide scientists is lacking in the field. Using intestinal biopsies (n = 40) from patients with inflammatory bowel disease (IBD) of varying disease states and disease locations and non-diseased controls, we systematically compared two imaging based spatial transcriptomics platforms (CosMx and Xenium) to guide translational work for two NIDDK supported IBD consortiums and the Crohn’s and Colitis Foundation Plexus Biorepository. In vitro experiments were conducted to validate key biologic findings. We present a comprehensive data resource of over 1.5 million spatially profiled intestinal cells from healthy and IBD samples. We observed CosMx to have overall better data quality than Xenium in both ulcerative colitis and Crohn’s disease across the full spectrum of commercially available panels. The performance of Xenium, but not CosMx, was significantly influenced by block quality and panel size, with a decline in data quality as the panel size increased. We demonstrate operational feasibility for CosMx in multi-center studies, and CosMx uniquely identified Treg-associated biology in both ulcerative colitis and Crohn’s disease which was validated by in vitro experiments. This study highlights the performance differences between CosMx and Xenium, demonstrating the strengths of CosMx for biology discovery in IBD research. Further studies are needed to explore the broader applicability of CosMx in other gastrointestinal conditions.
• 🔗 查看原文

5. ⭐ GSE317338 EBV 感染结果由单核细胞和 Treg 驱动的免疫动力学在体外 PBMC 模型中决定 [RNA-Seq Mock]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、monocyte、RNA-seq
• 📝 描述：Contributors : Leena Yoon ; Lauren N MacMullen ; Leonardo J Muñoz ; Alina Gu ; Jamie Bregman ; Mary S Campion ; Avi Srivastava ; Rena R Xian ; Richard F Ambinder ; Andrew Kossenkov ; Samantha S Soldan ; Paul M LiebermanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEpstein-Barr virus (EBV) infects >95% of the adult population with diverse outcomes ranging from benign latency to cancers and autoimmune diseases. Immunological control of EBV infection is known to be an important determinant of EBV infection outcomes. However, species-specific viral tropism and limited infection models have impeded mechanistic insights into early host–immune control of EBV infection. Here, we use ex vivo infection of peripheral blood mononuclear cells (PBMCs), rather than routinely used B cell enriched culture systems, to study immune and viral dynamics during primary EBV infection. We combined bulk RNA sequencing, EBV transcript enrichment, and flow cytometry to characterize cellular responses across Days 1, 7–8, and 14 post-infection. Early infection triggered a monocyte-specific antiviral response marked by changes in the expression of genes associated with lipid metabolism (LIPA, lysosomal acid lipase) and chemotaxis (CCR1 and CCR2). Inhibitors of LIPA increased EBV titers during primary infection, indicating that LIPA is part of an early monocyte-driven antiviral response. At later timepoints post-infection, donor-dependent variability in lymphoblastoid cell line (LCL) outgrowth was associated with divergent immune states. Donors that failed to generate LCLs demonstrated increased frequencies of CD8+ T cells and reduced numbers of regulatory T cells (CD4⁺CD25⁺FOXP3⁺). EBV transcriptomics revealed that LCL-failed donors exhibited elevated early lytic gene expression but did not establish a type III latency program. Our findings suggest that individual variations in immune cell composition and gene expression may account for differences in the immune response to EBV. These findings define temporal immune and viral signatures that predict transformation outcome and highlight intact PBMCs as a tractable model to study EBV pathogenesis in a genetically diverse, human-specific context.
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6. ⭐ GSE317329 EBV 感染结果由单核细胞和 Treg 驱动的免疫动力学在体外 PBMC 模型中决定 [RNA-Seq EBV 富集]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、monocyte、RNA-seq
• 📝 描述：Contributors : Leena Yoon ; Lauren N MacMullen ; Leonardo J Muñoz ; Alina Gu ; Jamie Bregman ; Mary S Campion ; Avi Srivastava ; Rena R Xian ; Richard F Ambinder ; Andrew Kossenkov ; Samantha S Soldan ; Paul M LiebermanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEpstein-Barr virus (EBV) infects >95% of the adult population with diverse outcomes ranging from benign latency to cancers and autoimmune diseases. Immunological control of EBV infection is known to be an important determinant of EBV infection outcomes. However, species-specific viral tropism and limited infection models have impeded mechanistic insights into early host–immune control of EBV infection. Here, we use ex vivo infection of peripheral blood mononuclear cells (PBMCs), rather than routinely used B cell enriched culture systems, to study immune and viral dynamics during primary EBV infection. We combined bulk RNA sequencing, EBV transcript enrichment, and flow cytometry to characterize cellular responses across Days 1, 7–8, and 14 post-infection. Early infection triggered a monocyte-specific antiviral response marked by changes in the expression of genes associated with lipid metabolism (LIPA, lysosomal acid lipase) and chemotaxis (CCR1 and CCR2). Inhibitors of LIPA increased EBV titers during primary infection, indicating that LIPA is part of an early monocyte-driven antiviral response. At later timepoints post-infection, donor-dependent variability in lymphoblastoid cell line (LCL) outgrowth was associated with divergent immune states. Donors that failed to generate LCLs demonstrated increased frequencies of CD8+ T cells and reduced numbers of regulatory T cells (CD4⁺CD25⁺FOXP3⁺). EBV transcriptomics revealed that LCL-failed donors exhibited elevated early lytic gene expression but did not establish a type III latency program. Our findings suggest that individual variations in immune cell composition and gene expression may account for differences in the immune response to EBV. These findings define temporal immune and viral signatures that predict transformation outcome and highlight intact PBMCs as a tractable model to study EBV pathogenesis in a genetically diverse, human-specific context.
• 🔗 查看原文

7. ⭐ GSE314519 破坏 SOX2 自缔合和凝聚体以克服肺鳞状细胞癌的化疗药物耐药性 [RNA-Seq, 2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、resistance、RNA-seq
• 📝 描述：Contributors : Juehan Wang ; Yulin Wen ; Sainan Huang ; Yanjiang Liu ; Hongjie YaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy remains one of the most important treatments for lung squamous cell carcinoma (LSCC), yet overcoming chemotherapeutic drug resistance poses a significant challenge. The high frequency of SOX2 copy number amplification observed in LSCC patients underscores its potential role as a regulator in this context. Our investigation reveals a strong correlation between SOX2 amplification and expression levels in LSCC patients. Notably, overexpression of SOX2 confers resistance to chemotherapeutic drugs in LSCC cell lines. We elucidate that SOX2 undergoes phase separation, forming condensates that sequester chemotherapeutic agents used in LSCC treatment, thereby exacerbating chemotherapeutic drug resistance in LSCC cells. To address this, we design a small peptide containing 16 amino acids conjugated with 8 arginine, specifically targeting α-helix within HMG domain to disrupt SOX2 self-association. Our data demonstrate that this peptide effectively prevents SOX2 droplet formation, consequently reversing chemotherapy tolerance in LSCC without compromising SOX2 transcriptional activity. Collectively, our findings unveil a novel mechanism of chemotherapy resistance in LSCC mediated by SOX2 phase separation and propose a promising peptide-based therapeutic strategy to combat chemoresistance in LSCC.
• 🔗 查看原文

8. ⭐ GSE289045 破坏 SOX2 自缔合和凝聚体以克服肺鳞状细胞癌的化疗药物耐药性 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、resistance、RNA-seq
• 📝 描述：Contributors : Juehan Wang ; Yulin Wen ; Sainan Huang ; Yanjiang Liu ; Hongjie YaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy remains one of the most important treatments for lung squamous cell carcinoma (LSCC), yet overcoming chemotherapeutic drug resistance poses a significant challenge. The high frequency of SOX2 copy number amplification observed in LSCC patients underscores its potential role as a regulator in this context. Our investigation reveals a strong correlation between SOX2 amplification and expression levels in LSCC patients. Notably, overexpression of SOX2 confers resistance to chemotherapeutic drugs in LSCC cell lines. We elucidate that SOX2 undergoes phase separation, forming condensates that sequester chemotherapeutic agents used in LSCC treatment, thereby exacerbating chemotherapeutic drug resistance in LSCC cells. To address this, we design a small peptide containing 16 amino acids conjugated with 8 arginine, specifically targeting α-helix within HMG domain to disrupt SOX2 self-association. Our data demonstrate that this peptide effectively prevents SOX2 droplet formation, consequently reversing chemotherapy tolerance in LSCC without compromising SOX2 transcriptional activity. Collectively, our findings unveil a novel mechanism of chemotherapy resistance in LSCC mediated by SOX2 phase separation and propose a promising peptide-based therapeutic strategy to combat chemoresistance in LSCC.
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9. GSE324653 HIV-1 通过 H4K5 组蛋白乙酰化增强人星状细胞对革兰氏阳性微生物产物的 IL-8 反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:micro(b|be|bial|organism)、histone
• 📝 描述：Contributors : Lumin Zhang ; Rabab O Ali ; Naichaya Chamroonkul ; Parissa Tabrizia ; Myron Schwart ; Ganesh Gunasekaran ; Maria Isabel Fiel ; Thomas Schiano ; Steven C Ward ; Meena B BansalSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Homo sapiensPatients living with Human Immunodeficiency Virus (PLWH) develop accelerated liver fibrosis, but the exact mechanism remains unknown. Unlike gram-negative bacterial products, the impact of gram-positive microbial products in Human Immunodeficiency Virus 1 (HIV-1) associated liver inflammation and fibrosis remains poorly understood. In this study, we investigated the effect of lipoteichoic acid (LTA), a major gram-positive bacterial component, on HSCs in the context of HIV-1 infection. Our data revealed that HIV-1 infection sensitizes HSCs to LTA stimulation, leading to an amplified IL-8 response mediated through histone acetylation that may accelerate liver fibrosis progression in PLWH. As microbial translocation persists despite effective antiretroviral therapy, these findings underscore the need for targeted strategies to mitigate liver fibrosis in HIV-1 infected patients.
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10. GSE324781 亲代 U2OS 细胞中 MYC 的 ChIP-Seq 及参考外源基因组 (ChIP-Rx)

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Sihan Li ; Zehua Wang ; Da YangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensEmerging evidence suggests that MYC binds RNAs, but its functional consequences remain unclear. Here, we integrate multi-omics data and reveal that MYC broadly binds enhancer RNAs (eRNAs), which exhibit high cancer- and tissue-specific expression in cancer cell lines and patient tumors. Moreover, we developed a computational pipeline to identify potential cis-regulatory MYC-eRNA target genes, with most predicted eRNA-target pairs supported by RNA polymerase II-mediated chromatin interaction data. Among these, we functionally characterized MERG1 as an oncogenic eRNA that promotes breast cancer tumorigenesis. Mechanistically, MERG1 interacts with MYC to enhance its occupancy at the GREB1 promoter, driving chromatin remodeling and epigenetic activation. This process specifically amplifies GREB1 expression and promotes tumor progression. Finally, nanoparticle-mediated delivery of antisense oligonucleotides targeting MERG1 suppresses MYC-mediated breast cancer growth. These results advance our understanding of the enhancer-driven regulation of gene expression and tumorigenesis and provide insights into the regulatory landscape of MYC in cancer.
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1. ⭐ 产生血清素的肠道细菌可能是治疗肠易激综合征的关键。

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Researchers have identified two gut bacteria that can produce serotonin, a key chemical that regulates bowel movements. In experiments with mice lacking serotonin, the microbes boosted serotonin levels, increased nerve cells in the colon, and normalized intestinal movement. The study also found that people with IBS have lower levels of one of these bacteria. The discovery suggests gut microbes could become a powerful new target for treating digestive disorders.
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2. 利用GPU在几秒钟内完成RNA测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：A new GPU implementation of kallisto enables RNA sequencing analysis in seconds, accelerating transcript quantification and dramatically reducing computation time for large transcriptomic datasets.
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3. 研究顾问 – 计算RNA基因组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：genomics
• 📝 描述：A Lilly Research Advisor position highlights the growing importance of RNA sequencing and bioinformatics for analyzing transcriptome data and advancing genetic medicine programs and therapeutic development…
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4. 重症新冠肺炎或流感可能会在数年后增加患肺癌的风险。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A severe case of COVID-19 or influenza could increase the risk of lung cancer later on, according to new research. Scientists discovered that serious viral infections can alter immune cells in the lungs, leaving behind chronic inflammation that may help tumors develop months or years later. The increased risk was seen mainly after severe infections that required hospitalization. Vaccination, however, appears to prevent the dangerous lung changes.
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5. 研究发现，两种类型的结肠息肉可使肠癌风险增加五倍。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers studying over 8,400 colonoscopies discovered that having both adenomas and serrated polyps in the bowel can raise the risk of serious precancerous changes by up to five times. These two polyp types may represent separate cancer pathways that can occur at the same time. Nearly half of patients with serrated polyps also had adenomas, making this high-risk combination more common than expected. The results emphasize the importance of early detection and regular colonoscopy monitoring.
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6. 微塑料可能正在悄无声息地损害你的大脑，并加剧阿尔茨海默病和帕金森病的发生。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Tiny plastic particles may be quietly threatening brain health. New research suggests microplastics—now widely found in food, water, and even household dust—could trigger inflammation and damage in the brain through multiple biological pathways. Scientists estimate adults may consume about 250 grams of these particles each year, and some can accumulate in organs including the brain.
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• GSE303826 基于液体活检的甲基化生物标志物的鉴定和验证：生殖细胞肿瘤亚型特异性研究[7]
• GSE303825 基于液体活检的甲基化生物标志物的鉴定和验证：生殖细胞肿瘤亚型特异性研究[3]
• GSE303824 基于液体活检的甲基化生物标志物的鉴定和验证：生殖细胞肿瘤亚型特异性研究[2]
• GSE324324 来自野生稻（Oryza rufipogon L.）的11号染色体上一个结构动态的基因位点赋予其对细菌性枯萎病的广谱隐性抗性
• GSE314516 破坏 SOX2 自缔合和凝聚体以克服肺鳞状细胞癌的化疗耐药性 [Cut & Run, 2]
• GSE289048 通过破坏 SOX2 自缔合和凝聚体来克服肺鳞状细胞癌的化疗耐药性
• GSE289046 破坏 SOX2 自缔合和凝聚体以克服肺鳞状细胞癌的化疗耐药性 [CUT&Run]
• GSE315060 神经发育障碍小鼠模型中的母胎免疫冲突。
• GSE313719 GFI1 调节 NK 细胞的成熟和功能 [scMultiome-seq]。
• GSE311364 基于 CRISPR 的基因激活的 gRNA 的错配容忍度赋予了广泛的活性，这对细胞重编程至关重要 [RNA-Seq]
• GSE307214 多柔比星对人类心脏电生理的年龄和性别特异性调节。
• GSE263671 基质细胞-肥大细胞通讯协调脑膜中的抗病毒免疫
• GSE307271 谷氨酰胺缺乏触发 TRIB3 依赖的 G4-DNA 解离以维持 DNA 修复和肿瘤存活 [TRIB3]
• GSE307270 谷氨酰胺缺乏触发 TRIB3 依赖的 G4-DNA 解离以维持 DNA 修复和肿瘤存活 [谷氨酰胺缺乏]
• GSE306768 谷氨酰胺缺乏触发 TRIB3 依赖的 G4-DNA 解离以维持 DNA 修复和肿瘤存活 [CUT&Tag]
• GSE303531 CHI3L1 促进高侵袭性脑转移瘤中免疫抑制的肿瘤微环境
• GSE303360 TET3 介导的 DNA 去甲基化促进番茄中稳定表观等位基因的形成 [RNA-seq]
• GSE302679 果蝇三龄幼虫，全身单核转录组分辨率
• GSE324335 多组学表征鼻上皮细胞中SIRT3代谢及其对β-淀粉样蛋白寡聚体的适应性
• GSE292031 Senataxin促进抗原受体基因多样化过程中的重组保真度
• GSE292003 靶向抑制从头脂肪生成诱导癌细胞衰老