详细内容（前10条）

1. ⭐ GSE255516 通过体内 CRISPR 激活筛选肿瘤微环境调节剂，合理设计免疫基因治疗组合 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment、scRNA
• 📝 描述：Contributors : Feifei Zhang ; Ryan D Chow ; Chuanpeng Dong ; Emily He ; Lvyun Zhu ; Shan Xin ; Daniyal Mirza ; Yanzhi Feng ; Xinyu Ling ; Qin Han ; Sidi Chen ; Guangchuan WangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe hostile tumor microenvironment (TME) is major challenge for cancer immunotherapies. Here, we design and perform TME-targeted in vivo CRISPR activation (CRISPRa) screens to uncover factors that promote anti-tumor immunity, culminating in rationally designed immune gene therapy combinations. Through adeno-associated virus (AAV) delivery, we find that multiplexed activation of pooled immunoregulatory genes encoding antigen presentation, cytokine, and co-stimulation molecules (APCM) leads to enhanced anti-tumor immunity. A CRISPRa screen targeting APCM genes in metastatic tumors identifies CD80, TNFSF14, CXCL10, TNFSF18, TNFSF9, and IFNG as the top immunostimulatory candidates. Further optimization pinpoints 4-1BBL(TNFSF9) + IFNG + IL12B (4II) as a potent streamlined therapeutic combination. AAV delivered 4II has potent in vivo anti-tumor efficacy in multiple tumor models, by enhancing tumor antigen presentation while simultaneously promoting the infiltration, activation, and expansion of anti-tumor T cells. We further demonstrate that APCM therapy synergizes with CAR-T therapy against human solid tumors in vivo. CRISPRa screens and gene activation systems targeting APCM factors thus represent a powerful approach for rapid development of off-the-shelf immune gene therapies against solid tumors.
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2. ⭐ GSE255514 通过体内 CRISPR 激活筛选肿瘤微环境调节剂，合理设计免疫基因治疗组合 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment、RNA-seq
• 📝 描述：Contributors : Feifei Zhang ; Ryan D Chow ; Chuanpeng Dong ; Emily He ; Lvyun Zhu ; Shan Xin ; Daniyal Mirza ; Yanzhi Feng ; Xinyu Ling ; Qin Han ; Sidi Chen ; Guangchuan WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe hostile tumor microenvironment (TME) is major challenge for cancer immunotherapies. Here, we design and perform TME-targeted in vivo CRISPR activation (CRISPRa) screens to uncover factors that promote anti-tumor immunity, culminating in rationally designed immune gene therapy combinations. Through adeno-associated virus (AAV) delivery, we find that multiplexed activation of pooled immunoregulatory genes encoding antigen presentation, cytokine, and co-stimulation molecules (APCM) leads to enhanced anti-tumor immunity. A CRISPRa screen targeting APCM genes in metastatic tumors identifies CD80, TNFSF14, CXCL10, TNFSF18, TNFSF9, and IFNG as the top immunostimulatory candidates. Further optimization pinpoints 4-1BBL(TNFSF9) + IFNG + IL12B (4II) as a potent streamlined therapeutic combination. AAV delivered 4II has potent in vivo anti-tumor efficacy in multiple tumor models, by enhancing tumor antigen presentation while simultaneously promoting the infiltration, activation, and expansion of anti-tumor T cells. We further demonstrate that APCM therapy synergizes with CAR-T therapy against human solid tumors in vivo. CRISPRa screens and gene activation systems targeting APCM factors thus represent a powerful approach for rapid development of off-the-shelf immune gene therapies against solid tumors.
• 🔗 查看原文

3. ⭐ GSE230944 通过表观遗传学靶向 NPM1 促进心肌梗死后修复，重编程修复性巨噬细胞代谢 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、metabolism、cardiac、RNA-seq
• 📝 描述：Contributors : Zhenzhen Zhan ; Sheng ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Post-infarction heart failure is attributed to ischemia-induced myocardial inflammation and unfavorable remodeling, with reparative macrophages playing a crucial role in limiting excessive fibrosis and promoting cardiac repair via cytokine secretion and cross-cell interactions. Hence, a timely and adequate transition of macrophage phenotypes is essential for proper wound healing post-MI, but the precise mechanisms underlying this process remain incompletely elucidated. Methods: To elucidate the function of NPM1 in post-infarct cardiac repair, we generated macrophage-specific NPM1 knockout mouse models. Additionally, Cut&Tag assays were conducted on cardiac macrophages for the first time to explore the epigenetic mechanisms underlying NPM1-mediated regulation of macrophage metabolic reprogramming. Results: Macrophage-specific deletion of NPM1 in MI mouse models resulted in reduced tissue fibrosis and enhanced cardiac repair by promoting the phenotypic transition of macrophages towards a reparative state. NPM1 deletion also led to a shift in macrophage metabolism from glycolysis to mitochondrial OXPHOS via inactivation of the mTOR cascades. Mechanistically, we demonstrated that IL-4 induced NPM1 oligomerization, which recruited histone demethylase KDM5b to the promoter region of Tsc1, ultimately leading to macrophage metabolic rewiring. Antisense oligonucleotides and inhibitory compounds targeting NPM1 exhibited notable protective effects on cardiac repair post-MI. Conclusions: Our study demonstrates that NPM1 may serve as a promising prognostic biomarker and a valuable therapeutic target for ischemia-induced heart failure, shedding new light on the understanding of post-infarct cardiac repair and may pave the way for the development of innovative therapeutic strategies.
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4. ⭐ GSE304687 线粒体代谢和信号传导直接调控树突状细胞在抗肿瘤免疫中的功能 [ATAC-seq2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、dendritic cell、metabolism
• 📝 描述：Contributors : Hao Shi ; Zhiyuan You ; Hongbo ChiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusATAC-seq profiling of intratumoral cDC1s
• 🔗 查看原文

5. ⭐ GSE304510 线粒体代谢和信号传导直接调控树突状细胞在抗肿瘤免疫中的功能 [microarray3]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、dendritic cell、metabolism
• 📝 描述：Contributors : Hao Shi ; Zhiyuan You ; Hongbo ChiSeries Type : Expression profiling by arrayOrganism : Mus musculusTranscriptional dissection of intratumoral cDC1s
• 🔗 查看原文

6. ⭐ GSE298478 诱导肾脏发育细胞状态与预后良好型 Wilms 肿瘤的化疗耐药性相关 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、resistance、RNA-seq
• 📝 描述：Contributors : Andrew J Murphy ; Hongjian JinSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChildren with favorable histology Wilms tumor (FHWT) who experience disease relapse or whose tumors exhibit blastemal predominance after chemotherapy often have poor outcomes. We established a FHWT patient-derived xenograft model, KT-47, that exhibited blastemal predominance after chemotherapy treatment with vincristine, actinomycin, and doxorubicin (VAD) and ultimately developed complete resistance to VAD after serial exposures to this combination. Histologic analyses and comprehensive multi-omics approaches were used to evaluate changes associated with resistance. CUT&TAG identified increased transcriptionally active H3K4me3 at stem cell and nephrogenesis gene promoters among the most different regions in KT-47 resistant compared to the KT-47 pretreatment model including the HOXB cluster, HOXC cluster, MYCN, SIX2, IGF2, CITED1, and OSR1. In contrast, decreased H3K27me3 was identified at HOX gene cluster and nephrogenesis gene promoter regions. The most significantly upregulated transcript and protein that associated with resistance in KT-47 was the let7 microRNA processor LIN28B. LIN28B upregulation was associated with copy number gain at MYCN and plasticity of cancer cells marked by open chromatin at the LIN28B locus rather than expansion of a minor subclone expressing LIN28B present in the original primary tumor material. The stem cell-associated multidrug resistance protein ABCB1 was upregulated in epithelial cells in association with an inter-chromosomal interaction between chromosomes 1 and 7. The impact of these findings at MYCN, LIN28B, and ABCB1 were validated in additional WT models and samples. Overall, these results support de-differentiation of FHWT cancer cells to a stem-like state which is associated with chemotherapy resistance. Targeting epigenetic modifiers that modulate differentiation of cancer cells with a stem-like phenotype could be a future treatment strategy in chemotherapy resistant FHWT.
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7. ⭐ GSE298463 诱导肾脏发育细胞状态与预后良好型 Wilms 肿瘤的化疗耐药性相关 [甲基化]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、resistance、methylation
• 📝 描述：Contributors : Andrew J Murphy ; Hongjian JinSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensChildren with favorable histology Wilms tumor (FHWT) who experience disease relapse or whose tumors exhibit blastemal predominance after chemotherapy often have poor outcomes. We established a FHWT patient-derived xenograft model, KT-47, that exhibited blastemal predominance after chemotherapy treatment with vincristine, actinomycin, and doxorubicin (VAD) and ultimately developed complete resistance to VAD after serial exposures to this combination. Histologic analyses and comprehensive multi-omics approaches were used to evaluate changes associated with resistance. CUT&TAG identified increased transcriptionally active H3K4me3 at stem cell and nephrogenesis gene promoters among the most different regions in KT-47 resistant compared to the KT-47 pretreatment model including the HOXB cluster, HOXC cluster, MYCN, SIX2, IGF2, CITED1, and OSR1. In contrast, decreased H3K27me3 was identified at HOX gene cluster and nephrogenesis gene promoter regions. The most significantly upregulated transcript and protein that associated with resistance in KT-47 was the let7 microRNA processor LIN28B. LIN28B upregulation was associated with copy number gain at MYCN and plasticity of cancer cells marked by open chromatin at the LIN28B locus rather than expansion of a minor subclone expressing LIN28B present in the original primary tumor material. The stem cell-associated multidrug resistance protein ABCB1 was upregulated in epithelial cells in association with an inter-chromosomal interaction between chromosomes 1 and 7. The impact of these findings at MYCN, LIN28B, and ABCB1 were validated in additional WT models and samples. Overall, these results support de-differentiation of FHWT cancer cells to a stem-like state which is associated with chemotherapy resistance. Targeting epigenetic modifiers that modulate differentiation of cancer cells with a stem-like phenotype could be a future treatment strategy in chemotherapy resistant FHWT.
• 🔗 查看原文

8. ⭐ GSE285156 线粒体代谢和信号传导直接影响树突状细胞在抗肿瘤免疫中的功能 [microarray1]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、dendritic cell、metabolism
• 📝 描述：Contributors : Hao Shi ; Zhiyuan You ; Hongbo ChiSeries Type : Expression profiling by arrayOrganism : Mus musculusTranscriptional dissection of cDC1s with polarized mitochondria or cDC1s with depolarized mitochondria
• 🔗 查看原文

9. ⭐ GSE285155 线粒体代谢和信号传导直接影响树突状细胞在抗肿瘤免疫中的功能 [microarray2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、dendritic cell、metabolism
• 📝 描述：Contributors : Hao Shi ; Zhiyuan You ; Hongbo ChiSeries Type : Expression profiling by arrayOrganism : Mus musculusTranscriptional dissection of splenic WT and OPA1-deficient cDC1s
• 🔗 查看原文

10. ⭐ GSE255515 通过体内 CRISPR 激活筛选肿瘤微环境调节剂，合理设计免疫基因治疗组合 [CRISPR]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment
• 📝 描述：Contributors : Feifei Zhang ; Ryan D Chow ; Chuanpeng Dong ; Emily He ; Lvyun Zhu ; Shan Xin ; Daniyal Mirza ; Yanzhi Feng ; Xinyu Ling ; Qin Han ; Sidi Chen ; Guangchuan WangSeries Type : OtherOrganism : Mus musculusThe hostile tumor microenvironment (TME) is major challenge for cancer immunotherapies. Here, we design and perform TME-targeted in vivo CRISPR activation (CRISPRa) screens to uncover factors that promote anti-tumor immunity, culminating in rationally designed immune gene therapy combinations. Through adeno-associated virus (AAV) delivery, we find that multiplexed activation of pooled immunoregulatory genes encoding antigen presentation, cytokine, and co-stimulation molecules (APCM) leads to enhanced anti-tumor immunity. A CRISPRa screen targeting APCM genes in metastatic tumors identifies CD80, TNFSF14, CXCL10, TNFSF18, TNFSF9, and IFNG as the top immunostimulatory candidates. Further optimization pinpoints 4-1BBL(TNFSF9) + IFNG + IL12B (4II) as a potent streamlined therapeutic combination. AAV delivered 4II has potent in vivo anti-tumor efficacy in multiple tumor models, by enhancing tumor antigen presentation while simultaneously promoting the infiltration, activation, and expansion of anti-tumor T cells. We further demonstrate that APCM therapy synergizes with CAR-T therapy against human solid tumors in vivo. CRISPRa screens and gene activation systems targeting APCM factors thus represent a powerful approach for rapid development of off-the-shelf immune gene therapies against solid tumors.
• 🔗 查看原文

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1. 揭示癌症中隐藏的 oncRNA 特征——从发现到液体活检

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Large-scale RNA sequencing reveals cancer-specific orphan RNAs that act as molecular barcodes, drive tumor growth, and enable blood-based monitoring of cancer burden and patient outcomes…
• 🔗 查看原文

2. 一种用于纳米孔直接RNA测序的双重上下文感知碱基识别器

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：A new dual context-aware basecaller, Coral, markedly improves nanopore direct RNA sequencing accuracy, enabling better detection of transcript isoforms and more reliable haplotype phasing…
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3. 科学家们刚刚破解了癌症进化的隐藏规律。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Cancer doesn’t evolve by pure chaos. Scientists have developed a powerful new method that reveals the hidden rules guiding how cancer cells gain and lose whole chromosomes—massive genetic shifts that help tumors grow, adapt, and survive treatment. By tracking thousands of individual cells over time, the approach shows which chromosome combinations give cancer an edge and why some tumors become especially resilient.
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4. 这些常见的食品防腐剂可能与癌症有关。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A large French study tracking more than 100,000 people over a decade has found that higher consumption of certain food preservatives—commonly found in processed foods and drinks—is linked to a modestly higher cancer risk. While many preservatives showed no association, several widely used ones, including potassium sorbate, sulfites, sodium nitrite, and potassium nitrate, were tied to increased risks of overall cancer and specific types such as breast and prostate cancer.
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• GSE230949 通过表观遗传学靶向 NPM1 重编程修复性巨噬细胞代谢促进梗死后心脏修复
• GSE230938 通过表观遗传学靶向 NPM1 促进心肌梗死后修复，重编程修复性巨噬细胞代谢 [CUT&Tag]
• GSE273378 血管侵袭相关基因表达可在 I 期肺腺癌术前活检中检测到 [空间转录组学]
• GSE317327 通过空间和单细胞转录组学揭示人类肌腱在整个生命周期中的细胞和分子图谱
• GSE312719 对 HUVEC 单层细胞单独培养或暴露于（细菌感染的）巨噬细胞样 U937 细胞 8 小时后的单细胞 RNA 测序分析。
• GSE311583 通过抑制 cGAS-STING 通路减弱 AAV 触发的成年小鼠神经系统中的先天免疫
• GSE298482 诱导肾脏发育细胞状态与预后良好型 Wilms 肿瘤的化疗耐药性相关 [HiC]
• GSE298479 诱导肾脏发育细胞状态与预后良好的 Wilms 肿瘤的化疗耐药性相关 [CUT&Tag]
• GSE270217 反式作用长链非编码RNA调节与致癌MYC信号相关的长程染色质相互作用[RNA-seq]
• GSE270212 反式作用长链非编码 RNA 调节与致癌 MYC 信号相关的长程染色质相互作用 [ATAC-seq]
• GSE208740 反式作用长链非编码RNA调节与致癌MYC信号相关的长程染色质相互作用[RNA-seq]
• GSE316386 Rpd3 组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要 – HDACi 组蛋白乙酰化 ChIP-seq (PE)
• GSE316355 Rpd3 组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要——HDAC 突变体组蛋白乙酰化 ChIP-seq
• GSE316185 Rpd3 组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要 – HDACi 组蛋白乙酰化 ChIP-seq (SE)
• GSE316184 Rpd3组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要——HDAC突变体TF ChIP-seq
• GSE316014 Rpd3组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要 – HDACi TF ChIP-seq
• GSE315932 Rpd3组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要——HDAC突变体RNA测序
• GSE315800 Rpd3 组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要——HDACi RNA-seq
• GSE295353 优化单细胞长读长测序以增强胰岛同工型检测 [sc_islet]
• GSE295352 优化单细胞长读长测序以增强胰岛中同工型的检测 [sc_spleen]
• GSE295351 优化单细胞长读长测序以增强胰岛中异构体检测 [bulk_islet]
• GSE292142 超越 BRCA 缺陷：BRCA 缺陷型输卵管卵巢高级别浆液性癌患者生存的临床和分子预测因子 [RNA-Seq]
• GSE292140 超越 BRCA 缺陷：BRCA 缺陷型输卵管卵巢高级别浆液性癌患者生存的临床和分子预测因子 [甲基化]
• GSE317702 TCR亲和力以抗原剂量依赖的方式控制CD8 T细胞的竞争适应性，但不能可靠地预测其命运。
• GSE314315 X射线活化铂复合物通过远隔效应诱导DNA损伤并增强癌症免疫疗法
• 利用 H3、H3K4me1、H3K4me2 和 H3K4me3 抗体对水稻 NiP 和 osldl3 中的组蛋白修饰进行 ChIP-seq 分析（GSE289852）
• 利用 H3、H3K4me1、H3K4me2、H3K4me3、H3K36me1、H3K36me2 和 H3K36me3 抗体对水稻 NiP、ehd3-1、sdg724-1 和 ehd3sdg724 中的组蛋白修饰进行 ChIP-seq 分析（GSE266898）。
• GSE316932 AMPK 突变体 dauer 转录组 [RNA-seq daf2_aak_alg34]
• GSE316835 3’tRNAAsp(GTC)衍生片段将炎症与骨关节炎期间软骨细胞的转录后重编程联系起来。[软骨小RNA测序]
• GSE316834 3’tRNAAsp(GTC)衍生片段将炎症与骨关节炎期间软骨细胞的转录后重编程联系起来。[原代软骨细胞小RNA测序]
• GSE296345 对暴露于未感染或细菌感染的 PMA 分化巨噬细胞样 U937 8 或 24 小时的原代人脐静脉内皮细胞 (HUVEC) 进行双端 RNA 测序
• GSE288127 H3K27me3 表观遗传标记对愈伤组织细胞特性和再生能力至关重要 [ChIP-seq]
• GSE316913 缬氨霉素处理的拟南芥转录组分析
• GSE311009 人类iPSC构建的Tau蛋白病模型，经基因工程改造后可内源性表达4R Tau亚型，并发展为晚期神经元Tau蛋白病理。
• GSE310475 靶向肉瘤融合基因 (FUS)：治疗特发性肺纤维化的新型反义策略 [RNA-Seq PCLS]
• GSE310473 靶向肉瘤融合基因 (FUS)：治疗特发性肺纤维化的新型反义策略 [RNA-Seq IPF]
• GSE310070 宫颈癌患者和健康对照组血浆细胞外囊泡 miRNA 谱分析
• GSE309995 反式作用长链非编码RNA调节与致癌MYC信号相关的长程染色质相互作用[VCaP_HiChIP]
• GSE309994 反式作用长链非编码 RNA 调节与致癌 MYC 信号相关的长程染色质相互作用 [SMARCA1_ATAC-Seq]
• GSE309829：对人多能干细胞来源的心脏心外膜-心肌类器官进行单细胞转录组分析，揭示了人心外膜来源细胞分化和冠状血管丛发育的原理
• GSE302462 AtNUDT11 介导的 dpCoA-RNA-seq 定义了表观转录组 dpCoA 加帽 RNA [dpCoA_seq]
• GSE302461 AtNUDT11 介导的 dpCoA-RNA-seq 定义了表观转录组 dpCoA 加帽 RNA [RNA-Seq]
• GSE208743 反式作用长链非编码 RNA 调节与致癌 MYC 信号传导相关的长程染色质相互作用 [Iso-Seq]
• GSE316691 Rpd3 组蛋白去乙酰化酶对人类真菌病原体组织胞浆菌的温度介导的形态发生和毒力至关重要
• GSE291427 核仁定位的 KANSL2 作为胶质母细胞瘤细胞中核糖体生物合成的表观遗传调节因子。
• GSE266911 水稻（Oryza sativa）、莱茵衣藻（Chlamydomonas reinhardtii）和小立碗藓（Physcomitrella patens）的高通量测序数据
• GSE266910 小立碗藓 (Physcomitrium patens) 野生型的转录组数据 (mRNA-seq)。
• GSE266909 莱茵衣藻野生型转录组数据（mRNA-seq）。
• GSE266906 NiP、ehd3-1、sdg724-1 和 ehd3 sdg724 的转录组数据（mRNA-seq）。
• GSE266905 使用 HA 或 GFP 抗体对 Ehd3 和 SDG724 进行 ChIP-seq 分析。
• GSE266903 小立碗藓 (Physcomitrella patens) 的 ChIP-seq。
• GSE266902 莱茵衣藻 H3K4me1、H3K4me2、H3K4me3、H3K36me1、H3K36me2 和 H3K36me3 的 ChIP-seq。
• GSE237299 基于DNA甲基化的血液淋巴系统肿瘤分类
• GSE317371 协同靶向 eIF4A 介导的翻译起始和急性髓系白血病中的细胞凋亡
• GSE317300 线粒体基因组比较和 atp8 功能分析，揭示苜蓿细胞质雄性不育症。
• GSE317288 研究发现，卵巢僵硬程度增加（模拟卵巢衰老）会诱导卵泡发生纤维炎症反应，并损害卵母细胞质量。
• GSE317275 SAGA/ATAC复合物维持异常染色质调控并促进弥漫性中线胶质瘤的肿瘤发生
• GSE317041 长病方治疗放射性肠炎大鼠模型肠道组织转录组分析
• GSE317025 Wnt 激活和双重 SMAD 抑制诱导和维持 hiPSCs 中类似后脑的神经干细胞 [scRNA-seq]
• GSE317019 慢性TCR信号驱动的FOXO1-KLHL6轴抑制促进T细胞耗竭
• GSE315930 比较转录组学揭示了兰科植物 Dactylorhiza majalis 原球茎对田间和体外生长条件的反应主要在幅度上存在差异，而不是模式上的差异
• GSE291437 哺乳动物细胞中 PspCas13b 和 RfxCas13d 的 gRNA 依赖性和 gRNA 非依赖性脱靶结合位点的表征 [RNA-Seq]
• GSE261461 定义血液和大脑细胞类型之间一致的转录组特征，并与普拉德-威利综合征的严重程度相关。