科研日报 2026-01-14
📅 Daily Report - 2026-01-14
今日筛选出 76 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点:
- BTK抑制剂在神经损伤修复中的潜力:多项研究(GSE279103, GSE278773)显示,BTK抑制剂可逆转B细胞介导的淋巴毒素-α释放引起的神经损伤,提示其在神经系统疾病治疗中的新应用。
- GATA1 N-端在红细胞发育中的关键代谢作用:通过RNA-seq、CUT&RUN等技术(GSE315981, GSE316151, GSE315986, GSE315985, GSE299583)揭示了GATA1 N-端在红细胞发育过程中的重要代谢调控功能。
主要方向:
- 肿瘤微环境与免疫治疗:深入研究激素敏感性乳腺癌(GSE304998)和急性髓系白血病(GSE300371, GSE300370)的肿瘤微环境及其对免疫治疗(ICB)和靶向疗效的影响。
- 细胞发育与表观遗传调控:探索肠道上皮Tet2缺陷(GSE307332)、ATRX基因丢失(GSE291201, GSE291197)以及γδ T细胞发育(GSE308703)中的关键分子机制。
- 单细胞转录组学在疾病诊断与机制解析中的应用:利用scRNA-seq技术解析结直肠癌(GSE299651)、B细胞功能(GSE271012, GSE155585)、中枢神经系统脱髓鞘疾病(GSE308212, GSE286541)以及甲壳类免疫(GSE289112)等。
技术亮点:
- Hi-C技术在癌症基因组学中的应用:用于检测淋巴瘤样本中的增强子-劫持重排(GSE289531)。
- 多组学联合分析:结合RNA-seq、ATAC-seq、CUT&RUN等技术,全面解析基因功能、表观遗传调控及代谢通路。
🧪 博客更新
今日焦点: 新型脑信号模式有望在阿尔茨海默病确诊前预测疾病进展;一种新型抗生素测试能区分真正杀灭细菌的药物。
主要方向:
- 精准医疗:开发能区分杀菌与抑菌的抗生素测试。
- 神经科学:探索早期阿尔茨海默病诊断的脑信号。
- 生物技术:实现无仪器高通量单细胞DNA测序及多组学分析。
- 空间组学:整合空间转录组学与RNA测序预测缺失基因表达,解析组织结构。
技术亮点:
- 新型抗生素敏感性测试,追踪单个细菌存活。
- 非侵入性脑扫描技术,识别早期阿尔茨海默病风险。
- VISTA整合空间信息,提升基因表达预测精度。
📚 分类浏览
🧬 数据前沿 (72条)
详细内容(前10条)
1. ⭐ GSE304998 肿瘤微环境和免疫动力学在激素敏感性乳腺癌中的作用:来自大鼠模型中免疫检查点阻断和靶向治疗的启示
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer、immune、tumor microenvironment
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusThis SuperSeries is composed of the SubSeries listed below.
- 🔗 查看原文
2. ⭐ GSE307332 肠道上皮Tet2缺陷通过胆汁酸代谢改变重编程肠道菌群
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
- 📝 描述:Contributor : Hailiang LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEpigenetic mechanisms are increasingly recognized as critical regulators of host-microbiota interactions. Here, we report that intestinal epithelial-specific deletion of Tet2, a key DNA demethylase, leads to structural abnormalities, impaired barrier function, and remarkable reprogramming of the gut microbial community. Mechanistically, Tet2 deficiency significantly downregulated the expression of the apical sodium-dependent bile acid transporter (ASBT/Slc10a2), resulting in altered bile acid homeostasis with specific accumulation of hyocholic acid (HCA) in the intestinal lumen. This metabolic shift created a favorable niche for selective expansion of bile salt hydrolase (BSH)-expressing Lactobacillus species. Furthermore, we identified an age-dependent regulatory role of HCA in shaping microbial composition, promoting Lactobacillus in young mice while enriching Akkermansia in aged animals. Our findings unveil an epigenetic-metabolic-microbial axis centered on Tet2-mediated regulation of bile acid metabolism, providing new insights into how host epigenetic factors shape the gut microbial ecosystem.
- 🔗 查看原文
3. ⭐ GSE279103 布鲁顿酪氨酸激酶抑制剂可挽救由B细胞介导的淋巴毒素-α释放引起的神经元损伤
- ✍️ 作者:未知作者
- 🏷️ 关键词:B cell、Neuronal、kinase
- 📝 描述:Contributors : Paul Götz ; Nesrin Sharif ; Nicholas Hanuscheck ; Josef Shin ; Frauke ZippSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAlthough B cell depletion slows disability accrual in people with multiple sclerosis (pwMS), the role of B cells in MS-associated neuronal injury remains elusive. B cells release cytokines such as lymphotoxin-α (LTα), and this proinflammatory protein is also present in the cerebrospinal fluid (CSF) and meninges of pwMS. B cell-specific ablation of LTα alleviates disease severity in a preclinical model of MS. To further study the impact of B cell-derived cytokines on neuronal function, we performed patch-clamp recordings on human iPSC-derived neurons. Coculture with proinflammatory human B cells led to depolarization and aberrant firing. Pretreatment of proinflammatory B cells with a Bruton’s tyrosine kinase inhibitor (BTKi), reported in patients to beneficially affect disability progression even in the absence of inflammatory relapse activity, prevented neuronal impairment and inhibited LTα release from B cells. Blocking LTα, tumor necrosis factor receptor 1 (TNFR1), or receptor-interacting protein kinase 1 or 3 also prevented neuronal impairment, but blocking TNFα or LTβ had no such effect. Neuronal impairment was reversible by BTKi or blockage of LTα, and this reversibility was dependent on the activity of acid sphingomyelinase. In pwMS, LTα correlated with elevated neurofilament light chain (NfL) abundance in CSF, and anti-CD20 B cell-depletion therapy led to a reduction in circulating LTα, supporting the role of B cells as a regulator for LTα. These findings highlight the negative impact of B cell-derived LTα on neurons and suggest potential treatment avenues for MS-associated neuronal injury.
- 🔗 查看原文
4. ⭐ GSE278773 布鲁顿酪氨酸激酶抑制剂可挽救由B细胞介导的淋巴毒素-α释放引起的神经元损伤
- ✍️ 作者:未知作者
- 🏷️ 关键词:B cell、Neuronal、kinase
- 📝 描述:Contributors : Paul Götz ; Nesrin Sharif ; Nicholas Hanuscheck ; Josef Shin ; Frauke ZippSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAlthough B cell depletion slows disability accrual in people with multiple sclerosis (pwMS), the role of B cells in MS-associated neuronal injury remains elusive. B cells release cytokines such as lymphotoxin-α (LTα), and this proinflammatory protein is also present in the cerebrospinal fluid (CSF) and meninges of pwMS. B cell-specific ablation of LTα alleviates disease severity in a preclinical model of MS. To further study the impact of B cell-derived cytokines on neuronal function, we performed patch-clamp recordings on human iPSC-derived neurons. Coculture with proinflammatory human B cells led to depolarization and aberrant firing. Pretreatment of proinflammatory B cells with a Bruton’s tyrosine kinase inhibitor (BTKi), reported in patients to beneficially affect disability progression even in the absence of inflammatory relapse activity, prevented neuronal impairment and inhibited LTα release from B cells. Blocking LTα, tumor necrosis factor receptor 1 (TNFR1), or receptor-interacting protein kinase 1 or 3 also prevented neuronal impairment, but blocking TNFα or LTβ had no such effect. Neuronal impairment was reversible by BTKi or blockage of LTα, and this reversibility was dependent on the activity of acid sphingomyelinase. In pwMS, LTα correlated with elevated neurofilament light chain (NfL) abundance in CSF, and anti-CD20 B cell-depletion therapy led to a reduction in circulating LTα, supporting the role of B cells as a regulator for LTα. These findings highlight the negative impact of B cell-derived LTα on neurons and suggest potential treatment avenues for MS-associated neuronal injury.
- 🔗 查看原文
5. ⭐ GSE271012:从8周龄C57BL/6J小鼠转移的B1-8抗原特异性B细胞的单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:antigen、RNAseq、single-cell
- 📝 描述:Contributors : Xiaoming Wang ; Jingjing Chen ; Yuliang WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe aim of this study is to characterize the accurate cell cluster of transferred B1-8 antigen-specific B cells.
- 🔗 查看原文
6. GSE315981 揭示 GATA1 N 端在红细胞发育中的关键代谢作用 [批量 RNA 测序]
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic、RNA-seq
- 📝 描述:Contributors : Te Ling ; Rashid Mehmood ; John D CrispinoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMutations in GATA1 that result in skipping of exon 2, which encodes the N-terminus, are associated with the myeloid leukemia of Down syndrome and Diamond-Blackfan anemia (DBA). To elucidate the molecular functions of the N-terminus, we employed single-cell RNA sequencing (scRNA-seq) of fetal liver cells derived from Gata1 mutant embryos that express the GATA1 short (GATA1s) isoform in place of full-length GATA1 (GATA1FL). scRNA-seq highlighted defects in erythropoiesis and revealed that the absence of the N-terminus resulted in elevated expression of genes involved in glycolysis, such as the rate-limiting pyruvate kinase PKM. To elucidate the regulation of the PKM gene, we performed precision nuclear run-on sequencing and cleavage under targets and release using nuclease on erythroid cells following acute deletion of GATA1 and determined that PKM is a direct target of GATA1. Mechanistically, we found that substitution of GATA1FL with GATA1s led to increased glycolysis in erythroid progenitor cells but did not affect oxidative phosphorylation. We further discovered that the expression of PKM is significantly elevated in DBA patients with RPS19 mutations, consistent with a role for GATA1 regulation of glycolysis in erythropoiesis. Together, these findings reveal that GATA1 controls not just heme metabolism, but also glycolysis.
- 🔗 查看原文
7. GSE299651 结直肠癌单细胞筛选鉴定出由癌基因激活的具有临床意义的转录模块
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、single-cell
- 📝 描述:Contributors : Viola Hollek ; Francisca Böhning ; Markus Morkel ; Nils BlüthgenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWhile oncogenic mutations shape colorectal cancer biology and therapy response, their prognostic value remains low. Cluster-based classification of patient cancer transcriptomes has shown greater promise for prognosis, yet these systems do not account for the roles of oncogenes in establishing cancer phenotypes. Here, we create and validate a prognostic classifier for colorectal cancer based on transcriptional programs induced by oncogenes.To systematically investigate oncogenic drivers, we employed a barcoded library of colorectal cancer-associated oncogene variants across a panel of genetically diverse colorectal cancer cell lines. We profiled the transcriptomes of over 100,000 transgenic cells and used machine learning to define transcriptional modules capturing key functional traits.Our analysis revealed heterogeneity on the cell-to-cell level and context-dependent gene expression patterns induced by oncogenes. We identified overarching gene expression modules reflecting core oncogenic processes, including cancer cell plasticity, inflammatory response, replicative stress, and epithelial-to-mesenchymal transition. These modules enabled a functional classification that linked oncogenic signalling states to distinct transcriptional profiles. We demonstrated their prognostic value by stratifying clinical colorectal cancer cohorts into high- and low-risk groups. Although partially correlated with established clinical parameters, the modules provided additional prognostic information, improving survival prediction and therapy stratification beyond existing classification systems.In summary, our study establishes a framework that connects oncogenic mutations to core transcriptional modules. By integrating experimental models with clinical data, we provide a resource for investigating colorectal cancer progression and oncogene-specific vulnerabilities, facilitating future research and precision oncology.
- 🔗 查看原文
8. GSE291201 ATRX 缺失将富含 G 的重复序列处的基因组不稳定性与人类 α-珠蛋白表达失调联系起来 [scRNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:scRNA、genome
- 📝 描述:Contributors : Yuqi Shen ; Sean WenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGermline mutations in the chromatin remodelling protein ATRX cause a severe developmental disorder associated with α-thalassemia. In addition, ATRX is amongst the twenty genes most frequently mutated in cancer. How ATRX mutations alter gene expression remains unclear. Using the α-globin locus as a model, here we show that ATRX deficiency downregulates α-globin in a subset of cells exhibiting DNA damage. A G-rich repeat at the α-globin locus serves as a potential site of G-quadruplex formation and DNA damage. ATRX binds this repeat co-transcriptionally, and its loss increases R-loop accumulation at this site, leading to local DNA damage and transcriptional disruption in cis. Deletion of this repeat abolishes this effect, while targeted DNA damage reinstates it. These findings reveal a mechanism linking ATRX’s role in genome stability to transcriptional regulation, and uncover a molecular basis of human genetic disease mediated by a long-range G-rich repeat.
- 🔗 查看原文
9. GSE291197 ATRX 缺失将富含 G 的重复序列处的基因组不稳定性与人类 α-珠蛋白表达失调联系起来 [ChIP-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:ChIP-seq、genome
- 📝 描述:Contributor : Yuqi ShenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensGermline mutations in the chromatin remodelling protein ATRX cause a severe developmental disorder associated with α-thalassemia. In addition, ATRX is amongst the twenty genes most frequently mutated in cancer. How ATRX mutations alter gene expression remains unclear. Using the α-globin locus as a model, here we show that ATRX deficiency downregulates α-globin in a subset of cells exhibiting DNA damage. A G-rich repeat at the α-globin locus serves as a potential site of G-quadruplex formation and DNA damage. ATRX binds this repeat co-transcriptionally, and its loss increases R-loop accumulation at this site, leading to local DNA damage and transcriptional disruption in cis. Deletion of this repeat abolishes this effect, while targeted DNA damage reinstates it. These findings reveal a mechanism linking ATRX’s role in genome stability to transcriptional regulation, and uncover a molecular basis of human genetic disease mediated by a long-range G-rich repeat.
- 🔗 查看原文
10. GSE289112 泥蟹(Scylla paramamosain)血细胞在感染白斑综合征病毒(WSSV)前后的单细胞转录组测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、transcriptome
- 📝 描述:Contributor : Hu HangSeries Type : Expression profiling by high throughput sequencingOrganism : Scylla paramamosainWe used the BDA DNBelabC4 platform to conduct single-cell RNA transcriptome sequencing on hemocytes before and after infection with WSSV, and to study the changes in hemocytes composition and antiviral mechanism of a crustacean virus infection represented by mud crab. The blood cells, or hemocytes, of the mud crab (Scylla paramamosain) play crucial roles in its innate immune system. These cells are involved in various immune responses, including phagocytosis, encapsulation, and the production of antimicrobial peptides. The hemocytes can be isolated and characterized using techniques such as flow cytometry, which helps in understanding their functions and interactions within the crab’s immune system. White Spot Syndrome Virus (WSSV) is a highly contagious and lethal virus that primarily infects crustaceans, particularly shrimp and crabs. It is an enveloped double-stranded DNA virus, typically oval-shaped, measuring about 320nm in length and 100nm in width, making it one of the largest known viruses. WSSV is the causative agent of White Spot Syndrome, a disease that has caused significant economic losses in the aquaculture industry.
- 🔗 查看原文
💡 该来源还有 62 条内容,详见 文末
🧪 博客更新 (4条)
详细内容(全部4条)
1. Factorial Biotechnologies 和 Honeycomb Biotechnologies 合作提供高通量、无需仪器的单细胞 DNA 测序服务
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、single-cell
- 📝 描述:A new partnership enables scalable single-cell WGS and multi-omics, complementing RNA…
- 🔗 查看原文
2. 一项新测试揭示了哪些抗生素真正能杀死细菌
- ✍️ 作者:未知作者
- 🏷️ 关键词:bacteria、regex:bacter(ia|ial|ium)
- 📝 描述:Some antibiotics stop bacteria from growing without actually killing them, allowing infections to return later. Scientists at the University of Basel created a new test that tracks individual bacteria to see which drugs truly eliminate them. When tested on tuberculosis and other serious lung infections, the method revealed big differences in how bacteria tolerate treatment. The findings could lead to more precise therapies and better predictions of treatment success.
- 🔗 查看原文
3. VISTA——连接基因表达和空间背景
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial
- 📝 描述:VISTA integrates spatial transcriptomics with RNA sequencing to predict missing gene expression, enabling enhanced mapping of tissue organization, cell interactions, and spatially driven gene activity patterns…
- 🔗 查看原文
4. 隐藏的大脑信号可能在确诊前很久就揭示阿尔茨海默病的症状。
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Researchers have discovered a brain activity pattern that can predict which people with mild cognitive impairment are likely to develop Alzheimer’s disease. Using a noninvasive brain scanning technique and a custom analysis tool, they detected subtle changes in electrical signals tied to memory processing years before diagnosis. The findings point to a new way of spotting Alzheimer’s early—by listening directly to how neurons behave.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| cancer | 10 |
| RNA-seq | 8 |
| metabolic | 7 |
| genome | 7 |
| sequencing | 5 |
| single-cell | 5 |
| antigen | 5 |
| Neuronal | 4 |
| scRNA | 4 |
| transcriptome | 4 |
| carcinoma | 4 |
| enrichment | 3 |
| methylation | 3 |
| spatial | 2 |
| ChIP-seq | 2 |
| immune | 2 |
| regex:intestin(e | al) |
| leukemia | 2 |
| ATAC-seq | 2 |
| Hi-C | 2 |
📎 更多内容
🧬 数据前沿 其他内容 (62条)
- GSE301058 对模拟肠液中共生大肠杆菌溶原菌的转录组分析揭示了基因组核心区和辅助区的广泛变化。
- GSE300371 急性髓系白血病微环境通过 NFκB 信号通路损害中性粒细胞的成熟和功能 [ATAC-seq]
- GSE300370 急性髓系白血病微环境通过 NFκB 信号通路损害中性粒细胞的成熟和功能 [scRNA-seq]
- GSE289531 Hi-C 用于淋巴癌常规临床活检中增强子劫持重排的全基因组检测
- GSE304911 激素受体阳性乳腺癌大鼠模型中靶向和免疫联合疗法的评估 [RNA]
- GSE155585:8周龄C57BL/6J小鼠脾脏生发中心B细胞的单细胞RNA测序
- GSE308212 表达 EBV 潜伏膜蛋白 1 的 B 细胞在中枢神经系统中捕获髓鞘抗原,导致脱髓鞘病变形成 [RNA-Seq]
- GSE286541 表达 EBV 潜伏膜蛋白 1 的 B 细胞在中枢神经系统中捕获髓鞘抗原,导致脱髓鞘病变形成 [scRNA-Seq]
- GSE316151 揭示 GATA1 N 端在红细胞发育中的关键代谢作用
- GSE315986 揭示 GATA1 N 端在红细胞发育中的关键代谢作用 [CUT&RUN 人类]
- GSE315985 揭示 GATA1 N 端在红细胞发育中的关键代谢作用 [CUT&RUN]
- GSE314456 脂肪基质细胞衍生的癌相关成纤维细胞通过SFRP4信号通路促进胰腺腺癌的发生
- GSE308703 人类γδ T细胞发育的体内模型揭示末端脱氧核苷酸转移酶是3型Vδ2 T细胞发育的关键调控因子
- GSE306513 CCL18 作为 ABC 弥漫性大 B 细胞淋巴瘤预后的免疫抑制生物标志物
- GSE299583 揭示 GATA1 N 端在红细胞发育中的关键代谢作用 [CUT&Run]
- GSE298761 揭示 GATA1 N 端在红细胞发育中的关键代谢作用
- GSE296540 高分辨率图谱预测神经元身份的谱系和出生顺序
- GSE287648 ComBO:一种结合了人类骨骼和淋巴-髓系骨髓的类器官,用于造血系统疾病的临床前建模。
- GSE117546 APOBEC3B 对肝细胞癌的影响
- GSE316098 人乳头瘤病毒相关宫颈内膜腺癌侵袭模式的空间转录组图谱
- GSE315141 转座子测序揭示了伯克霍尔德氏菌基因在与太空飞行相关的植物-病原体互作中的适应性。
- GSE312186 利用 5-甲基胞嘧啶糖苷酶富集 DNA 低甲基化区域以发现生物标志物 [mouse_DMNseq]
- GSE312185 利用 5-甲基胞嘧啶糖苷酶富集 DNA 低甲基化区域以发现生物标志物 [human_DMNseq]
- GSE311748 RBProximity-CLIP 能够以核苷酸分辨率对 RNA 结合蛋白相互作用进行亚细胞定位 [RNA-seq]
- GSE309434 利用5-甲基胞嘧啶糖苷酶富集DNA低甲基化区域以发现生物标志物
- GSE308256 趋同的抗体突变轨迹将 IGHV4-34 B 细胞中的功能性自身耐受性转化为遗传性自身耐受性。
- GSE305990 cmLumiOpto 基因疗法联合化疗治疗三阴性乳腺癌。
- GSE304375转录组分析揭示TOE1在肝细胞癌中的潜在作用
- GSE302640 Cal27口腔癌细胞中角蛋白转录组分析
- GSE301630 健康犬外周血白细胞的单细胞转录组图谱
- GSE301074 小鼠卵巢排卵过程中壁层颗粒细胞和卵丘细胞的转录组分析
- GSE300533 性腺和染色体性别对肝脏转录组的影响
- GSE300149 研究发现,使用单域抗体靶向固有无序核蛋白1 (NUPR1) 可缓解体内三阴性乳腺癌 (TNBC) 的进展。
- GSE297214 葡萄糖对三阴性乳腺癌中MIR503HG调控基因的分子效应
- GSE293411 TWIST1 驱动内皮细胞向间质细胞转化以稳定动脉粥样硬化斑块 [AEBP1 RNA-Seq]
- GSE293410 TWIST1 驱动内皮细胞向间质细胞转化以稳定动脉粥样硬化斑块 [Twist1 RNA-Seq]
- GSE292327 脑膜瘤复发风险预测新型甲基化分类器的开发、验证和临床应用
- GSE292326 脑膜瘤复发风险预测的新型甲基化分类器的开发、验证和临床应用[数据集 2]
- GSE292325 脑膜瘤复发风险预测的新型甲基化分类器的开发、验证和临床应用[数据集 1]
- GSE291588 总 CD45+ 主动脉细胞的 scRNA-seq 及细胞哈希
- GSE281118 前列腺癌发生过程中维生素D信号通路的研究
- GSE278596 TWIST1 驱动内皮细胞向间质细胞转化以稳定动脉粥样硬化斑块 [单细胞 RNA 测序]
- GSE267007 HeLa细胞中hnRNPA1敲低的RNA测序
- GSE255158 不同条件下耳念珠菌和白色念珠菌的RNA测序
- GSE243837 CD4+ T 细胞中 CTCF 调控的三维增强子网络分析 [原位 Hi-C]
- GSE243713 CD4+ T 细胞中 CTCF 调控的三维增强子网络分析 [RNA-seq]
- GSE243710 CD4+ T 细胞中 CTCF 调控的三维增强子网络分析 [ChIP-seq]
- GSE243709 CD4+ T 细胞中 CTCF 调控的三维增强子网络分析 [ATAC-seq]
- GSE234454 LINC00862 通过 RBM47 介导的正反馈环路抑制肝细胞癌
- GSE285674 野生型和 Gls CD19cre B KO 或 Efnb1 ai3 B KO 或 Kdm6b OE CD83+ly75+GCB 细胞中 H3K27me3 修饰的全基因组图谱
- GSE270909:B细胞不同亚群中H3K27me3和H3K4me3修饰的全基因组图谱
- GSE270617 野生型和 Kdm6b B KO 前浆生发中心 B 细胞中 H3K27me3 修饰的全基因组图谱。
- GSE316061 夏威夷短尾鱿鱼共生菌 Leisingera sp. ANG-M7 采用“联合武器”策略来克服竞争对手的抵抗力
- GSE315968 靶向 Alk4 通路可预防与年龄相关的骨质流失。
- GSE308407 表达 EBV 潜伏膜蛋白 1 的 B 细胞在中枢神经系统中捕获髓鞘抗原,导致脱髓鞘病变形成 [BRB-seq]
- GSE308213 表达EBV潜伏膜蛋白1的B细胞在中枢神经系统中捕获髓鞘抗原,导致脱髓鞘病变形成
- GSE306473 一项 II 期临床试验,研究伊沙佐米联合吉西他滨和多柔比星治疗 SMARCB1 缺陷型肾髓质癌患者的疗效
- GSE302984 用癌相关成纤维细胞 (CAFs) 条件培养基 (CM) 处理诱导胰腺癌细胞基因表达的分析
- GSE297515 研究发现,Piezo1 依赖性基质细胞激活可引发运动和损伤时的肌肉炎症,并与炎症衰老相关。
- GSE291050:在化疗和/或新型类干细胞制剂二氢杨梅素的临床前治疗过程中,小鼠异种移植模型中人基质细胞的全转录组分析
- GSE272221 RNA-seq 分析 FLO-1 食管腺癌中 EpCAM-GFP 和 GFP 的过表达
- GSE222871 神经元 miR-17-5p 导致产前酒精暴露引起的半球间皮层连接缺陷
📅 报告生成时间:2026-01-13 21:40
🤖 由 GitHub Actions 自动生成