详细内容（前10条）

1. ⭐ GSE333285 Ago2 缺失可恢复免疫难治性肺癌对免疫检查点抑制剂的敏感性 [RNA-seq vitro]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq
• 📝 描述：Contributors : Dario Pasquale Anobile ; Layla Barbar ; Emile Maucotel ; Alexis Cornec ; Valeria Manriquez ; Wilfrid Richer ; Jordan Denizeau ; Christine Sedlik ; Charlie Bories ; Elodie Couderc ; Renaud Leclere ; Judith Sobas ; Emeline Papillon ; Rafael Mena Osuna ; Jimena Tosello-Boari ; Marianne Burbage ; Eliane Piaggio ; Enzo PoirierSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOne of the first-line treatments for advanced non-small cell lung cancer (NSCLC) are immune checkpoint inhibitors (ICI), which activate the antitumor immune response. Despite their success, ICI remain ineffective in many patients, highlighting the need for strategies to overcome resistance. Most efforts have focused on promoting immune cell infiltration into refractory tumors to improve ICI efficacy. In this work, we mobilize this approach by focusing on Argonaute 2 (Ago2), a pivotal member of the RNA interference pathway. Using two murine models of immunorefractory NSCLC, we demonstrate that tumoral Ago2 suppresses interferon signaling, leading to poor immunogenicity and failure of ICI therapy. Genetic deletion of Ago2 in cancer cells restores interferon signaling and supports immune infiltration of the tumor. Consequently, whereas wild-type tumors are resistant to ICI, tumors devoid of Ago2 become sensitive to treatment. In NSCLC patients treated with ICI, high Ago2 expression and a low interferon signature in tumors correlates with reduced survival. Ago2 is thus a driver of the immunorefractory phenotype observed in NSCLC and may represent a therapeutic target when aiming to sensitize patients to ICI.
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2. ⭐ GSE330941 Ago2 缺失可恢复免疫难治性肺癌对免疫检查点抑制剂的敏感性 [RNA-seq vivo]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq
• 📝 描述：Contributors : Dario Pasquale Anobile ; Layla Barbar ; Emile Maucotel ; Alexis Cornec ; Valeria Manriquez ; Wilfrid Richer ; Jordan Denizeau ; Christine Sedlik ; Charlie Bories ; Elodie Couderc ; Renaud Leclere ; Judith Sobas ; Emeline Papillon ; Rafael Mena Osuna ; Jimena Tosello-Boari ; Marianne Burbage ; Eliane Piaggio ; Enzo PoirierSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOne of the first-line treatments for advanced non-small cell lung cancer (NSCLC) are immune checkpoint inhibitors (ICI), which activate the antitumor immune response. Despite their success, ICI remain ineffective in many patients, highlighting the need for strategies to overcome resistance. Most efforts have focused on promoting immune cell infiltration into refractory tumors to improve ICI efficacy. In this work, we mobilize this approach by focusing on Argonaute 2 (Ago2), a pivotal member of the RNA interference pathway. Using two murine models of immunorefractory NSCLC, we demonstrate that tumoral Ago2 suppresses interferon signaling, leading to poor immunogenicity and failure of ICI therapy. Genetic deletion of Ago2 in cancer cells restores interferon signaling and supports immune infiltration of the tumor. Consequently, whereas wild-type tumors are resistant to ICI, tumors devoid of Ago2 become sensitive to treatment. In NSCLC patients treated with ICI, high Ago2 expression and a low interferon signature in tumors correlates with reduced survival. Ago2 is thus a driver of the immunorefractory phenotype observed in NSCLC and may represent a therapeutic target when aiming to sensitize patients to ICI.
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3. ⭐ GSE287965 瘢痕疙瘩发病机制中的表观遗传失调：新型甲基化特征的全基因组鉴定和验证

• ✍️ 作者：未知作者
• 🏷️ 关键词：genome、epigenetic、methylation
• 📝 描述：Series Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensKeloid scars are related to genetic factors and some environmental factors. Currently, most molecular studies on keloids have primarily focused on epigenetic mechanisms, involving gene expression regulation mechanisms, particularly DNA methylation, where methylation changes have been reported to cause many complex diseases. These studies investigate DNA methylation changes that have been linked to keloid scars. This study aimed to enhance our understanding of keloid scars by examining the epigenetic mechanisms involved from 12 keloid scar fibroblasts and 6 normal skin fibroblasts, using the Infinium MethylationEPIC BeadChip (Illumina, San Diego, CA, USA). The findings revealed 3,564 differentially methylated CpG sites, 828 were hypomethylated (TSS200: 17.11%, TSS1500:37.76%, body: 44.84%, 3’UTR: 0.29%), and 2,736 were hypermethylated (TSS200: 14.81%, TSS1500: 37.34%, body: 47.50%, 3’UTR: 0.18%). This study may serve as a guideline for managing patients with keloid scars in the future.
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4. GSE328435 DSS结肠炎模型中同窝Gpr15l-/-和Gpr15l+/+小鼠的全基因组鸟枪法宏基因组测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、genome
• 📝 描述：Contributors : Miriana Leggio ; Sebastian Schramm ; Tanja M Müller ; Stefan Wirtz ; Sebastian ZundlerSeries Type : OtherOrganism : feces metagenomeObjective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
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5. GSE317764 高脂饮食通过微生物群驱动的炎症导致肠道第3组固有淋巴细胞快速丢失

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、regex:intestin(e|al)
• 📝 描述：Contributors : Eva C Torrico ; Paulien Kaptein ; Fatiha Laalouhmi ; Sara Guendouzi ; Abdellatif E Khayari ; Chaymae E Baha ; Elly D Htite ; Sophie chawluk ; christian D Gauthier ; Nadhir M Djekidel ; Gopal Murugaiyan ; James A Lederer ; Scott B Sapper ; Roni Nowarski ; Rachid E Fatimy ; Howard L Weiner ; Selma BoulenouarSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusGroup 3 innate lymphoid cells (ILC3s) are critical sensory hubs to maintain intestinal immunity while adapting to environmental changes, including food intake and microbiota composition. Nutritional stress such as feeding on a high-fat diet (HFD) impairs ILC3s homeostasis, but the drivers underlying this phenotype remain elusive. Here, we found that intestinal ILC3s are depleted in overweight and obese humans, similarly to HFD-induced obese mice. However, we identified that ILC3s loss is not dependent on excessive calorie intake, weight gain, or glucose intolerance. Instead, we found that ILC3s impairment starts upon hours of HFD consumption, inducing microbial efflux. As a result, tissue-resident mononuclear phagocytes (MNPs) become proinflammatory, driving ILC3 cell death. We determined that the microbiota-driven stimulation overrides lipid-laden ILC3s ability to perform fatty acid oxidation, causing mitochondrial damage due to the accumulation of lipid peroxides. Collectively, our findings define the mechanism driving ILC3s maladaptation to fat-microbiota crosstalk and raise new considerations for understanding intestinal homeostasis and inflammation.
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6. GSE308469 MLL4 复合物在 H3K4 甲基化和 p53 依赖性转录激活中的分子机制 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、methylation
• 📝 描述：Contributors : Jianfeng Sun ; Douglas Barrows ; Robert G RoederSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMLL4 is a mammalian H3K4 mono-methyltransferase that plays a critical role in enhancer-regulated gene activation and tissue-specific gene expression during development. Here, we utilized a reconstituted MLL4 complex (MLL4C) containing a truncated MLL4 “fusion” protein (MLL4F) that retains its catalytic SET domain and N-terminal functional regions for comprehensive structural and functional analyses. In vitro H3K4 methyltransferase assays demonstrated that MLL4 catalytic activity is notably stimulated by p53 and CBP/p300. Cryo-electron microscopy (cryo-EM) analysis revealed that the MLL4 fusion core complex engages the nucleosome in three major distinct conformational states, providing mechanistic insights into the regulation of MLL4 and other MLL family methyltransferases by two structurally rigid modules: the SET–ASH2L–DPY30 module and the RBBP5–WDR5 module. In addition, we delineated a third structurally rigid module within the functional region upstream of MLL4 SET domain, encompassing the tandem PHD4–6, PHD7, and FYR domains, which is essential for MLL4- and p53-dependent transcription. Comparative structural analyses reveal that this third module is evolutionarily conserved across MLL1 to MLL4. Furthermore, we employed crosslinking mass spectrometry and integrative modeling to generate a complete model of the nine-subunit MLL4FC complex and elucidated its functional interactions with p53. Finally, genomic studies in the human colon cancer cell line HCT116 revealed that MLL4 colocalizes with p53 at active enhancers of p53 target genes. MLL4 knockout led to significant downregulation of p53-regulated genes, coupled with the reduction of p53 binding at active enhancers. These findings provide molecular insights into the catalytic and transcriptional functions of the MLL4 complex in establishing active enhancers and facilitating p53-dependent transcription activation.
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7. GSE308265 MLL4 复合物在 H3K4 甲基化和 p53 依赖性转录激活中的分子机制 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、methylation
• 📝 描述：Contributors : Jianfeng Sun ; Douglas Barrows ; Robert G RoederSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMLL4 is a mammalian H3K4 mono-methyltransferase that plays a critical role in enhancer-regulated gene activation and tissue-specific gene expression during development. Here, we utilized a reconstituted MLL4 complex (MLL4C) containing a truncated MLL4 “fusion” protein (MLL4F) that retains its catalytic SET domain and N-terminal functional regions for comprehensive structural and functional analyses. In vitro H3K4 methyltransferase assays demonstrated that MLL4 catalytic activity is notably stimulated by p53 and CBP/p300. Cryo-electron microscopy (cryo-EM) analysis revealed that the MLL4 fusion core complex engages the nucleosome in three major distinct conformational states, providing mechanistic insights into the regulation of MLL4 and other MLL family methyltransferases by two structurally rigid modules: the SET–ASH2L–DPY30 module and the RBBP5–WDR5 module. In addition, we delineated a third structurally rigid module within the functional region upstream of MLL4 SET domain, encompassing the tandem PHD4–6, PHD7, and FYR domains, which is essential for MLL4- and p53-dependent transcription. Comparative structural analyses reveal that this third module is evolutionarily conserved across MLL1 to MLL4. Furthermore, we employed crosslinking mass spectrometry and integrative modeling to generate a complete model of the nine-subunit MLL4FC complex and elucidated its functional interactions with p53. Finally, genomic studies in the human colon cancer cell line HCT116 revealed that MLL4 colocalizes with p53 at active enhancers of p53 target genes. MLL4 knockout led to significant downregulation of p53-regulated genes, coupled with the reduction of p53 binding at active enhancers. These findings provide molecular insights into the catalytic and transcriptional functions of the MLL4 complex in establishing active enhancers and facilitating p53-dependent transcription activation.
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8. GSE288617 配对转录组学揭示细胞因子刺激的类器官与溃疡性结肠炎上皮反应之间的相似性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、transcriptomics
• 📝 描述：Contributors : Gunnar A Walaas ; Arun Sridhar ; Lusie F Kuraas ; Siri Sæterstad ; Atle v Granlund ; Arne K Sandvik ; Ann E Østvik ; Ingunn Bakke ; Torunn BrulandSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe intestinal epithelium mediates critical crosstalk between microbiota and immune cells in inflammatory bowel disease. While patient-derived intestinal organoids offer potential for modeling ulcerative colitis, their ability to replicate in vivo inflammation and utility for precision medicine remain unclear. By comparing transcriptomic profiles from microdissected colonic epithelium of ulcerative colitis patients with paired patient-derived organoids under various inflammatory conditions, we demonstrated that organoids established from uninflamed biopsies can effectively model epithelial inflammation. Combined IFNγ and TNF stimulation or a cocktail of pro- and anti-inflammatory signals induced inflammatory signatures matching in vivo ulcerative colitis patterns, including upregulation of interferon signaling, antigen presentation, and unfolded protein response pathways. Strong correlations between in vivo and in vitro expression of over 200 disease-relevant genes validate intestinal organoids as a suitable preclinical model. These findings substantiate intestinal epithelial organoids’ value for investigating ulcerative colitis pathogenesis and developing personalized medicine approaches.
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9. GSE333058 来自 CD14 阳性单核细胞 (ENCSR465SUK) 的 Mint-ChIP-seq。

• ✍️ 作者：未知作者
• 🏷️ 关键词：monocyte、ChIP-seq
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensH3K27me3 Mint-ChIP-seq on human CD14-positive monocyteFor data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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10. GSE333018 来自 CD14 阳性单核细胞 (ENCSR167XYG) 的 Mint-ChIP-seq。

• ✍️ 作者：未知作者
• 🏷️ 关键词：monocyte、ChIP-seq
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensH3K9me3 Mint-ChIP-seq on human CD14-positive monocyteFor data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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1. 加快 R 包开发者的 Stan 模型构建速度

• ✍️ 作者：未知作者
• 🏷️ 关键词：R package
• 📝 描述：Introduction In my previous job my work computer was a Windows desktop – yes, those were the days before laptops and hotdesking! My PhD student was interested in Bayesian methods and we put together an R package which included some Stan models. … Continue reading: Speeding up Stan model builds for R package developers
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详细内容（全部2条）

1. 科学家称，他们用一种简单的鼻喷雾剂逆转了大脑衰老。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Researchers at Texas A&M have developed a nasal spray that appears to reverse brain aging by calming inflammation and restoring the brain’s energy systems. After just two doses, memory and cognitive function improved for months, raising hopes for future treatments targeting dementia and brain fog.
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2. 科学家们对维生素B12与癌症的关系提出了新的疑问

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Vitamin B12 has long been seen as a health hero, helping the body make red blood cells, repair DNA, and keep nerves functioning properly. But scientists are discovering that the story may be more complicated than simply “more is better.” While too little B12 can damage DNA and raise cancer risk, some studies suggest that extremely high levels — especially from long-term high-dose supplements — may also be linked to certain cancers or poorer outcomes in cancer patients.
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• GSE332901 来自幼稚胸腺来源的 CD4 阳性 αβ T 细胞的 Mint-ChIP-seq (ENCSR994PGV)
• GSE332897 来自 Karpas-422 的组蛋白 ChIP-seq (ENCSR978BQI)
• GSE332884 横结肠组蛋白 ChIP-seq (ENCSR933BVL)
• GSE332880 来自 Karpas-422 的组蛋白 ChIP-seq (ENCSR910XKX)
• GSE332874 活化的幼稚 CD8 阳性 αβ T 细胞 (ENCSR897UBR) 的对照 Mint-ChIP-seq
• GSE332866 来自 Karpas-422 的组蛋白 ChIP-seq (ENCSR867UKC)
• GSE332863 OCI-LY3 (ENCSR867TPP) 的组蛋白 ChIP-seq
• GSE332855 OCI-LY3 (ENCSR857GMX) 的组蛋白 ChIP-seq
• GSE332844 横结肠组蛋白 ChIP-seq (ENCSR840VWD)
• GSE332833 乙状结肠组蛋白 ChIP-seq (ENCSR812POE)
• GSE332830 KMS-11 的组蛋白 ChIP-seq (ENCSR806XIU)
• GSE332827 活化的幼稚 CD8 阳性 αβ T 细胞 (ENCSR803FCO) 的对照 Mint-ChIP-seq
• GSE332826 横结肠组蛋白 ChIP-seq (ENCSR791LZY)
• GSE332813 DOHH2 的组蛋白 ChIP-seq (ENCSR784AQY)
• GSE332805 来自活化的幼稚 CD8 阳性 αβ T 细胞 (ENCSR772HRO) 的 Mint-ChIP-seq
• GSE332795 升主动脉组蛋白 ChIP-seq (ENCSR736PKV)
• GSE332791 脾脏组蛋白 ChIP-seq (ENCSR726HTS)
• GSE332775 升主动脉组蛋白 ChIP-seq (ENCSR707AEW)
• GSE332771 来自活化的幼稚 CD8 阳性 αβ T 细胞 (ENCSR701EUC) 的 Mint-ChIP-seq
• GSE332762 来自幼稚胸腺来源的 CD4 阳性 αβ T 细胞 (ENCSR662VXY) 的 Mint-ChIP-seq
• GSE332760 脾脏组蛋白 ChIP-seq (ENCSR659RJP)
• GSE332746 背外侧前额叶皮层组蛋白 ChIP-seq (ENCSR653OJO)
• GSE332742 背外侧前额叶皮层组蛋白 ChIP-seq (ENCSR639RKS)
• GSE332741 OCI-LY3 组蛋白 ChIP-seq (ENCSR638FRE)
• GSE332737 DOHH2 (ENCSR627TNG) 的组蛋白 ChIP-seq
• GSE332725 OCI-LY3 (ENCSR604JFH) 的组蛋白 ChIP-seq
• GSE332720 背外侧前额叶皮层组蛋白 ChIP-seq (ENCSR597RXN)
• GSE332719 来自活化 CD4 阳性 αβ T 细胞 (ENCSR594FUA) 的 Mint-ChIP-seq
• GSE332717 脾脏组蛋白 ChIP-seq (ENCSR589TCU)
• GSE332707 SU-DHL-6 (ENCSR587FCM) 的组蛋白 ChIP-seq
• GSE332706 Histone ChIP-seq from OCI-LY3 (ENCSR581LZU)
• GSE332693 Histone ChIP-seq from SU-DHL-6 (ENCSR494LJG)
• GSE332692 Histone ChIP-seq from MCF-7 (ENCSR493NBY)
• GSE332691 Control Mint-ChIP-seq from activated CD4-positive, alpha-beta T cell (ENCSR490HRA)
• GSE332688 Histone ChIP-seq from GM23248 (ENCSR479HKJ)
• GSE332687 Histone ChIP-seq from DOHH2 (ENCSR460SEN)
• GSE332685 Histone ChIP-seq from OCI-LY1 (ENCSR449AYM)
• GSE332684 Histone ChIP-seq from OCI-LY7 (ENCSR447ZGY)
• GSE332683 Mint-ChIP-seq from activated CD4-positive, alpha-beta T cell (ENCSR440SZD)
• GSE332682 Histone ChIP-seq from dorsolateral prefrontal cortex (ENCSR438KQU)
• GSE332680 Histone ChIP-seq from OCI-LY1 (ENCSR422JNY)
• GSE332677 Mint-ChIP-seq from activated naive CD8-positive, alpha-beta T cell (ENCSR392MYU)
• GSE332676 Histone ChIP-seq from OCI-LY7 (ENCSR389WWC)
• GSE332669 Histone ChIP-seq from DOHH2 (ENCSR350RYG)
• GSE332666 Histone ChIP-seq from SU-DHL-6 (ENCSR316KHQ)
• GSE332664 Histone ChIP-seq from Karpas-422 (ENCSR306VSH)
• GSE332657 polyA plus RNA-seq from cardiac muscle cell (ENCSR294NDO)
• GSE332654 Mint-ChIP-seq from activated naive CD8-positive, alpha-beta T cell (ENCSR260TLP)
• GSE332653 Histone ChIP-seq from uterus (ENCSR249INE)
• GSE332652 Histone ChIP-seq from OCI-LY7 (ENCSR243AIS)
• GSE332645 Histone ChIP-seq from transverse colon (ENCSR208QRN)
• GSE332639 Histone ChIP-seq from spleen (ENCSR197QDK)
• GSE332632 Histone ChIP-seq from OCI-LY1 (ENCSR189AGR)
• GSE332624 Histone ChIP-seq from stomach (ENCSR166CNR)
• GSE332622 Histone ChIP-seq from spleen (ENCSR161FEJ)
• GSE332600 Histone ChIP-seq from dorsolateral prefrontal cortex (ENCSR128YOH)
• GSE332599 Histone ChIP-seq from SU-DHL-6 (ENCSR114GLZ)
• GSE332597 Histone ChIP-seq from spleen (ENCSR105URN)
• GSE332589 Histone ChIP-seq from ascending aorta (ENCSR103QHX)
• GSE332583 Control Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR069ZFG)
• GSE332582 Histone ChIP-seq from DOHH2 (ENCSR052WRV)
• GSE332570 Mint-ChIP-seq from activated naive CD8-positive, alpha-beta T cell (ENCSR012DUX)
• GSE317919 Single nuceli RNA sequencing of pancreatic tumors to determine how SCAP loss affects tumor development
• GSE306231 Single cell RNA sequencing of pancreata to determine how SCAP loss affects pancreata on a cellular transcriptome level
• GSE288517 Paired transcriptomics reveals similarities between cytokine-stimulated organoids and ulcerative colitis epithelial responses
• GSE332923 单核细胞中的基线干扰素信号传导和注射部位抗体介导的先天激活影响 mRNA 疫苗的反应原性 [mouse_scRNAseq]
• GSE331536 骨关节炎中的口腔-肠-关节轴：一项多组学病例对照研究
• GSE290746 KLF4 促进鳞状肺癌中 KRT13+ 丘状体样状态 [scRNA-Seq]
• GSE290745 KLF4 促进鳞状肺癌中 KRT13+ 丘状体状态 [RNA-Seq]
• GSE332947 自闭症谱系障碍男性全外显子组测序和转录组分析的综合研究
• GSE309797 TMEM161A在结直肠癌中的高表达与肿瘤增殖和不良预后相关
• GSE290317 血液透析患者的免疫过度活跃与干扰素γ诱导的训练免疫相关
• GSE330849 MERFISH 空间转录组分析：小鼠出生后脑内 Sst+ 中间神经元的分析
• GSE327543 RNA-seq 分析了 DSS 结肠炎模型中 GPR15L KO 小鼠与 WT 小鼠结肠和 LPMC 的 RNA 测序结果
• GSE327541 16S rRNA测序数据来自共饲养实验中的Gpr15l-/-和野生型小鼠
• GSE327479 16S rRNA测序数据来自同窝饲养的Gpr15l-/-小鼠和对照小鼠
• GSE327478 16S rRNA 测序来自同窝 Gpr15l 转基因小鼠和同窝对照小鼠。
• GSE327477 16S rRNA测序，来自DSS结肠炎模型中接受直肠GPR15L或安慰剂治疗的同窝Gpr15l-/-小鼠。
• GSE327476 16S rRNA测序，来自DSS结肠炎模型中同窝Gpr15l-/-和Gpr15l+/+小鼠的比较
• GSE325397 社会调控基因在蚂蚁大脑中与增强子表现出过度连接 [RNA-seq]
• GSE316117 粪肠球菌上清液处理HeLa细胞的转录组分析：RNA-seq揭示差异基因表达
• GSE312236 综合蛋白质基因组学分析鉴定微卫星稳定型和不稳定型结直肠癌中的免疫靶点
• GSE289072 促炎混合物刺激后结肠上皮类器官的差异表达
• GSE285197 脑雌激素缺乏对脑特异性芳香化酶敲除小鼠模型海马转录组变化和记忆缺陷的性别特异性影响
• GSE333352 衰老小鼠脑白质中衰老和疾病相关小胶质细胞的空间分布
• GSE333349 超越糖原储存：AMPKγ2 通过肌球蛋白相互作用调节心脏肥大和电生理
• GSE333297 重组N蛋白（rNP）刺激的NK细胞
• GSE333134 心脏左心室对照 ChIP-seq (ENCSR979YKY)。
• GSE333132 脾脏 TF ChIP-seq (ENCSR967BSF)。
• GSE333125 H9 的 TF ChIP-seq (ENCSR871MKQ)。
• 来自活化的 CD4 阳性 αβ 记忆 T 细胞 (ENCSR810IIV) 的 GSE333111 snATAC-seq。
• GSE333108 脑组织 Mint-ChIP-seq (ENCSR804EYS)。
• GSE333107 DNA克隆样本（ENCSR798ALS）的混合克隆测序。
• GSE333094 神经嵴细胞的对照 Mint-ChIP-seq (ENCSR713YQD)。
• GSE333091 H9 的对照 ChIP-seq (ENCSR686HII)。
• GSE333090 来自内分泌胰腺祖细胞的 Mint-ChIP-seq (ENCSR673CVD)。
• GSE333083 来自活化的幼稚 CD4 阳性 αβ T 细胞 (ENCSR600UDB) 的 snATAC-seq。
• GSE333078 来自活化的 CD4 阳性 αβ T 细胞 (ENCSR569ZMI) 的 snATAC-seq。
• GSE333075 骨细胞对照 Mint-ChIP-seq (ENCSR554CUI)。
• GSE333072 内分泌胰腺祖细胞的对照 Mint-ChIP-seq (ENCSR546XZC)。
• GSE333061 来自活化的 CD8 阳性 αβ T 细胞 (ENCSR472HFJ) 的 snATAC-seq。
• GSE333059 软骨细胞对照 Mint-ChIP-seq (ENCSR466ZEA)。
• GSE333043 对照 Mint-ChIP-seq 来自 B 型胰腺细胞 (ENCSR380ZKL)。
• GSE333036 神经祖细胞（ENCSR322GAX）的对照 ChIP-seq。
• GSE333026 B 细胞的 DNase-seq (ENCSR224YYX)。
• GSE333022 来自活化的 CD8 阳性 αβ 记忆 T 细胞 (ENCSR196EOO) 的 snATAC-seq。
• GSE333014 来自活化的幼稚 CD8 阳性 αβ T 细胞 (ENCSR110IID) 的 snATAC-seq。
• GSE332899 来自 HepG2 (ENCSR985KAT) 的 polyA plus RNA-seq
• GSE332898 子宫对照 ChIP-seq (ENCSR979XBX)
• GSE332895 背外侧前额叶皮层对照 ChIP-seq (ENCSR968XKG)
• GSE332892 来自 S2 的 siRNA RNA-seq (ENCSR961OTL)
• GSE332890 K562 的 TF ChIP-seq (ENCSR948QLZ)
• GSE332881 GM23248 (ENCSR922FLS) 的对照 ChIP-seq
• GSE332876 来自中脑的 polyA plus RNA-seq (ENCSR908JWT)
• GSE332873 polyA plus RNA-seq 来自 GM12878 (ENCSR889TRN)
• GSE332870 来自 S2 的 siRNA RNA-seq (ENCSR881SWI)
• GSE332858 来自 S2 的 siRNA RNA-seq (ENCSR859XFS)
• GSE332856 肝细胞 polyA 加 RNA 测序 (ENCSR859HWB)
• GSE332851 来自胚胎面部突出部位的 polyA 加 RNA-seq (ENCSR851HEC)
• GSE332847 polyA plus RNA-seq 来自 GM12878 (ENCSR843RJV)
• GSE332839 横结肠对照 ChIP-seq (ENCSR828XQV)
• GSE332814 来自 S2 的 siRNA RNA-seq (ENCSR787CRI)
• GSE332803 来自 MCF-7 (ENCSR768LHG) 的对照 ChIP-seq
• GSE332800 肢体多聚腺苷酸化加RNA测序 (ENCSR750YSX)
• GSE332797 来自 GM23338 (ENCSR748GVH) 的 polyA 加 RNA-seq
• GSE332796 来自 S2 的 siRNA RNA-seq (ENCSR739YWV)
• GSE332768 来自 S2 的 siRNA RNA-seq (ENCSR679ARY)
• GSE332744 肝脏 polyA 加 RNA-seq (ENCSR648YEP)
• GSE332743 前脑 polyA 加 RNA-seq (ENCSR647QBV)
• GSE332705 Control ChIP-seq from OCI-LY1 (ENCSR569IIN)
• GSE332704 siRNA RNA-seq from S2 (ENCSR566KSW)
• GSE332703 siRNA RNA-seq from S2 (ENCSR556HGK)
• GSE332702 in situ Hi-C from K562 (ENCSR545YBD)
• GSE332700 Control ChIP-seq from dorsolateral prefrontal cortex (ENCSR534KYQ)
• GSE332699 TF ChIP-seq from dorsolateral prefrontal cortex (ENCSR525VXD)
• GSE332698 siRNA RNA-seq from S2 (ENCSR522GIE)
• GSE332697 polyA plus RNA-seq from GM23248 (ENCSR510QZW)
• GSE332696 polyA plus RNA-seq from neural tube (ENCSR508GWZ)
• GSE332695 siRNA RNA-seq from S2 (ENCSR505DDG)
• GSE332694 siRNA RNA-seq from S2 (ENCSR500YVI)
• GSE332686 siRNA RNA-seq from S2 (ENCSR449SQC)
• GSE332681 dilution Hi-C from GM12878 (ENCSR423SYP)
• GSE332679 polyA plus RNA-seq from hindbrain (ENCSR420QTO)
• GSE332678 siRNA RNA-seq from S2 (ENCSR401EQD)
• GSE332672 Control ChIP-seq from Karpas-422 (ENCSR367UDO)
• GSE332671 polyA plus RNA-seq from forebrain (ENCSR362AIZ)
• GSE332670 Control ChIP-seq from OCI-LY3 (ENCSR361GKY)
• GSE332668 siRNA RNA-seq from S2 (ENCSR340GYZ)
• GSE332659 siRNA RNA-seq from S2 (ENCSR295STB)
• GSE332658 Control ChIP-seq from dorsolateral prefrontal cortex (ENCSR295FXG)
• GSE332656 siRNA RNA-seq from S2 (ENCSR278IDU)
• GSE332648 polyA plus RNA-seq from smooth muscle cell (ENCSR236URT)
• GSE332640 Control ChIP-seq from HCT116 (ENCSR198WIH)
• GSE332633 Control ChIP-seq from spleen (ENCSR189UPU)
• GSE332617 TF ChIP-seq from MCF-7 (ENCSR155VDK)
• GSE332605 polyA plus RNA-seq from heart (ENCSR150CUE)
• GSE332603 polyA plus RNA-seq from muscle of leg (ENCSR144UVO)
• GSE332602 siRNA RNA-seq from S2 (ENCSR129TSA)
• GSE332573 polyA plus RNA-seq from bipolar neuron (ENCSR023VVO)
• GSE332572 siRNA RNA-seq from S2 (ENCSR023FIP)
• GSE332565 polyA plus RNA-seq from G1E-ER4 (ENCSR000CIA)
• GSE325399 Socially regulated genes display hyper-connectivity to enhancers in the ant brain [CUT&Tag and ATAC-seq]
• GSE324328 A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein [HK2_bulk RNA-seq]
• GSE324326 A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein [UUO_bulk RNA-seq]
• GSE317692 B cell αv integrin regulates tissue specialization and clonal expansion of lung germinal center and memory B cells after viral infection
• GSE308886 The role of Sulf1 during cardiac regeneration in zebrafish
• GSE277623 Co-Treatment with Empagliflozin and Pirfenidone Improves Cardiac Functions and Reverses Hypertrophic Remodeling in Heart Failure with Preserved Ejection Fraction in a Two-Hit Rat Model
• GSE241436 Uncoupling the TFIIH Core and Kinase Modules Leads to High CTD Serine 5 Phosphorylation Throughout Transcription
• GSE333343 DCLK1 调控化疗耐药性卵巢癌的干性及 IL-6/STAT3 依赖性转移微环境形成
• GSE333160 延迟处理CPT采集的血液可保留循环肿瘤细胞的转录组和基因组特征
• GSE333139 B细胞上的Siglec-G通过在阳性选择过程中控制T细胞辅助来抑制生发中心反应。
• GSE316413 KLF4 促进鳞状肺癌中 KRT13+ 丘状体样状态 [类器官切割与运行]
• GSE316412 KLF4 促进鳞状肺癌中 KRT13+ 丘状体样状态 [SNL_Organoids_RNA-seq]
• GSE303650 NR5A2 控制肝脏中必需昼夜节律代谢基因的基因表达和染色质接触
• GSE298582 硝唑啉上调LDLR表达，增强脂质代谢，并减少Apoe-/-小鼠的肝脂肪变性和动脉粥样硬化
• GSE294250 NAC转录因子ZmNAC24：从水通道蛋白调控到全基因组靶标和植物发育
• GSE291730 KLF4促进鳞状肺癌中KRT13+丘状样状态
• GSE290744 KLF4 促进鳞状肺癌中 KRT13+ 丘状体样状态 [BEAS_RNA-seq]
• GSE131395 CRTC1 在神经元中的全基因组占位情况
• GSE332825 H4K16ac 促进有丝分裂和减数分裂转变过程中染色质区室的重组 [Hi-C 2]
• GSE332824 H4K16ac 促进有丝分裂和减数分裂转变过程中染色质区室的重组 [Hi-C 2b]
• GSE332823 H4K16ac 促进有丝分裂和减数分裂转变过程中染色质区室的重组 [Hi-C 2a]
• GSE330568 文拉法辛通过单细胞分辨率的上皮和真皮重编程逆转化疗引起的脱发
• GSE299092 H4K16ac 促进有丝分裂和减数分裂转变过程中染色质区室的重组 [Hi-C 1]
• GSE299090 H4K16ac 促进有丝分裂和减数分裂转变过程中染色质区室的重组 [RNA-seq]