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1. ⭐ 最新14+生信，通过单细胞分析识别HLA-DR +肿瘤细胞，并分析其对 CD8+T 细胞及预后的影响，思路新颖！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、T细胞、单细胞、生信、通路
• 📝 描述：点击查看详情
• 🔗 查看原文

2. ⭐ 最新14+热点好文，巨噬细胞胞葬驱动多胺代谢增强化疗后癌干细胞富集及耐药！生信发现现象，实验解释现象，探索机制！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：巨噬细胞、代谢、耐药、生信、富集
• 📝 描述：点击查看详情
• 🔗 查看原文

3. ⭐ 转录组学的生物信息学视角：批量与单细胞 RNA 测序分析的全面综述

• ✍️ 作者：BMELab
• 🏷️ 关键词：测序、单细胞、转录组、生物信息、生信
• 📝 描述：转录组学的生物信息学视角：批量与单细胞 RNA 测序分析的全面综述
• 🔗 查看原文

4. ⭐ 最新14+生信，单细胞识别MARCO+巨噬细胞抑制CD8T，阻断MARCO增强免疫治疗疗效。干湿结合经典高分思路！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、巨噬细胞、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

5. ⭐ 最新14+生信，单细胞识别PLAUR+中性粒细胞塑造免疫抑制微环境，抑制PLAUR 增强抗 PD1 疗效。高分文章经典思路！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、免疫微环境、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

6. ⭐ Redox Biology双区TOP！巨噬细胞×衰老×胞葬作用的新机制，值得一学

• ✍️ 作者：同医济云Medfocus
• 🏷️ 关键词：衰老、T细胞、B细胞、巨噬细胞
• 📝 描述：南通大学崔志明/钱湛瑒团队近期在《Redox Biology》发表研究，首次证实：巨噬细胞因过度吞噬髓鞘碎片而提前衰老，是脊髓损伤后修复受阻的关键。
• 🔗 查看原文

7. ⭐ 最新14+干湿结合SCI，作者鉴定出干扰素诱导的衰老 CD8T 细胞并揭示其对免疫治疗的影响。衰老虽老，但是真的火！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、衰老、T细胞
• 📝 描述：点击查看详情
• 🔗 查看原文

8. ⭐ DMF释放mtDNA，激活cGAS-STING通路增强抗肿瘤免疫

• ✍️ 作者：同医济云Medfocus
• 🏷️ 关键词：肿瘤、免疫、通路
• 📝 描述：揭示“线粒体-cGAS-STING”轴在DMF抗肿瘤免疫中的核心地位。
• 🔗 查看原文

9. ⭐ 重磅研究！首次系统揭示三级淋巴结构在胃癌免疫微环境中的关键作用，开发创新工具精准预测免疫治疗反应

• ✍️ 作者：转化医学网
• 🏷️ 关键词：免疫、免疫微环境、淋巴
• 📝 描述：通过单细胞和空间转录组技术，首次系统揭示了三级淋巴结构在胃癌免疫微环境中的关键作用。
• 🔗 查看原文

10. ⭐ 【转化医学研究专场】单细胞测序入门大讲堂：助您锁定新靶点、破解耐药性、揭示毒性机制！

• ✍️ 作者：10x Genomics
• 🏷️ 关键词：耐药、测序、单细胞
• 📝 描述：直播时间：12月10日&11日｜下午 2:00-3:00
• 🔗 查看原文

💡 该来源还有 28 条内容，详见 文末

详细内容（前10条）

1. ⭐ GSE275681 MHC II 限制性新抗原疫苗逆转免疫微环境并克服冷肿瘤对免疫检查点抑制剂的耐药性。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、vaccine、MHC、resistance
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

2. ⭐ GSE282415 餐后全身代谢变化对 T 细胞免疫产生持久影响 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell、metabolism、ATAC-seq
• 📝 描述：Contributors : Alok Kumar ; Greg M Delgoffe ; Isha MehtaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusSystemic nutrient availability waxes and wanes with dietary input. Here we show that short periods of fasting and refeeding have long-lasting effects on T cell immunity. Human or murine T cells from fed hosts have higher metabolic capacity than those from fasted hosts ex vivo and show better/superior metabolic phenotype and immune response/functions in vitro and in vivo settings of virus infection or tumor model. Serum or chylomicrons enriched from lymphatics of fed mice restores the metabolic and immune functions of fasted T cells. Fed T cells had heightened mTORC1-dependent translation of key immunologic and metabolic genes independent of their epigenetic and transcriptional status. mTORC1 inhibition during the fed period mitigates the postprandial benefit of fed T cells over fasted cells. Our data highlight the need to consider diet content and timing as key factors in immune cell analysis, vaccination strategies, and the generation of cellular therapies.
• 🔗 查看原文

3. ⭐ GSE282410 餐后全身代谢变化对 T 细胞免疫产生持久影响 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell、metabolism、RNA-seq
• 📝 描述：Contributors : Alok Kumar ; Greg M Delgoffe ; Isha MehtaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSystemic nutrient availability waxes and wanes with dietary input. Here we show that short periods of fasting and refeeding have long-lasting effects on T cell immunity. Human or murine T cells from fed hosts have higher metabolic capacity than those from fasted hosts ex vivo and show better/superior metabolic phenotype and immune response/functions in vitro and in vivo settings of virus infection or tumor model. Serum or chylomicrons enriched from lymphatics of fed mice restores the metabolic and immune functions of fasted T cells. Fed T cells had heightened mTORC1-dependent translation of key immunologic and metabolic genes independent of their epigenetic and transcriptional status. mTORC1 inhibition during the fed period mitigates the postprandial benefit of fed T cells over fasted cells. Our data highlight the need to consider diet content and timing as key factors in immune cell analysis, vaccination strategies, and the generation of cellular therapies.
• 🔗 查看原文

4. ⭐ GSE254001 NFATc1 和 NFATc2 通过调节胆固醇生物合成和 WNT/β-catenin 通路控制儿童 T 细胞急性淋巴细胞白血病中的糖皮质激素抵抗

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、pathway
• 📝 描述：Series Type : Expression profiling by arrayOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

5. ⭐ GSE253999 NFATc1 和 NFATc2 通过调节胆固醇生物合成和 WNT/β-catenin 通路来调控儿童 T 细胞急性淋巴细胞白血病中的糖皮质激素抵抗

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、pathway
• 📝 描述：Contributors : Silvia Bresolin ; Valentina SerafinSeries Type : Expression profiling by arrayOrganism : Homo sapienshe glucocorticoid (GC) resistance onset in pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients remains one of the biggest challenges in current cancer treatment. The mechanisms driving this resistance are still not fully understood, making it difficult to predict patient outcomes and to develop effective therapies. Our study uncovered critical insights into the biological processes underlying GC resistance, offering potential breakthroughs for future treatments. Building on our previous research on LCK kinase hyperactivation in GC-resistant T-ALL patients, we have now delved deeper into the LCK downstream NFAT transcription factor family’s contribution to GC resistance. We discovered that, even at the time of diagnosis, GC resistant T-ALL patients exhibit an intrinsic low glucocorticoid receptor (GR) activity coupled with high NFATc1 and NFATc2 ones. This dysregulation creates a roadblock to effective GC therapy. Indeed, in the absence of either NFATc1 or NFATc2, the normal transcriptional activity of GR is restored, re-sensitizing the leukemia cells to dexamethasone treatment both in vitro and in vivo. This suggests that NFATc1 and NFATc2 are central to driving GC resistance, as they directly regulate crucial pathways like cholesterol biosynthesis and WNT/β-catenin signaling. The identification of NFAT transcription factors as key players in leukemia therapy resistance offers a promising target for future therapeutic strategies, potentially transforming the way we approach treatment for these challenging conditions or autoimmune disorders where glucocorticoids are a cornerstone of treatment.
• 🔗 查看原文

6. ⭐ GSE253998 NFATc1 和 NFATc2 通过调节胆固醇生物合成和 WNT/β-catenin 通路来调控儿童 T 细胞急性淋巴细胞白血病中的糖皮质激素抵抗

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、pathway
• 📝 描述：Contributors : Silvia Bresolin ; Valentina SerafinSeries Type : Expression profiling by arrayOrganism : Homo sapiensThe glucocorticoid (GC) resistance onset in pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients remains one of the biggest challenges in current cancer treatment. The mechanisms driving this resistance are still not fully understood, making it difficult to predict patient outcomes and to develop effective therapies. Our study uncovered critical insights into the biological processes underlying GC resistance, offering potential breakthroughs for future treatments. Building on our previous research on LCK kinase hyperactivation in GC-resistant T-ALL patients, we have now delved deeper into the LCK downstream NFAT transcription factor family’s contribution to GC resistance. We discovered that, even at the time of diagnosis, GC resistant T-ALL patients exhibit an intrinsic low glucocorticoid receptor (GR) activity coupled with high NFATc1 and NFATc2 ones. This dysregulation creates a roadblock to effective GC therapy. Indeed, in the absence of either NFATc1 or NFATc2, the normal transcriptional activity of GR is restored, re-sensitizing the leukemia cells to dexamethasone treatment both in vitro and in vivo. This suggests that NFATc1 and NFATc2 are central to driving GC resistance, as they directly regulate crucial pathways like cholesterol biosynthesis and WNT/β-catenin signaling. The identification of NFAT transcription factors as key players in leukemia therapy resistance offers a promising target for future therapeutic strategies, potentially transforming the way we approach treatment for these challenging conditions or autoimmune disorders where glucocorticoids are a cornerstone of treatment.
• 🔗 查看原文

7. ⭐ GSE253996 研究发现，NFATc1 和 NFATc2 通过调节胆固醇生物合成和 WNT/β-catenin 通路来调控儿童 T 细胞急性淋巴细胞白血病中的糖皮质激素抵抗。

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、pathway
• 📝 描述：Contributors : Silvia Bresolin ; Valentina SerafinSeries Type : Expression profiling by arrayOrganism : Homo sapiensThe glucocorticoid (GC) resistance onset in pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients remains one of the biggest challenges in current cancer treatment. The mechanisms driving this resistance are still not fully understood, making it difficult to predict patient outcomes and to develop effective therapies. Our study uncovered critical insights into the biological processes underlying GC resistance, offering potential breakthroughs for future treatments. Building on our previous research on LCK kinase hyperactivation in GC-resistant T-ALL patients, we have now delved deeper into the LCK downstream NFAT transcription factor family’s contribution to GC resistance. We discovered that, even at the time of diagnosis, GC resistant T-ALL patients exhibit an intrinsic low glucocorticoid receptor (GR) activity coupled with high NFATc1 and NFATc2 ones. This dysregulation creates a roadblock to effective GC therapy. Indeed, in the absence of either NFATc1 or NFATc2, the normal transcriptional activity of GR is restored, re-sensitizing the leukemia cells to dexamethasone treatment both in vitro and in vivo. This suggests that NFATc1 and NFATc2 are central to driving GC resistance, as they directly regulate crucial pathways like cholesterol biosynthesis and WNT/β-catenin signaling. The identification of NFAT transcription factors as key players in leukemia therapy resistance offers a promising target for future therapeutic strategies, potentially transforming the way we approach treatment for these challenging conditions or autoimmune disorders where glucocorticoids are a cornerstone of treatment.
• 🔗 查看原文

8. GSE287189：年轻和年老塞莱黑羊卵巢中m6A甲基化和转录组谱差异的综合分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：transcriptome、methylation
• 📝 描述：Contributors : Linlin Pei ; Chunjie LiuSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Ovis ariesOvarian aging results in follicular failure and atresia, leading to a decline in both the quantity and quality of oocytes. N6-methyladenosine (m6A) has been demonstrated to play a regulatory role in the reproductive functions of female animals; however, the regulatory mechanisms of m6A in the ovaries of sheep remain unclear. In the present study, ovarian tissues from 1~2 year-old and 5~6 year-old Cele black sheep were collected and analyzed using MeRIP-seq and RNA-seq sequencing. A total of 109 differentially methylated genes were identified, including 7 genes that were up-regulated in both methylation and mRNA expression, 55 genes that were up-regulated in methylation while down-regulated in mRNA expression, and 33 genes that were down-regulated in both methylation and mRNA expression. Additionally, 14 genes exhibited down-regulation in methylation and up-regulation in mRNA expression. Differential methylation peaks (DMPs) were found to be significantly enriched in the BMP signaling pathway, uterine embryonic development, histone acetyltransferase activity, and VEGF signaling pathway by GO and KEGG enrichment analysis. Differentially expressed genes (DEGs) were significantly enriched in negative regulation of the I-kappaB kinase/NF-kappaB signalling pathway, positive regulation of leukocyte adhesion to vascular endothelial cells, histone methyltransferase binding, transcriptional co-repressor activity, and cellular senescence. The results suggest that differentially expressed genes may influence various biological functions, including transcription, translation, aging, development, regeneration, and immune responses in the ovary of sheep. In this study, we constructed the first comprehensive whole transcriptome analysis map of the sheep ovary, which provides a theoretical foundation for investigating the transcriptional regulation mechanisms of m6A modification in the ovary.
• 🔗 查看原文

9. GSE272644 BRCA1 突变和表观突变携带者的血细胞全基因组甲基化谱、乳腺癌诊断前既无 BRCA1 突变也无表观突变的女性以及既无 BRCA1 突变也无表观突变的健康女性（对照组）

• ✍️ 作者：未知作者
• 🏷️ 关键词：genome、methylation
• 📝 描述：Contributors : Katarzyna E Sokolowska ; Jacek Antoniewski ; Marta Sobalska-Kwapis ; Dominik Strapagiel ; Jan Lubiński ; Tomasz Huzarski ; Tomasz K WojdaczSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensGenome-wide DNA methylation patterns were quantified in peripheral blood samples collected from 112 individuals (with determined BRCA1 mutation and epimutation status) using the Illumina Infinium HumanMethylationEPIC BeadChip
• 🔗 查看原文

10. GSE272599 使用TIGER对Recql4 -/- Klhdc3 -/- 与对照组进行全基因组测序（三重复），分析其复制时间。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、genome
• 📝 描述：Contributors : M F Smeets ; P A Buco ; A Koren ; A M Chalk ; C R WalkleySeries Type : OtherOrganism : Mus musculusAbstract TBC
• 🔗 查看原文

💡 该来源还有 34 条内容，详见 文末

详细内容（全部2条）

1. 晚期宫颈癌中，一线降级化疗加彭普利单抗和安洛替尼反应的分子和免疫相关性

• ✍️ 作者：未知作者
• 🏷️ 关键词：免疫
• 📝 描述：Secret hovertext: 晚期宫颈癌的标准护理包括化疗、抗血管生成和/或免疫检查点阻滞方案。虽然有效，但会导致多效性副作用。降级化疗结合免疫靶向疗法已被证明在其他癌症中有效且毒性较低。本研究中，我们进行了一项多中心、单臂、二期临床研究，针对一线降级铂类化疗加安洛替尼和彭普利单抗，随后仅用安洛替尼和彭普利单抗维持治疗治疗，治疗 PD-L1 阳性、持续性、复发或转移性宫颈癌患者。在 32 例有效性评估患者中，30 例（93.8%，95%置信区间：79.2%至 99.2%）获得研究者确认的客观反应。单核 RNA 测序暗示肿瘤浸润 T 细胞和活化生殖中心 B 细胞的趋化性和增殖活性增强，预示着最佳治疗反应。TLS 与肿瘤面积比较高的患者存活率较高。我们的发现为一线降级化疗加安洛替尼和彭普利单抗在转移性、持续性或复发性宫颈癌患者中的可行性奠定了基础。
• 🔗 查看原文

2. 对 CIC：:D UX4 肉瘤的建模揭示了癌基因介导的 MHCI 依赖免疫逃脱。

• ✍️ 作者：未知作者
• 🏷️ 关键词：免疫
• 📝 描述：Secret hovertext: CIC：:D UX4 肉瘤（CDS）是一种高度侵袭性的恶性肿瘤，治疗选择有限。本文介绍了一个可诱导多西环素的 CIC：:D UX4 嵌合小鼠模型及其衍生的癌症系 imChCDS，忠实地重现了人类 CDS 的分子、组织学和免疫学特征。我们证明仅 CIC：:D UX4 表达就足以驱动软结缔组织允许谱系的肿瘤发生。imChCDS 细胞系保留了其间充质细胞起源的转录足迹，在免疫功能正常的宿主中发生转移性肿瘤，并明显依赖 P300/CBP 转录共激活因子。值得注意的是，我们发现 CIC：:D UX4/P300/CBP 介导的 MHC I 类（MHCI）抑制是 CDS 免疫逃避的关键机制。CIC：:D UX4 的遗传失活或 P300/CBP 的药物抑制可诱导癌细胞周期停止，恢复 MHCI 表达，并触发强健的抗肿瘤免疫反应，从而将免疫学上“冷”的 CDS 微环境转变为“热”环境，推动肿瘤退缩。这些模型共
• 🔗 查看原文

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1. 一项历时二十年的研究表明，更清洁的水能大幅降低癌症和心脏病死亡率。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A 20-year project in Bangladesh reveals that lowering arsenic levels in drinking water can slash death rates from major chronic diseases. Participants who switched to safer wells had the same risk levels as people who were never heavily exposed. The researchers tracked individual water exposure with detailed urine testing. Their results show how quickly health improves once contaminated water is replaced.
• 🔗 查看原文

2. 你的身体可能已经存在一种有助于对抗阿尔茨海默病的分子。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Spermine, a small but powerful molecule in the body, helps neutralize harmful protein accumulations linked to Alzheimer’s and Parkinson’s. It encourages these misfolded proteins to gather into manageable clumps that cells can more efficiently dispose of through autophagy. Experiments in nematodes show that spermine also enhances longevity and cellular energy production. These insights open the door to targeted therapies powered by polyamines and advanced AI-driven molecular design.
• 🔗 查看原文

3. 纳米花增强干细胞活力，从而修复衰老细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Texas A&M researchers found a way to make stem cells produce double the normal number of mitochondria using nanoflower particles. These energized stem cells then transfer their surplus “power packs” to weakened cells, reviving their energy production and resilience. The method bypasses many limitations of current mitochondrial therapies and could offer long-lasting effects. It may open the door to treatments for aging tissues and multiple degenerative diseases.
• 🔗 查看原文

4. 这种微小的微生物或许是战胜永久性化学物质的关键。

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:micro(b|be|bial|organism)
• 📝 描述：A photosynthetic bacterium shows a surprising ability to absorb persistent PFAS chemicals, offering a glimpse into biological tools that might one day tackle toxic contamination. Researchers are now exploring genetic and synthetic biology approaches to enhance these early signs of PFAS-handling potential.
• 🔗 查看原文

• 肿瘤免疫 | TrendsCancer | 蛋白酶对肿瘤-免疫细胞共生关系的调控
• 基因组 | Nature | 通过体细胞表突变的克隆追踪揭示血液衰老的动态变化
• 最新Cancer Cell重磅，胰腺癌中首次证实神经元与癌细胞间存在 “神经元-癌细胞假性突触”，并形成正反馈增强肿瘤神经浸润！
• PDX小鼠DNA测序比对到人类或者小鼠参考基因组（你以为的比对并不是真正的比对）
• 《自然》：教科书又得改了！科学家首次发现，抑制T细胞抗癌活性的PD-1，竟然还是T细胞的保护伞，可以防止淋巴结内T细胞耗竭或死亡
• Cell Res | 林圣彩等团队发现通过代谢调控来调动体内固有免疫力，使肝癌小鼠实现寿终正寝——“代谢性免疫治疗”
• Science破题：这一分子决定肿瘤免疫能否真正被激活
• 戴磊团队CHOM：基于蛋白结构检索的人体肠道微生物组功能研究新范式 | Cell Press对话科学家
• 当导师只给我一个单细胞测序数据，我是怎么设计4个课题的1——如何挑选细胞群
• 话进七 | 从小用Windows，终于开始做生信
• 乙醇酸代谢途径（建议收藏）
• 还在苦苦比对微生物序列？Kraken2轻松实现超快速的微生物组分类，数据处理效率翻倍！
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• GSE306804 产后母体血液中细菌的快速清除，适用于胎膜早破并发妊娠的情况。
• GSE311151 脑癌患者体内代谢通量估算的数字孪生模型
• GSE310554 配对血管-实质单核测序揭示阿尔茨海默病中内皮-间质转化紊乱
• GSE298006 阶段特异性表观遗传启动在谱系决定过程中增强基因激活 [RNA-Seq]
• GSE298001 阶段特异性表观遗传启动在谱系决定过程中增强基因激活 [ATAC-Seq]
• GSE295550 染色质可及性和基因表达动态表明维生素 D3 在体内具有免疫调节作用 [ATAC-seq]
• GSE295549 染色质可及性和基因表达动态揭示维生素 D3 在体内的免疫调节作用 [RNA-Seq]
• GSE286942 DOT1L抑制剂通过激活乳腺癌细胞中的干扰素信号通路发挥抗肿瘤作用
• GSE235046 先天免疫和代谢信号将受损线粒体滞留在细胞膜上以进行线粒体氧化损伤
• GSE221564 肿瘤细胞内在RIG-I激活足以驱动免疫介导的肿瘤排斥
• GSE302831 通过RNA测序鉴定银屑病中差异表达基因
• GSE292493 C-C趋化因子受体4的基因缺陷可保护小鼠免受血管紧张素II诱导的腹主动脉瘤形成
• GSE291310 L-苯丙氨酸对Th2细胞的代谢调控
• GSE288012 全基因组筛选鉴定出 Runx2 是造血干细胞扩增和 T 细胞分化的新型调控因子
• GSE285478 外泌体 CLOCK 稳定 lncRNA 赋予结核病抵抗者先天记忆 [RNAseq]
• GSE281009 间充质IL-33激活修复性巨噬细胞，促进血管内损伤诱导的新内膜增生[scRNA-Seq]
• GSE281008 间充质IL-33激活修复性巨噬细胞，促进血管内损伤诱导的新内膜增生[RNA-Seq]
• GSE273174 在全基因组 CRISPR/Cas9 拯救筛选中鉴定与 Recql4 的新型基因相互作用。
• GSE273006 在全基因组 CRISPR/Cas9 合成致死筛选中鉴定与 Recql4 的新型基因相互作用。
• GSE311318 软骨寡聚基质蛋白（COMP）基因与高级别膀胱癌相关并促进膀胱癌细胞增殖
• GSE311202 大肠杆菌感染期间与 Th17 细胞共培养的口腔角质形成细胞的转录组分析
• GSE310377 胎盘外泌体 miR-24-1-5p 在 LPS 诱导的炎症中的作用
• GSE307410 莫哈维芽孢杆菌后生元：对结肠癌细胞的转录组学和抗癌作用
• GSE298010 阶段特异性表观遗传启动增强谱系定向过程中的基因激活 [Micro-C]
• GSE298008 阶段特异性表观遗传启动增强谱系定向过程中的基因激活 [多组]
• GSE298005 阶段特异性表观遗传启动增强谱系定向过程中的基因激活 [RELACS]
• GSE298002 阶段特异性表观遗传启动增强谱系定向过程中的基因激活 [CUT&Run]
• GSE298000 阶段特异性表观遗传启动在谱系决定过程中增强基因激活 [4C]
• GSE291575 体外循环通过剪切力介导的钙库操纵性内流激活经典单核细胞 [scRNA-seq]
• GSE279595 A-to-I RNA 编辑可预防脂肪组织中炎症介导的脂肪营养不良
• GSE221529 疾病相关的 p63 DBD 突变通过不同的机制和不同程度损害 DNA 结合 [RNA-seq]
• GSE221525 疾病相关的 p63 DBD 突变通过不同的机制和不同程度损害 DNA 结合 [ChIP-seq]
• GSE221520 疾病相关的 p63 DBD 突变通过不同的机制和不同程度损害 DNA 结合 [ATAC-seq]
• GSE221088 基于循环小细胞外囊泡的 miRNA 分类器在滤泡性甲状腺癌诊断中的应用：一项多中心诊断研究