详细内容（前10条）

1. ⭐ GSE335211 H3K36M癌组蛋白抑制NSD2，从而激活KRAS驱动的肺癌中SETD2依赖的抗病毒样免疫反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、KRAS
• 📝 描述：Contributors : Amy C Gladstein ; Akino Mercy Charles Solomon ; Carson D Poltorack ; Sharan Venkatesh ; Keren M Adler ; Maggie R Robertson ; Stephanie Stransky ; Valerie M Irizarry-Negron ; Dain A Ruiz ; Dingwen Tao ; Nelson F Freeburg ; Simone Sidoli ; Irfan A Asangani ; Sydney M Shaffer ; David M FeldserSeries Type : OtherOrganism : Mus musculusMutations in histone 3 at or near lysine 36 (H3K36) have dominantly acting oncogenic effects in multiple tumor types by limiting H3K36-directed methyltransferases. Paradoxically, we find that expression of the H3K36M oncohistone unexpectedly inhibits tumor formation in KRAS-driven lung adenocarcinoma by inducing a potent immune-mediated tumor clearance. Mechanistically, oncohistone expression derepresses endogenous retroviral element transcription, results in the accumulation of double-stranded RNA (dsRNA), and activates an innate antiviral-like immune response that eradicates tumor growth. Surprisingly, while inactivation of the H3K36 di-methyltransferase NSD2 replicated all effects of oncohistone expression, inactivation of the H3K36 tri-methyltransferase SETD2 abolished element derepression and all associated downstream anti-cancer effects that are induced by oncohistone expression. These observations restructure our understanding of the roles of H3K36 methylation, the consequences of its deregulation in cancer, and shape our expectations for therapeutic interventions targeting H3K36 methyltransferases.
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2. ⭐ GSE334916 组蛋白3赖氨酸甲基转移酶的拮抗作用决定肿瘤免疫监视

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、histone
• 📝 描述：Contributors : Amy C Gladstein ; Akino Mercy Charles Solomon ; Carson D Poltorack ; Sharan Venkatesh ; Keren M Adler ; Maggie R Robertson ; Stephanie Stransky ; Valerie M Irizarry-Negron ; Dain A Ruiz ; Dingwen Tao ; Nelson F Freeburg ; Simone Sidoli ; Irfan A Asangani ; Sydney M Shaffer ; David M FeldserSeries Type : OtherOrganism : Mus musculusHistone H3 lysine 36 (H3K36) methyltransferases are recurrently altered in cancer, but how distinct H3K36 methylation states influence tumorigenesis remains incompletely understood. Using KRAS-driven lung cancer models, we show that NSD2, SETD2, and EZH2 form an epigenetic circuit that regulates endogenous retroviral elements (ERVs) and tumor immune surveillance. Although SETD2 is a potent tumor suppressor in KRAS-driven lung adenocarcinoma, expression of the H3K36M oncohistone, which broadly inhibits H3K36 methylation, does not phenocopy Setd2 loss. Instead, H3K36M expression suppresses tumor growth by reducing H3K36me2, derepressing ERV transcripts, inducing cytoplasmic dsRNA, and activating RIG-I/MDA5-dependent antiviral-like immune clearance. Genetic inactivation of histone dimethyltransferase Nsd2 phenocopies H3K36M expression, nominating H3K36me2 loss as a trigger of this viral-mimicry response. In Setd2-deficient contexts, EZH2-dependent H3K27me3 restores ERV repression, prevents dsRNA accumulation, and permits immune escape. Pharmacologic inhibition of NSD2 induces dsRNA in human lung adenocarcinoma cells, whereas concurrent SETD2 inhibition blunts this response while additional EZH2 inhibition restores it. These findings define opposing roles for NSD2- and SETD2-dependent H3K36 methylation in lung tumor immunity and reveal an NSD2–SETD2–EZH2 axis that can be targeted to modulate viral mimicry and immune surveillance in cancer.
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3. ⭐ GSE303917 靶向调控神经元-癌细胞-免疫细胞三方串扰可增强化疗和免疫疗法的疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Dolly Jain ; Nishant Pandey ; Somesh K Jha ; Shreya Sinha ; Ragini Singh ; Junaid Alam ; Bharti Aggarwal ; Neelam Chauhan ; Arunima Acharya ; Anu P V ; Vandana Dhangar ; Ritika Bhargava ; Nikhil K Chourasiya ; Ali Khan ; Arnab K Sahoo ; Debasish Nath ; Lalita Mehra ; Kajal Rana ; Poonam Yadav ; Jahanvi Ralhan ; Saroj Rajput ; Ashish Pal ; Arindam Maitra ; Shantiswarup Singha ; Rajesh Panwar ; Satish Khurana ; Ujjaini Dasgupta ; Sandeep K Bhoriwal ; Jyoti S Prabhu ; Prasenjit Das ; Veena S Patil ; Avinash BajajSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNeurotransmitter-mediated crosstalk between nerve fibers, cancer cells, and immune cells in the tumor microenvironment (TME) have been shown to promote cancer progression and immunosuppression. While there are extensive reports on sympathetic nerve fibers, effect of parasympathetic neurons on cancer progression and immunosuppression still remains elusive. In colorectal cancer tissues, we observed presence of cholinergic parasympathetic nerve fibers near tumor stroma and elevated acetylcholine levels as compared to adjacent normal. To disrupt this crosstalk, we used Bupivacaine (BUP), an FDA-approved local anesthetic, delivered via a hydrogel (BUP-Gel) for localized release. BUP-Gel inhibited tumor growth across multiple murine models. Further, single cell RNA analysis revealed reshaping of TME, enhancing M1-like macrophages and cytotoxic T-cell activation. Additionally, BUP-Gel therapy amplified the efficacy of systemic chemotherapy, immune checkpoint blockade, and adoptive T-cell therapy. These findings highlight localized cholinergic inhibition as a promising therapeutic strategy.
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4. ⭐ GSE338984 肿瘤靶向一氧化氮纳米疗法克服索拉非尼耐药性并重编程肝细胞癌的抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immunity、resistance
• 📝 描述：Contributors : Chen Yunching ; Yang ShengSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTherapeutic responses in hepatocellular carcinoma (HCC) are often limited by resistance-associated survival signaling and immune escape. Resistance to sorafenib, a first-line tyrosine kinase inhibitor (TKI) for advanced HCC, has been associated with activation of the AKT–mTOR pathway, suggesting that suppression of this axis may improve therapeutic efficacy. Here, we developed NanoNOSOR, an HCC-targeted SP94 peptide-functionalized lipid–PLGA nanoplatform for tumor-targeted, pH-responsive co-delivery of the nitric oxide donor DNIC and sorafenib. DNIC sensitized murine and human HCC cells to sorafenib by suppressing AKT–mTOR signaling. Co-loading DNIC and sorafenib into SP94-functionalized nanoparticles enhanced HCC cell uptake, promoted pH-responsive payload release, and achieved synergistic AKT–mTOR pathway suppression and cytotoxicity in vitro. In orthotopic HCC-bearing mice, NanoNOSOR preferentially accumulated in tumors and showed superior antitumor activity over single-agent nanoparticle formulations, as indicated by suppression of primary tumor growth and lung metastasis, together with increased tumor cell apoptosis. This antitumor effect was accompanied by transcriptional remodeling of the tumor microenvironment, with reduced proliferation-associated programs and increased immune-activation pathways. In addition, NanoNOSOR-mediated AKT–mTOR axis suppression downregulated PD-L1 immune checkpoint expression and enhanced intratumoral CD8⁺ T-cell infiltration and activation, linking tumor-intrinsic pathway inhibition to reduced immune escape. Biosafety analysis showed no overt hepatotoxicity, nephrotoxicity, or major organ damage. Together, these findings establish NanoNOSOR as a tumor-targeted NO–TKI co-delivery strategy that enhances therapeutic response and reprograms the HCC tumor microenvironment, providing a potential nanotherapeutic platform for overcoming therapeutic resistance in HCC.
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5. ⭐ GSE312794 CD73抑制可克服前列腺癌模型中PARP抑制引起的适应性免疫抵抗

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、resistance
• 📝 描述：Contributors : Ping Xie ; Renqiang Ma ; Minghui Zhang ; Jie Fan ; Hui Tang ; longzhen Song ; Bin ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMetastatic castration-resistant prostate cancer (mCRPC) remains a major cause of cancer-related mortality in the male population. While poly(ADP-ribose) polymeraseinhibitors (PARPi) are approved for selected mCRPC patients with homologous recombination repair (HRR) deficiencies, combinations with PD-1/PD-L1 inhibitors immunotherapy have demonstrated limited efficacy in unselected populations. To investigate the immunomodulatory effects of PARPi in an unbiased manner, we performed bulk RNA sequencing on HRR-proficient MyC-CaP cells treated with PARPi Olaparib or control vehicle. Pathway enrichment analysis revealed a marked upregulation of CD73 (NT5E), an emerging immune checkpoint ectoenzyme that generates extracellular adenosine, suggesting an adaptive mechanism that undermines PARPi efficacy and enables unwanted immunosuppression. CD73 induction by PARPi was confirmed in both human and mouse prostate cancer cell lines, with more pronounced effects in the HRR-compromised PTEN knock-out (KO) cells. Mechanistically, Olaparib-driven CD73 expression was mediated through the DNA damage-activated ATR-CHEK1-IRF1 and TGF-β1-ΑΚΤ signaling pathways. Concurrently, PARPi enhanced tumor cell immunogenicity by activating the type I interferon pathway and antigen presentation machinery. In vivo, combining Olaparib with CD73 blockade therapy delayed tumor growth, improved T-cell infiltration, and augmented antigen-specific CD8⁺ T-cell effector function across HRR-proficient and PTEN KO prostate cancer models. These findings highlight PARPi-induced CD73 upregulation as a novel resistance mechanism and support PARPi plus CD73 blockade as a promising therapeutic strategy for mCRPC, irrespective of HRR status.
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6. GSE337533 早期B细胞发育过程中转录和免疫球蛋白库演化的单细胞图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell、single-cell
• 📝 描述：Contributors : Charlotte DiBiase ; Jonathan Hurtado ; Bryan BrineySeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensThe development of human B cells in the bone marrow can be separated into functionally and transcriptionally distinct subsets, which while canonically described have yet to be profiled deeply and individually and with NGS and bioinformatic techniques. In this study, single-cell RNA sequencing was performed on 65,110 B cells from six healthy donors to observe the foundation of the diversity observed in mature immune repertoires. Following the established narrative of development, committed B cells undergo heavy and light chain recombination, which together form the functional BCR. However, a granular per-subset phenotypic analysis reveals proliferative bursts following each recombination event, an aspect of BCR recombination previously undescribed in the pro-B phase of development. Heavy and light chain pairing becomes more similar to that of mature, circulating B cells with progress through lymphopoiesis, deleting features associated with autoreactivity. Prominent among these repertoire alterations is a substantial shortening of heavy chain CDR3s, and changes in V, D, and J gene usage. This study provides a detailed snapshot of the transcriptomic and repertoire genetics landscape of developing B cells, providing a deeper understanding of the repertoire-shaping influence of early selection processes, and introducing new avenues for repertoire development research.
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7. GSE338797 产前炎症使肺部免疫细胞对产后高氧诱导的肺损伤更加敏感

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、inflammation
• 📝 描述：Contributors : Anabalagan Saminathan ; Papah Michael B ; Glazewski Lisa ; Hesek Anne ; Karl Franke ; Erin Crowgey ; Alapati DeepthiSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusBronchopulmonary dysplasia (BPD) arises from a combination of prenatal and postnatal environmental factors, but the impact of prenatal inflammation on subsequent postnatal lung injury remains unclear. We aimed to investigate how prenatal lipopolysaccharide (LPS)-induced chorioamnionitis alters the composition of resident pulmonary immune cells and modifies the response to hyperoxia-induced lung injury in neonatal rats. Pregnant Sprague-Dawley rats received intra-amniotic injections of LPS or normal saline (NS) at embryonic day 20. Pups were euthanized on postnatal day 1 (P1) or exposed to 85% oxygen (O₂) or room air (RA) for 14 days and euthanized on postnatal day 14 (P14) for analysis. Resident pulmonary immune cells were quantified by flow cytometry. Mann–Whitney and ANOVA tests were used for group comparisons (p<0.05). mRNA from pulmonary immune cells collected on P1 was subjected to RNA sequencing and differential gene expression analysis. On P1, prenatal LPS exposure did not change the overall percentage of CD45⁺ pulmonary immune cells but decreased the percentages of CD3⁺CD4⁺ T cells, CD3⁺CD8⁺ T cells, and CD45R⁺ B cells compared with the NS+RA group. In contrast, CD161⁺ NK cells and CD43⁺ monocytes were significantly increased. Upregulated genes were enriched in inflammatory biological processes. By P14, cell composition in the LPS+RA group normalized. However, a second insult with postnatal hyperoxia resulted in an increased proportion of CD161⁺ NK cells in the LPS+O₂ group only and an increased proportion of CD43⁺ monocytes in the NS+O₂ group only, with a relative reduction in monocytes in the LPS+O₂ group at P14. In this rat model of BPD, LPS-mediated in-utero inflammation primes neonatal lung immune cells for a dysregulated response to postnatal hyperoxia. Dual prenatal and postnatal injuries result in persistent elevation of NK cells and reduction of monocytes, while other immune subsets respond differentially, suggesting that prenatal events condition the neonatal lung immune system in ways that may influence BPD pathogenesis.
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8. GSE308570 果蝇 Rumpelstiltskin 改变 Polycomb 染色质关联，并维持 Homie 绝缘子的正确 3D 基因组组织和屏障活性 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genome
• 📝 描述：Contributors : Savanna F Lyda ; Catherine E McManus ; Juan Manuel Caravaca ; Dagyeong Yang ; Yuejun Wang ; Hernan A Lorenzi ; Fedor Kouzine ; David Levens ; Leah F Rosin ; Elissa P LeiSeries Type : Expression profiling by high throughput sequencingOrganism : Drosophila melanogasterThree-dimensional genome organization is maintained in part by chromatin insulators, DNA-protein complexes that create boundaries between active and inactive chromatin and regulate enhancer-promoter interactions. In Drosophila, the Homing insulator at eve (Homie) sequence prevents repressive Polycomb (PcG) chromatin at even-skipped (eve) from spreading into the neighboring essential gene, TER94. Use of an in vivo reporter assay identified the requirement of the hnRNP M homolog, Rumpelstiltskin (Rump), for Homie barrier activity. Interestingly, Rump depletion resulted in no changes to chromatin insulator protein binding at Homie but extensive chromatin association changes to the Polycomb response element (PRE)-associated protein Crooked legs (Crol) at Crol-bound PREs. Furthermore, global chromatin association changes were detected for a subset of Polycomb repressive complex 1 and 2 (PRC1 and PRC2) components. Finally, we observed increased cis-compaction within the eve PcG domain and increased distances between eve and other PcG domains in trans after Rump depletion. These data suggest a regulatory role of Rump for both cis and trans interactions of PcG proteins, likely promoting Homie barrier activity independently of chromatin insulator proteins.
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9. GSE308569 果蝇 Rumpelstiltskin 改变 Polycomb 染色质关联，并维持 Homie 绝缘子的正确 3D 基因组组织和屏障活性 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Savanna F Lyda ; Catherine E McManus ; Juan Manuel Caravaca ; Dagyeong Yang ; Yuejun Wang ; Hernan A Lorenzi ; Fedor Kouzine ; David Levens ; Leah F Rosin ; Elissa LeiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Drosophila melanogasterThree-dimensional genome organization is maintained in part by chromatin insulators, DNA-protein complexes that create boundaries between active and inactive chromatin and regulate enhancer-promoter interactions. In Drosophila, the Homing insulator at eve (Homie) sequence prevents repressive Polycomb (PcG) chromatin at even-skipped (eve) from spreading into the neighboring essential gene, TER94. Use of an in vivo reporter assay identified the requirement of the hnRNP M homolog, Rumpelstiltskin (Rump), for Homie barrier activity. Interestingly, Rump depletion resulted in no changes to chromatin insulator protein binding at Homie but extensive chromatin association changes to the Polycomb response element (PRE)-associated protein Crooked legs (Crol) at Crol-bound PREs. Furthermore, global chromatin association changes were detected for a subset of Polycomb repressive complex 1 and 2 (PRC1 and PRC2) components. Finally, we observed increased cis-compaction within the eve PcG domain and increased distances between eve and other PcG domains in trans after Rump depletion. These data suggest a regulatory role of Rump for both cis and trans interactions of PcG proteins, likely promoting Homie barrier activity independently of chromatin insulator proteins.
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10. GSE293116 野生型、TREM2 敲除、GPR34 敲除或 TREM2/GPR34 双敲除野生型和 APP 敲入小鼠（17 个月）原代小胶质细胞的单细胞转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptome
• 📝 描述：Contributors : Karthik Raju ; Sophia M Guldberg ; David Tatarakis ; Shan V Andrews ; Connie Ha ; Thomas Sandmann ; Joseph W Lewcock ; Jim Ray ; Kathryn M MonroeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMicroglia are broadly implicated in modifying disease risk in the central nervous system (CNS). Identifying regulators of microglia state is critical for elucidating their role in disease and identifying novel drug targets. GPR34 is a G-protein coupled receptor expressed in homeostatic microglia where its function is not well understood. Like TREM2, GPR34 detects lipid ligands. In both healthy and amyloid mouse models, Gpr34 KO accelerated microglial state transcriptionally and histologically consistent conversion of homeostatic microglia to a disease-associated microglia (DAM) state. Shifts in microglial state were accompanied by increased expression of multiple metabolic gene sets.
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1. ⭐ scCap——基于单细胞RNA测序数据的知识增强聚类方法的无注释表型预测

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、clustering
• 📝 描述：RNA sequencing combined with annotation-free artificial intelligence improved phenotype prediction by identifying disease-associated cell populations without relying on predefined…
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2. 科学家在海洋中最难以捉摸的鲸鱼之一体内发现了神秘细菌

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Scientists studying decades of pygmy sperm whale strandings have uncovered three previously unknown types of Helicobacter bacteria hiding in the animals’ stomachs. All four infected whales showed serious digestive damage, including inflammation, ulcers, scarring, and parasite infestations, although the bacteria were not confirmed as the cause of death.
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3. 新型抗体药物可阻止侵袭性前列腺癌扩散

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、antibody
• 📝 描述：Scientists have developed a fully human antibody that halted the growth and spread of aggressive prostate cancer in preclinical research. Although more testing is needed, the drug’s unusual mechanism could open the door to a safer new treatment for advanced cancer.
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4. DNA和RNA测序揭示了导致严重早期儿童龋齿的真正罪魁祸首

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing identified metabolically active bacteria driving severe early childhood caries, revealing Lactobacillus casei as a major contributor to dentin lesion progression…
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• GSE293041 野生型、TREM2 敲除、GPR34 敲除或 TREM2/GPR34 双敲除野生型和 APP 敲入小鼠（8 个月）原代小胶质细胞的单细胞转录组分析
• GSE293040 对野生型、TREM2 敲除、GPR34 敲除或 TREM2/GPR34 双敲除的野生型和 APP 敲入小鼠（4 个月）的原代小胶质细胞进行单细胞转录组分析
• GSE279603 疾病定义性催化失活蛋白激酶 C α 突变通过显性负性机制驱动脊索样胶质瘤的发生
• GSE274126 时间戳追踪描绘天然条件下胸腺调节性 T 细胞的个体发育 [RNA-seq]
• GSE274125 时间戳追踪描绘了天然条件下胸腺调节性 T 细胞的个体发育 [scRNA-seq]
• GSE339049 研究发现，重度长新冠是由单核细胞重编程和与疱疹病毒激活相关的广泛免疫失调驱动的。
• GSE338779 骨关节炎对照患者滑液细胞的单细胞RNA测序
• GSE274117 常见变异型免疫缺陷患者淋巴结中细胞毒性 CD4 T 细胞簇的扩增
• GSE339344 EBNA1特异性CD4+ T细胞将遗传风险与多发性硬化症的免疫病理联系起来
• GSE325054 时间分辨多组学鉴定 mRNA 疫苗接种即时反应的生物标志物 [RNA-Seq]
• GSE323995 CReP 介导的 eIF2a 磷酸化控制是高危髓母细胞瘤的中心节点 [RNA-Seq 3]
• GSE305969 整合单细胞分析揭示多发性骨髓瘤的恶性原型和增殖层级 [第 3 部分（共 4 部分）：Illumina NovaSeq 6000；MARS_v2]
• GSE305968 整合单细胞分析揭示多发性骨髓瘤的恶性原型和增殖层级 [第 2 部分（共 4 部分）：Illumina NextSeq 500；MARS]
• GSE305967 整合单细胞分析揭示多发性骨髓瘤的恶性原型和增殖层级 [第 1 部分（共 4 部分）：Illumina NovaSeq 6000；MARS]
• GSE297713 T细胞受体γδ是独特组织监视机制的关键实时决定因素
• GSE212322 链霉菌（Streptomyces clavuligerus）抗生素生产菌株驯化过程中的基因组进化
• GSE183780 时间分辨转录组学和基因网络分析揭示了黑杨根系中脱落酸信号传导的主要靶标
• GSE339326 通过上下文匹配的扰动特征对活性蛋白质组进行建模
• GSE328214 小鼠小胶质细胞单细胞分析，携带小鼠 Nlrp3 野生型基因座、人类 NLRP3 野生型敲入基因或人类 NLRP3 D305N 变体敲入基因。
• GSE327449 造血干细胞的异质性使其能够适应衰老的微环境 [scRNA-seq]
• GSE325266 果蝇 Rumpelstiltskin 改变 Polycomb 染色质关联，并维持 Homie 绝缘体的正确 3D 基因组结构和屏障活性
• GSE324215 人类腓肠神经小RNA测序
• GSE318645 双重免疫检查点阻断在复发性胶质母细胞瘤中诱导不同的全身性和肿瘤内免疫激活
• GSE308884 研究表明，可穿透中枢神经系统的 NLRP3 抑制剂 TN-783 能够实现持久的体重减轻，并逆转饮食诱导肥胖症中的下丘脑炎症。
• GSE293117 GPR34 功能缺失可挽救 TREM2 代谢功能障碍并促进反应性小胶质细胞状态
• GSE293037 对野生型、TREM2 敲除型、GPR34 敲除型或 TREM2/GPR34 双敲除型 iPSC 衍生的人类小胶质细胞进行批量转录组分析，这些小胶质细胞分别用 PBS 或髓鞘处理。
• GSE291963 CCR8 在调节性 T 细胞上的表达揭示了组织适应的轨迹并能预防心肌梗死 [scRNA-seq]
• GSE291962 CCR8 在调节性 T 细胞上的表达揭示了组织适应的轨迹并能预防心肌梗死 [bulk RNA-seq]
• GSE339098 野生型和 Gata2；Mx1-Cre 杂合子 HSC 的下一代测序
• GSE310229 利用大鼠单核测序技术鉴定和验证中央杏仁核FGFR1作为酒精使用障碍的治疗靶点
• GSE338987 条纹跳甲（Phyllotreta striolata）的发育阶段和性别特异性转录组
• GSE334049 黑色素瘤来源的外泌体 miRNA 和角质形成细胞来源的 LL-37 定义了黑色素瘤中表皮与肿瘤之间的军备竞赛
• GSE328737 成年小鼠脑微血管碎片的 RNA 测序
• GSE324154 治疗诱导的衰老通过降低 EZH2 活性促进急性髓系白血病的免疫原性
• GSE313643 采用 Smart-seq2 方法对小鼠脑微血管片段进行单细胞 RNA 测序
• GSE311449 利用 Smart-seq2 方法对小鼠脑血管细胞进行单细胞 RNA 测序