详细内容（前10条）

1. ⭐ GSE317984 靶向癌视网膜抗原PDE6G的mRNA-LNP疫苗可诱导针对乳腺癌的强效抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、vaccine、antigen
• 📝 描述：Contributors : Yue Zhao ; Yichun Pan ; Wei Zhang ; Zhao ZuoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe development of effective mRNA vaccines for breast cancer has been constrained by the lack of highly immunogenic and tumor-specific antigens. Here, we identify PDE6G, an immune-privileged retina-enriched antigen aberrantly overexpressed in breast tumors, and develop a PDE6G mRNA-LNP vaccine. Vaccination elicited robust CD8+ T cell responses, promoted clonal expansion of effector and IFN-competent T cell subsets, and suppressed tumor growth without detectable toxicity. Single-cell RNA sequencing (scRNA-seq) revealed that vaccination of PDE6G mRNA-LNP reshapes the tumor immune microenvironment (TIME) by expanding antigen-presenting Cd74+ tumor-associated macrophages (TAMs) while reducing immunosuppressive Maf+ macrophages, and enhancing crosstalk between macrophages and CD8+ T cells. Moreover, combining PDE6G mRNA-LNP with PD-1 blockade further improved anti-tumor efficacy. These findings establish cancer-retina antigens as promising vaccine targets and demonstrate that PDE6G mRNA-LNP coordinates adaptive immunity and tumor microenvironment remodeling, providing a safe and potent strategy for breast cancer immunotherapy.
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2. ⭐ GSE287028 PDGFC 通过自分泌激活 RAP1-MAPK 通路促进前列腺癌产生恩扎卢胺耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、pathway
• 📝 描述：Contributors : Bingqian Deng ; Saipeng Chen ; Dan Zhong ; Guojing SongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensProstate cancer (PCa) is a highly heterogeneous malignant tumor within the male genitourinary system, characterized by its invasive and metastatic potential. Although the second-generation androgen receptor (AR) antagonist enzalutamide has shown therapeutic efficacy in PCa patients, enzalutamide resistance (EnzaR) will be inevitably develops and the underlying mechanisms are not fully understood. In this study, we confirmed that the expression of Platelet-Derived Growth Factor C (PDGFC) elevated in EnzaR PCa and promoted the proliferation of PCa in vitro and in vivo. Silencing PDGFC in EnzaR cells notably enhances the sensitivity of EnzaR PCa cells to enzalutamide, thereby inhibiting the progressive of PCa. Mechanistically, overexpressed PDGFC activates the PDGFR-RAP1-MAPK signaling cascade in an autocrine fashion within EnzaR cells. PDGFR inhibitors alone or combined with enzalutamide significantly suppressed the progression of EnzaR PCa xenografts. Additionally, we demonstrated that the transcription factor STAT4 binds to a specific DNA sequence in the PDGFC promoter region, which is essential for PDGFC upregulation. Collectively, our results confirmed the pivotal role of PDGFC in PCa cells developing resistant to enzalutamide therapy, suggesting that targeting PDGFC may serve as a promising therapeutic strategy for EnzaR PCa.
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3. GSE317951 PI3δγ激酶和IFN-γ通路，是在一项无偏激酶药物筛选中发现的，是细胞因子释放综合征的关键介质。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、kinase
• 📝 描述：Contributors : Amatya Parmeshwar ; O’Neal Julie ; Jayasinghe Reyka ; DiPersio JohnSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChimeric Antigen Receptor T (CAR-T) cell therapy can induce cytokine release syndrome (CRS), which ranges clinically from mild to life-threatening, and is universally characterized by elevation of multiple cytokines, including IL-6. To clarify mechanisms underlying CRS and identify potential new therapeutic agents, we screened a protein kinase inhibitor library using an in vitro model system where CART19 cells were co-cultured with CD19+ tumor target cells and cytokine-primed myeloid cells (pMC), and secreted IL-6 levels serving as the CRS readout. We identified duvelisib, a dual PI3Kdg inhibitor, which blocked pMC IL-6 secretion in in vitro and in vivo without negative impact on CART19 cell function. Immunophenotyping showed increased activation markers on CART19 cells CD137+(4-1BB); CD279+ (PD-1) and pMC cells (CD83+CD86+) when cultured with tumor target cells compared to cultures without target cells; these activation phenotypes were reduced in the presence of duvelisib. Single-cell RNA sequencing analyses identified four transcriptional clusters of pMCs. Among these, the activated pMC1 subset was the primary source of IL-6 expression, which was effectively reduced by duvelisib and by ruxolitinib, a JAK1/2 kinase inhibitor known to block CRS. Transcriptionally, IFNG expression in CART19 cells was significantly downregulated in the presence of duvelisib and ruxolitinib, and cell-cell communication between CART19 cells and pMCs suggests different mechanisms of action for the two inhibitors. Finally, pMC IL-6 production was significantly reduced by CRISPR/Cas9 deletion of IFNG in CART19 cells, the IFN-g receptor in pMC, or treatment with duvelisib which blocks both IFN-g production by CART19 and IFN-g receptor signaling. Our studies suggest that targeting PI3dg and IFN-g signaling pathways reduce CRS without altering CAR-T cell function.
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4. GSE308376 ACTB甲基化调控SMARCA4基因组占位，从而促进翻译并降低结直肠癌细胞的黏附性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、methylation
• 📝 描述：Contributor : Elina Abeav-SchneidermanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensACTB is a cytoskeletal protein involved in intracellular trafficking. In recent years, it has become evident that, in addition to its established roles in these compartments, ACTB also participates in the regulation of transcription. However, the molecular mechanisms underlying this function remain poorly understood. The methyltransferase SETD3 has previously been shown to methylate ACTB at H73, thereby regulating ACTB polymerization and smooth muscle contraction. Here, we show that the genomic distribution of ACTB is SETD3-dependent and that this regulation modulates the transcription of genes involved in cell adhesion and mRNA translation in colorectal cancer cells. Proteomic analyses reveal that ACTB and SETD3 interact with multiple large protein complexes, including complexes associated with transcriptional regulation. Specifically, we demonstrate that SETD3-mediated ACTB methylation is required for the co-localization of SMARCA4, a subunit of the SWI/SNF BAF complex, at specific genomic loci. Genomic analyses further show that this co-localization enables the coordinated occupancy of SMARCA4 and H73-methylated ACTB at genes involved in cell adhesion and mRNA translation. Finally, phenotypic assays confirm these regulatory effects. Together, these findings uncover a new mechanistic layer of selective transcriptional regulation mediated by an ACTB–SETD3–SMARCA4 axis in colorectal cancer cells.
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5. GSE308375 ACTB甲基化调控SMARCA4基因组占位，从而促进翻译并降低结直肠癌细胞的黏附性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、methylation
• 📝 描述：Contributor : Abeav-Schneiderman ElinaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensACTB is a cytoskeletal protein involved in intracellular trafficking. In recent years, it has become evident that, in addition to its established roles in these compartments, ACTB also participates in the regulation of transcription. However, the molecular mechanisms underlying this function remain poorly understood. The methyltransferase SETD3 has previously been shown to methylate ACTB at H73, thereby regulating ACTB polymerization and smooth muscle contraction. Here, we show that the genomic distribution of ACTB is SETD3-dependent and that this regulation modulates the transcription of genes involved in cell adhesion and mRNA translation in colorectal cancer cells. Proteomic analyses reveal that ACTB and SETD3 interact with multiple large protein complexes, including complexes associated with transcriptional regulation. Specifically, we demonstrate that SETD3-mediated ACTB methylation is required for the co-localization of SMARCA4, a subunit of the SWI/SNF BAF complex, at specific genomic loci. Genomic analyses further show that this co-localization enables the coordinated occupancy of SMARCA4 and H73-methylated ACTB at genes involved in cell adhesion and mRNA translation. Finally, phenotypic assays confirm these regulatory effects. Together, these findings uncover a new mechanistic layer of selective transcriptional regulation mediated by an ACTB–SETD3–SMARCA4 axis in colorectal cancer cells.
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6. GSE279149 CUL5 E3泛素连接酶通过抑制自噬来调节膀胱癌细胞逃避CD8+ T细胞介导的杀伤作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell
• 📝 描述：Contributors : Xincheng Gao ; Hui Zhang ; Guosong JiangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCD8+ T cells are capable of specifically targeting and eliminating malignant tumor cells, but tumor cells can develop resistance mechanisms to escape CD8+ T cell-mediated killing. Here, we performed a whole genome CRISPR-Cas9 knockout screen under CD8+ T cells pressure and identified the E3 ubiquitin ligase CUL5 as an essential factor required for escaping CD8+ T cells killing in bladder cancer cells. We found that CUL5 knockout promoted the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing both in vivo and in vitro. Mechanistically, CUL5 loss reduced the ubiquitination of PTBP1, which regulated alternative splicing of RUBCN pre-mRNA and led to an increase in the levels of the RUBCN-S isoform, thereby preventing immune evasion of bladder cancer cells by inhibiting autophagy. Importantly, CUL5 knockout significantly enhanced the efficacy of anti-PD-1 immunotherapy in a xenograft model. Collectively, these findings reveal a novel mechanism of bladder cancer immune evasion, providing potential targets for cancer immunotherapy.
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7. GSE317479 正常脂肪饮食和高脂肪饮食条件下小鼠心脏的单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Junichi Sadoshima ; Shin-ichi Oka ; Eun-Ah Sung ; Alexander Lemenze ; Mainul HoqueSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate transcriptional changes in the heart induced by diet, we performed single-cell RNA sequencing on pooled mouse hearts from normal fat diet (NFD, 10% kcal fat) and high fat diet (HFD, 60% kcal fat) groups using the Parse Biosciences Evercode WT Mini v3 kit.
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8. GSE307881 体外受精诱导雌性小鼠后代过早出现生殖衰老和多代表观遗传改变

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、epigenetic
• 📝 描述：Contributors : Eric A Rhon-Calderon ; Cassidy N Hemphill ; Alexandra J Savage ; Christopher J Krapp ; Zhengfeng Liu ; Laren Riesche ; Richard M Schultz ; Marisa S BartolomeiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIn vitro fertilization (IVF) is an assisted reproductive technology that has enabled millions of births. Although considered safe, emerging evidence suggests that IVF may have long-term health adverse outcomes in offspring, though its impact on female reproduction, especially on reproductive aging is largely unknown. Here, we use a mouse model to investigate how IVF influences female reproductive and transgenerational health outcomes. We assessed IVF-conceived fetal (E18.5) and adult (12-week and 39-week) female offspring, identifying alterations in ovarian-to-body weight ratios, ovarian morphology, serum sex hormone levels, and transcriptomic and DNA methylation profiles in ovaries, oocytes, and cumulus cells, consistent with biomarkers of accelerated reproductive aging. The offspring of IVF females and wild-type males exhibited altered fetal-to-placental weight ratios, placental morphology, and dysregulated placental gene expression. At 12-weeks-of-age, offspring showed increased body weight, disrupted lipid and glucose metabolism, and transcriptomic and epigenetic changes in liver and reproductive organs. Our results highlight the need for deeper mechanistic understanding of assisted reproduction’s long-term and multigenerational impacts on female reproductive health.
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9. GSE304224 PU.1 激活的基因组区域定义了以免疫失调和疾病进展为特征的低风险 MDS 亚群 [MDS-L ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、ChIP-seq
• 📝 描述：Contributors : Veronica Vallelonga ; Francesco Gandolfi ; Matteo Zampini ; Elena Riva ; Giulia Maggioni ; Denise Ventura ; Elena Saba ; Alberto Termanini ; Sara Polletti ; Elena Prosperini ; Laura Crisafulli ; Alessia Campagna ; Ivan Ferrari ; Nicole Pinocchio ; Gabriele Todisco ; Michela Calvi ; Clara Di Vito ; Domenico Mavilio ; Francesca Ficara ; Matteo Giovanni Della Porta ; Serena GhislettiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMyelodysplastic syndromes (MDS) are heterogeneous myeloid neoplasms with an increased risk of progression to secondary acute myeloid leukemia (sAML). This study investigates the genomic correlates of disease progression in MDS by profiling active genomic regulatory regions and their transcriptional impact through H3K27ac ChIP-seq and RNA-seq analysis on CD34+ bone marrow progenitors cells isolated from a prospective cohort of 86 and 357 patients, respectively. Our analysis revealed distinct patterns of genomic region activation and transcriptional regulation across different disease stages (low-risk MDS, high-risk MDS and sAML). Unexpectedly, unsupervised clustering revealed a subset of low-risk MDS patients displaying regulatory and transcriptional profiles similar to those of high-risk MDS and sAML, highlighting early molecular events that may predispose patients to disease progression. This subset is characterized by PU.1 genomic occupancy in regions linked to immune and inflammatory responses, increased T-cell and NK activation, and a higher frequency of SRSF2 mutations. Clinically, patients in this group exhibit greater susceptibility to infections and cardiovascular events, along with an elevated risk of disease progression, resulting in a significantly reduced overall survival. Functional studies demonstrate that PU.1 inhibition suppresses MDS cell proliferation and clonogenicity, as impaired PU.1 binding inhibits the activation of key transcriptional programs involved in disease advancement. Collectively, these findings identify epigenetic factors that predispose low-risk MDS patients to progression into high-risk MDS and, ultimately, sAML. Moreover, they provide proof of concept for targeting PU.1 as a potential strategy to prevent disease progression in low-risk MDS.
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10. GSE303742 PU.1 激活的基因组区域定义了以免疫失调和疾病进展为特征的低风险 MDS 亚群 [MDS-L RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、RNA-seq
• 📝 描述：Contributors : Veronica Vallelonga ; Francesco Gandolfi ; Matteo Zampini ; Elena Riva ; Giulia Maggioni ; Denise Ventura ; Elena Saba ; Alberto Termanini ; Sara Polletti ; Elena Prosperini ; Laura Crisafulli ; Alessia Campagna ; Ivan Ferrari ; Nicole Pinocchio ; Gabriele Todisco ; Silvia Pedretti ; Michela Calvi ; Clara Di Vito ; Domenico Mavilio ; Francesca Ficara ; Matteo Giovanni Della Porta ; Serena GhislettiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMyelodysplastic syndromes (MDS) are heterogeneous myeloid neoplasms with an increased risk of progression to secondary acute myeloid leukemia (sAML). This study investigates the genomic correlates of disease progression in MDS by profiling active genomic regulatory regions and their transcriptional impact through H3K27ac ChIP-seq and RNA-seq analysis on CD34+ bone marrow progenitors cells isolated from a prospective cohort of 86 and 357 patients, respectively. Our analysis revealed distinct patterns of genomic region activation and transcriptional regulation across different disease stages (low-risk MDS, high-risk MDS and sAML). Unexpectedly, unsupervised clustering revealed a subset of low-risk MDS patients displaying regulatory and transcriptional profiles similar to those of high-risk MDS and sAML, highlighting early molecular events that may predispose patients to disease progression. This subset is characterized by PU.1 genomic occupancy in regions linked to immune and inflammatory responses, increased T-cell and NK activation, and a higher frequency of SRSF2 mutations. Clinically, patients in this group exhibit greater susceptibility to infections and cardiovascular events, along with an elevated risk of disease progression, resulting in a significantly reduced overall survival. Functional studies demonstrate that PU.1 inhibition suppresses MDS cell proliferation and clonogenicity, as impaired PU.1 binding inhibits the activation of key transcriptional programs involved in disease advancement. Collectively, these findings identify epigenetic factors that predispose low-risk MDS patients to progression into high-risk MDS and, ultimately, sAML.
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1. ⭐ 单细胞RNA测序揭示了能够帮助塑造癌症免疫疗法的抗体产生免疫细胞。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、antibody、regex:immuno(logy|therapy|suppression)、scRNA
• 📝 描述：RNA sequencing and immune profiling reveal that IgG1-producing plasma cells support effective PD-1 immunotherapy responses by coordinating antibody and T cell activity in cancer patients…
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2. 一种已有20年历史的癌症疫苗或许是延长癌症患者生存期的关键。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、vaccine
• 📝 描述：Two decades after a breast cancer vaccine trial, every participant is still alive—an astonishing result for metastatic disease. Scientists found their immune systems retained long-lasting memory cells primed to recognize cancer. By enhancing a key immune signal called CD27, researchers dramatically improved tumor elimination in lab studies. The findings suggest cancer vaccines may have been missing a crucial ingredient all along.
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3. 长期饮酒与直肠癌发病率急剧上升有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Drinking heavily over many years is linked to a higher risk of colorectal cancer, especially rectal cancer, according to new research tracking U.S. adults for two decades. People who drank heavily throughout adulthood faced sharply higher risks than light drinkers. Former drinkers did not show increased cancer risk and had fewer precancerous tumors. The results suggest that quitting alcohol may help lower long-term cancer risk.
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4. 脑癌可能在医生发现之前数年就已经存在。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists in South Korea have discovered that one of the most common malignant brain tumors in young adults may begin years before a tumor can be seen. IDH-mutant glioma, long treated by removing visible tumor tissue, actually starts when normal-looking brain cells quietly acquire a cancer-linked mutation and spread through the brain’s cortex. Using advanced genetic mapping and animal models, researchers traced the cancer’s true origin to glial progenitor cells that appear healthy at first.
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5. 一种特洛伊木马式癌症疗法显示出惊人的效果

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists at Mount Sinai have unveiled a bold new way to fight metastatic cancer by turning the tumor’s own defenses against it. Instead of attacking cancer cells head-on, the experimental immunotherapy targets macrophages—immune cells that tumors hijack to shield themselves from attack. By eliminating or reprogramming these “bodyguards,” the treatment cracks open the tumor’s protective barrier and allows the immune system to flood in and destroy the cancer.
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• GSE298019 PU.1 激活的基因组区域定义了以免疫失调和疾病进展为特征的低风险 MDS 亚群 [RNA-seq]
• GSE297914 PU.1 激活的基因组区域定义了以免疫失调和疾病进展为特征的低风险 MDS 亚群 [ChIP-seq]
• GSE317927 胎儿生长受限小鼠海马小胶质细胞的单细胞RNA测序
• GSE317548 RUVBL2 转录调控胆囊癌细胞中的线粒体自噬通路
• GSE317515 库普弗细胞通过 VSIG4-CD5 相互作用校准 T 细胞反应促进肿瘤逃逸 [TCR-Seq]
• GSE317513 Kupffer 细胞通过 VSIG4-CD5 相互作用校准 T 细胞反应促进肿瘤逃逸 [bulkRNA]
• GSE317400 人类卵巢癌中CLDN6阳性实性区域和小簇区域的空间转录组分析
• GSE310853 CRAMP1 对组蛋白基因座内组蛋白 H1 表达的独特控制 [ChIP-seq]
• GSE310852 CRAMP1 对组蛋白基因座内组蛋白 H1 表达的独特控制 [ATAC-seq]
• GSE288459 肺免疫细胞群中结节病的单细胞转录组特征
• GSE288067 单细胞 RNA 测序结合多重免疫荧光探针揭示 MFAP5+ 成纤维细胞在胰腺导管腺癌微环境中的作用。
• GSE317696 人类性腺组织转录组分析（发表于《性别发育差异》期刊）
• GSE312455 酿酒酵母不同菌株中保守的 HOG 通路表现出令人惊讶的调控可塑性
• GSE317728 成年小鼠背根神经节胶质细胞单细胞转录组图谱鉴定出多能祖细胞
• GSE301514 ID3 缺陷改变 DSB 位点的染色质可及性并增强对 HDAC 抑制的敏感性 [ATAC-seq]
• GSE301513 ID3 缺陷改变 DSB 位点的染色质可及性并增强对 HDAC 抑制的敏感性 [RNA-seq]
• GSE298020 PU.1 激活的基因组区域定义了以免疫失调和疾病进展为特征的低风险 MDS 亚组。
• GSE297740 儿童B细胞印记会损害针对血凝素茎的抗体
• GSE289389 研究显示，系统性红斑狼疮的皮肤光反应以表皮炎症失调和炎症性髓系细胞浸润为特征。
• GSE301229 转谷氨酰胺酶 2 在脓毒症巨噬细胞活化过程中调节波形蛋白依赖性蛋白质稳态
• GSE279695 人类诱导多能干细胞来源的心肌细胞和畸胎瘤移植后的代谢变化
• GSE231494 猪肺对胸膜肺炎放线杆菌反应的单细胞图谱
• GSE317999 宫内生长受限对海马小胶质细胞转录组的影响
• GSE317924 宫内生长受限对海马小胶质细胞DNA甲基化的影响
• GSE317483 用钙调磷酸酶抑制剂处理的永生化人足细胞的 RNA 测序
• GSE316921 敲低肝内胆管癌（ICC）癌相关成纤维细胞（CAFs）中SLC2A1对正常和缺氧条件下内皮细胞出芽的影响
• GSE315861 靶向先天免疫抑制疗法与抗生素治疗复发性急性膀胱炎的比较
• GSE315735 NIH:OVCAR-3异种移植瘤中基因表达情况（载体或卡铂治疗）
• GSE315733 NIH:OVCAR-3 异种移植瘤中基因表达（载体或卡铂治疗）[进展]
• GSE314786 揭开 WRN 解旋酶的奥秘：结构解析揭示构象状态及 MSI-H 癌症药物研发的机遇
• GSE312730 Simtuzumab 可减弱 Loxl2 介导的细胞外基质重塑，并在 LMNA 突变诱导的扩张型心肌病中保护心脏功能
• GSE311986 一种基于CasRx的新方法鉴定出TRA2B是晚期前列腺癌中AR-V7的关键剪接调节因子
• GSE310913 CRAMP1 对组蛋白基因座内组蛋白 H1 表达的独特调控
• GSE310855 CRAMP1 对组蛋白基因座内组蛋白 H1 表达的独特控制 [BiSulfite-seq]
• GSE310854 RNA-seq 分析 CRAMP1 调控的基因表达
• GSE310036 piR-37524抑制后HCT116和HT29结直肠癌细胞的转录组分析
• GSE286977 鸡盲肠组织mRNA链特异性测序
• GSE286402 研究发现，BRAF抑制剂耐药性导致黑色素瘤对Chk1抑制剂敏感。