title: Comprehensive expression profile reveals dynamic changes in Xenopus gene expression depending on the duration of activin A treatment.

city: Toyama

first: Jun-Dal

last: Kim

state: Toyama

address: 2630 Sugitani

department: Department of Complex Biosystem Research (CBR), Institute of National Medicine (INM)

institute: University of Toyama

summary:
In amphibian embryo, the animal cap explants treated with activin A, which is a member of TGF-β family protein, have a potent of Spemann-Mangold organizer-like activities, leading the induction of mesendodermal tissue.  We report the temporal RNA expression profile of the mesendodermal cell lineage induced by activin A to Xenopus animal cap explants, which have multipotency.  Depending on the duration of activin A treatment to animal cap, dynamic changes of gene expressions were observed.
Overview of samples: As the sample for RNA-seq, animal cap explants from Xenopus blastulas (stage 8.5) were cultured in activin A solution (50 ng/mL) for 1, 3, 6, and 9 hours (Post 1h_, Post_3h_, Post 6h_, and Post 9h_activin), and activin A-untreated control (Pre_activin) were also prepared.
Results: We first tested the principal component analysis (PCA) for gene expression at individual time points, and found that three biological replicates of individual time points made clusters together.  To compare the gene expression between activin A-treated and -untreated samples, we then visualized gene expression of 45099 annotated genes.  The heat map visualization showed the distinct clusters between individual time points, and also revealed the significant changes of gene expression levels depending on the duration of activin A treatment.  Analysis for differentially expressed genes (DEGs) (fold change >2 with false discovery rate at p<0.05) showed upregulated and downregulated genes by activin A treatment, in comparison with Pre_activin sample.  Gene number of upregulated (up), downregulated (down) genes, and treatment time of activin A were described as follows; 2573 (up), 111 (down), 1h; 4149 (up), 1901 (down), 3h; 6323 (up), 4704 (down), 6h; 8858 (up), 6008 (down), 9h.  From the data set of analysis for enriched Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, we assessed the molecular functions and signaling pathway of upregulated DEGs at each time point of activin A treatment, in comparison with Pre_activin sample.
Conclusions: Regarding the temporal expression of organizer genes such as goosecoid (gsc), orthodenticle homeobox 2 (otx2) and chordin (chrd), our transcriptome data using mesendodermal cells derived from animal cap explants was correlated with previous findings using mesendodermal region from Xenopus embryos.  Our transcriptome data from animal cap assay may cover the transition of gene expression from undifferentiated cells to mesendodermal tissue during the normal early development.

overall_design: Time-course RNA expression data from Xenopus animal cap treated with activin A. mRNA profiles of animal caps were generated by RNA sequencing using the NextSeq 500 (Illumina).

first: Yumeko

last: Kobayashi

first: Makoto

last: Asashima

first: Akiyoshi

last: Fukamizu


title: p38-MAPK mediated rRNA processing and translation regulation enables PrE differentiation during mouse blastocyst maturation

status: Public on Jun 23 2021

city: Ceske Budejovice

first: Lenka

last: Gahurova

address: Branisovska 1760

department: Department of molecular biology and genetics

country: Czech Republic

institute: University of South Bohemia

type: Expression profiling by high throughput sequencing

summary: p38-MAPKs are stress activated kinases necessary for placental development and nutrient and oxygen transfer during murine post-implantation development. In preimplantation development, p38-MAPK activity is required for blastocyst formation. Additionally, we have previously reported its role in regulating specification of inner cell mass (ICM) towards primitive endoderm (PrE), although a comprehensive mechanistic understanding is currently limited. Adopting live embryo imaging, proteomic and transcriptomic approaches, we report experimental data that directly address this deficit. Chemical inhibition of p38-MAPK activity during blastocyst maturation causes impaired blastocyst cavity expansion, most evident between the third and tenth hours post inhibition onset. We identify an overlapping minimal early blastocyst maturation window of p38-MAPKi inhibition (p38-MAPKi) sensitivity, that is sufficient to impair PrE cell fate by the late blastocyst (E4.5) stage. Comparative proteomic analyses reveal substantial downregulation of ribosomal proteins, the mRNA transcripts of which are also significantly upregulated. Ontological analysis of the differentially expressed transcriptome during this developmental period reveals “translation” related gene transcripts as being most significantly, yet transiently, affected by p38-MAPKi. Moreover, combined assays consistently report concomitant reductions in de novo translation that are associated with accumulation of unprocessed rRNA precursors. Using a phospho-proteomic approach, ± p38-MAPKi, to potentially identify p38-MAPK effectors, we report that clonal siRNA mediated knockdown of Mybpp1a, an rRNA transcription and processing regulator gene, is associated with significantly diminished PrE contribution. Lastly, we show that defective PrE specification caused by p38-MAPKi (but not MEK/ERK signalling inhibition) can be partially rescued by activating the archetypal mTOR mediated translation regulatory pathway.

overall_design: 3 timepoints of mouse preimplantation development (E3.5+4 hours, E3.5+7 hours, E3.5+10 hours), for each timepoint there are two replicates of control (DMSO) dataset and two replicates of p38-inhibited dataset.

first: Pablo

last: Bora


title: Genome wide DNA methylation profiling of term and pre-term blood samples

status: Public on Jun 22 2021

city: Seoul

first: Young Ju

address: 1071, Anyangcheon-ro, Yangcheon-gu

country: South Korea

institute: Ewha Womans University

type: Methylation profiling by genome tiling array

summary: The Illumina Illumina HumanMethylation 450 BeadChip was used to obtain DNA methylation profiles across approximately 485,000 CpGs. Samples included 5 term blood samples, 5 pre-term blood samples.

overall_design: Bisulphite converted DNA from the 10 samples were hybridised to the Illumina HumanMethylation 450 BeadChip


title: Individual-specific functional epigenomics reveals genetic determinants of adverse metabolic effects of glucocorticoids

city: Philadelphia

first: Chunjie

last: Jiang

state: PA

address: 3400 Civic Center Boulevard

department: Institute for Diabetes, Obesity, and Metabolism

country: USA

institute: University of Pennsylvania

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Glucocorticoids (GCs) are widely used as anti-inflammatory drugs, but their long-term use has severe metabolic side effects. Here, by treating multiple patient-derived adipose stem cell-derived adipocytes and iPSC-derived hepatocytes with the potent GC dexamethasone (Dex), we uncovered cell type-specific and individual-specific GC-dependent transcriptomes and glucocorticoid receptor (GR) cistromes. Patient-specific GR binding could be traced to single nucleotide polymorphisms (SNPs) that altered the binding motifs of GR or its cooperating factors. We also discovered another set of genetic variants that modulated Dex response through affecting chromatin accessibility or chromatin architecture. Several SNPs that altered Dex-regulated GR binding and gene expression controlled Dex-driven metabolic perturbations and, remarkably, predicted metabolic side-effects of GC-treated patients. These data validate a patient stem cell-based experimental framework to discover genetic variants that impact GR function and individual responses to GC drugs, with implications for developing personalized therapies.

overall_design:
hACSs derived from consented healthy female patients undergoing elective abdominoplasty were differentiated into adipocytes; then treated with dexamethasone
HLCs derived from hiPSCs and treated with dexamethasone

first: Wenxiang

last: Hu


title: Influence of varying dietary ratios of ω6 to ω3 fatty acids on the hepatic global gene expression, and association with phenotypic traits (growth, somatic indices and tissue lipid composition) in Atlantic salmon (Salmo salar)

city: St. John's

first: Xi

last: Xue

state: NL

address: 1 Marine Lab Road

department: Department of Ocean Sciences

country: Canada

institute: Memorial University of Newfoundland

summary: The present study investigated the influence of plant-based diets (12-week exposure) with varying ω6:ω3 (0.4–2.7) on the hepatic transcriptome of Atlantic salmon, and the relationships with tissue (i.e. liver, muscle) lipid composition, and growth performance. The current microarray study identified several genes involved in immune and inflammatory response (lect2, itgb5, p43), lipid metabolism (helz2), cell growth (htra1), muscle development (mef2d), and translation (eif2a, eif4b1, p43), that were differentially expressed between the two extreme ω6:ω3 dietary treatments (i.e. high ω6 vs. high ω3).

overall_design:
Atlantic salmon were fed the two experimental diets (high ω6 and high ω3 ; four tanks per diet) for 12 weeks. Liver samples were taken from 5 fish from each tank at week 12. A universal reference design was used for the microarray experiment. For the test samples, RNA was used from individual livers of fish from the 2 treatment groups. For each treatment group we used 8 biological replicates (2 fish from each of 4 tanks). All test samples were labeled with Cy5. The common reference was a pool of 16 RNA samples from livers of fish from all individuals invovled in microarray experiment. The common reference was labeled with Cy3. Each individual test sample was hybridized together with the common reference sample on an array, so the experiment consisted of 16 arrays. Please note that sample titles represent 'diet_tank number_individual fish number' for each sample.
variable: Highω6_T3_F1, Highω6_T3_F5, Highω6_T7_F2, Highω6_T7_F4, Highω6_T21_F2,  Highω6_T21-F3, Highω6_T24_F3, Highω6_T24_F4
variable: Highω3_T2_F1, Highω3_T2_F4, Highω3_T8_F2, Highω3_T8_F5, Highω3_T20_F3, Highω3_T20_F5, Highω3_T26_F1, Highω3_T26_F2
biological replicate: Highω6_T3_F1, Highω6_T3_F5, Highω6_T7_F2, Highω6_T7_F4, Highω6_T21_F2,  Highω6_T21-F3, Highω6_T24_F3, Highω6_T24_F4
biological replicate: Highω3_T2_F1, Highω3_T2_F4, Highω3_T8_F2, Highω3_T8_F5, Highω3_T20_F3, Highω3_T20_F5, Highω3_T26_F1, Highω3_T26_F2

first: Tomer

last: Katan

first: Albert

last: Caballero-Solares

first: Richard

middle: G

last: Taylor

first: Christopher

middle: C

last: Parrish

first: Matthew

middle: L

last: Rise


title: Role of PML in ISG induction in primary postnatal sympathetic neurons

status: Public on Jun 21 2021

city: Charlottesville

first: Eugene

last: Ke

state: Virginia

address: P.O. Box 800734, 1340 Jefferson Park Avenue

department: MIC

institute: University of Virginia

summary: A previous study has shown that PML-dependent recruitment of HIRA to ISG promoters contributes to the up-regulation of gene expression as a result of cytokine release in response to HSV infection (McFarlane et al., 2019). Although carried out in non-neuronal cells, this study and others (Ulbricht et al., 2012, Kim and Ahn, 2015, Scherer et al., 2016, Chen et al., 2015) suggest that PML itself may contribute to ISG upregulation, so to determine whether PML was indeed required for ISG stimulation in SCG neurons, we carried out RNA sequence analysis in IFNα-treated neurons depleted of PML.

overall_design: Postnatal (P6) murine SCG neurons were transduced with lentiviral vectors expressing non-targeting control or PML-targeting shRNAs (shCtrl and shPML, respectively) and then mock treated or treated with IFNα (600 IU/ml) for 18h prior to RNA extraction.

first: Anna

last: Cliffe

first: Jon

last: Suzich


title: BAP1/ASXL complex modulation regulates Epithelial-Mesenchymal Transition during trophoblast differentiation and invasion

city: Cambridge

first: Felix

last: Krueger

address: Granta Park

department: Bioinformatics

country: United Kingdom

institute: Altos Labs

summary: The experiment  shows the transcriptional changes between mouse trophoblast stem cells transduced with non-targeting single-guide RNA (NT-sgRNA) or sgRNA against the promoter of the Bap1 gene (sgRNA1) at two different time points, 0 days (0d) -stem cell conditions- and after 3 days (3d) of differentiation

overall_design: RNA-seq experiment in triplicate comparing control  (NT-sgRNA) with Bap1- overexpressing mTSCs (sgRNA1) at two different time points, 0 days and 3 days of differentiation

first: Vicente

last: Perez-Garcia


title: Analysis of endothelial cells related gene in MC38 tumors

city: Suita city

first: Yumiko

last: Hayashi

address: 3-1 Yamadaoka

country: Japan

institute: Osaka University

summary: We show that endothelial cells from MC38 tumors in WT mice express high chemokine Ccl8 than in Apelin knockout mice. We found that Apelin induces Ccl8 expression in ECs and enhances anti-tumor immunity.

overall_design: We search for endothelial cells related gene of MC38 tumors in WT mice and Apelin knockout mice.

first: Liuying

first: Nobuyuki

last: Takakura


title: RAB38 Facilitates Energy Metabolism and Counteracts Cell Death in Glioblastoma Model Systems

city: Boston

first: Boston University

last: Microarray and Sequencing Resource

state: MA

address: 72 East Concord Street, E631

department: Microarray and Sequencing Resource

institute: Boston University

summary: Glioblastoma is a high-grade glial neoplasm with a patient survival of 12-18 months. Therefore, there is an urgent need for identification of novel therapeutic targets. RAB38 is a member of a family of small GTPase proteins and has been implicated in regulating cell proliferation and survival in tumors. The role of RAB38 in glioblastoma is unexplored. Here, we used human glioblastoma cell lines to test the hypothesis that RAB38 regulates glioblastoma growth. We found that genetic interference of RAB38 resulted in a marked decrease in glioblastoma growth, but not in astrocytes, through inhibition of proliferation and cell death induction accompanied by loss of mitochondrial membrane potential. Transcriptome analysis with subsequent gene set enrichment analysis (GSEA) showed that RAB38 silencing leads to changes in genes related to mitochondrial metabolism, intrinsic apoptosis (e.g. Bcl-xL) as well as a reduction in MYC targets.  Consistently, rescue experiments demonstrated that loss of RAB38 causes reduction of glioblastoma viability through downregulation of both Bcl-xL and c-Myc, respectively. Moreover, RAB38 knock-down inhibited both glycolysis and oxidative phosphorylation. Consistently, interference with RAB38 enhanced cell death induced by BH3-mimetics. RAB38 antagonists are under development, but not yet clinically available. We found that FDA approved statins led to a rapid reduction in RAB38 protein expression, increased cell death and phenocopied some of the molecular changes elicited by loss of RAB38. In summary, our findings suggest that RAB38 is a potential therapeutic target for glioblastoma treatment.

overall_design: LN229 human glioblastoma cell line was transfected with non-targeting (NT) or RAB38 specific siRNA (siRAB38). 48 hours following transfection, cells were subjected to RNA extraction and submitted for microarray and GSEA analysis.

first: Elena

last: Bianchetti

first: Kevin

last: Roth


title: FEC + OV treatment of TNBC tumors

city: Hamilton

first: Karen

last: Mossman

state: Ontario

address: 1280 Main St. West

department: Department of Pathology

institute: McMaster University

summary: E0771 subcutaneous tumors in C57/Bl6 mice were treated with saline, FEC (chemotherapy), oHSV-1 (oncolytic virus) or FEC + oHSV-1

overall_design: Examination of whole tumor lysates across various treatment groups

first: Alyssa

last: Vito

last: Dvorkin-Gheva


title: Single-cell sequencing of murine articular cartilage

status: Public on Jun 19 2021

city: Livermore

first: Stephen

middle: Patrick

last: Wilson

state: CA

address: 7000 East Ave

department: BBTD

institute: LLNL

summary: Osteoarthritis (OA) is a degenerative joint disease characterized by progressive cartilage loss, bone remodeling, synovial inflammation, and significant joint pain, often resulting in disability. Injury to the synovial joint such as the anterior cruciate ligament (ACL) tear is the major cause of OA in young adults. Currently, there are no approved therapies available to prevent joint degeneration or rebuild articular cartilage destroyed by OA, primarily because our understanding of the cellular and molecular changes that contribute to joint damage is very limited. The synovial joint is a complex structure composed of several tissues including articular cartilage, subchondral bone, synovium, synovial fluid, and tensile tissues including tendons and ligaments. In the present study, using single-cell RNA sequencing (scRNA-seq), we examined the cellular heterogeneity in articular cartilage from mouse knee joints and determined the knee joint injury-induced early molecular changes in the chondrocytes that could contribute to OA.

overall_design: Right knee joints of 10-week-old C57Bl/6J mice were injured using a tibial compression injury model. Uninjured and injured hindlimbs were collected at 3- and 7-days post-injury. Subsequently, knee joints were isolated, about ~1mm tissue was cut from the end of femur and tibia and digested to obtain single cell suspensions. After depleting CD45+ immune cells and Ter119+ erythrocytes, the remaining cells were sequenced to obtain single-cell level gene expression profiles.

first: Aimy

last: Sebastian

first: Gabriela

last: Loots


title: T cell-intrinsic CDK6 is dispensable for anti-viral and anti-tumor responses in vivo

city: Vienna

first: Veronika

last: Sexl

address: Veterinaerplatz 1

department: Pharmacology / Toxikology

country: Austria

institute: University of Veterinary Medicine Vienna

summary: The cyclin-dependent kinase 6 (CDK6) regulates the transition through the G1-phase of the cell cycle, but also acts as a transcriptional regulator. As such CDK6 regulates cell survival or cytokine secretion together with STATs, AP-1 or NF-κB. In the hematopoietic system, CDK6 regulates T cell development and promotes leukemia and lymphoma. CDK4/6 kinase inhibitors are FDA approved for treatment of breast cancer patients and have been reported to enhance T cell-mediated anti-tumor immunity. The involvement of CDK6 in T cell functions remains enigmatic. We here investigated the role of CDK6 in CD8+ T cells, using previously generated CDK6 knockout (Cdk6-/-) and kinase-dead mutant CDK6 (Cdk6K43M) knock-in mice. RNA-seq analysis indicated a role of CDK6 in T cell metabolism and interferon (IFN) signaling. To investigate whether these CDK6 functions are T cell-intrinsic, we generated a T cell-specific CDK6 knockout mouse model (Cdk6fl/fl CD4-Cre). T cell-intrinsic loss of CDK6 enhanced mitochondrial respiration in CD8+ T cells in vitro, but did not impact on CD8+ T cell effector function, as T cell-mediated tumor surveillance of MC38 tumors remained unaltered. Similarly, while we observed an impaired induction of early responses to type I IFN in CDK6-deficient CD8+ T cells, we failed to observe any differences in the response to LCMV infection in vivo. This apparent contradiction might at least partially be explained by the reduced expression of Socs1, a negative regulator of IFN signaling, in CDK6-deficient CD8+ T cells. Therefore, our data are in line with a dual role of CDK6 in IFN signaling; while CDK6 promotes early IFN responses, it is also involved in the induction of a negative feedback loop. These data assign CDK6 a role in the fine-tuning of cytokine responses.

overall_design: Splenic CD8+ T cells were ex vivo sorted from 8-10 week-old male wild-type (WT), Cdk6-/- and Cdk6K43M mice. Two mice were pooled for each of the three biological replicates per genotype.

first: Klara

last: Klein

first: Agnieszka

last: Witalisz-Siepracka

first: Dagmar

last: Gotthardt

first: Benedikt

last: Agerer

last: Locker

first: Reinhard

last: Grausenburger

first: Andreas

last: Bergthaler


title: Expression data from SIRT6 knockout, young WT and old WT mice brains

status: Public on Jun 18 2021

city: Beer Sheva

first: Debra

last: Toiber

state: Israel

address: Ben Gurion Road #1, Building 40, room 205

country: Israel

institute: Ben Gurion University of the Negev

summary: Brain-specific SIRT6-KO mice present increased DNA damage, learning impairments, and neurodegenerative phenotypes, placing SIRT6 as a key protein in preventing neurodegeneration. In the aging brain, SIRT6 levels/activity decline, which is accentuated in Alzheimer's patients. To understand SIRT6 roles in transcript pattern changes, we analyzed transcriptomes of young WT, old WT and young SIRT6-KO mice brains, and found changes in gene expression related to healthy and pathological aging. In addition, we traced these differences in human and mouse samples of Alzheimer's and Parkinson's diseases, healthy aging and calorie restriction (CR). Our results define four gene expression categories that change with age in a pathological or non-pathological manner, which are either reversed or not by CR. We found that each of these gene expression categories is associated with specific transcription factors, thus serving as potential candidates for their category-specific regulation. One of these candidates is YY1, which we found to act together with SIRT6 regulating specific processes. We thus argue that SIRT6 has a pivotal role in preventing age-related transcriptional changes in brains. Therefore, reduced SIRT6 activity may drive pathological age-related gene expression signatures in the brain.

overall_design:
Whole-exon microarray analysis of brain samples from either old, full-body SIRT6-KO or WT mice.
Overall 9 samples were analyzed: 3 Old WT (22-26 months old), 3 young WT/het (21 days old; no phenotypical difference between WT and heterozygous), 3 young SIRT6KO (21 days old).


title: Differential expression of  circulating exosomal microRNAs  in refractory intracranial  atherosclerosis associated with  antiangiogenesis

city: Los Angeles

first: Miguel

last: Quintero

institute: Cedars Sinai medical center

type: Non-coding RNA profiling by high throughput sequencing

summary:
Purpose:We aimed to investigate the role of circulating exosomal microRNAs (e-miRNAs) in recurrent ischemic events in ICAD
Methods: consecutive patients with severe ICAD undergoing intensive medical management (IMM) were prospectively enrolled. Those with recurrent ischemic events despite IMM during 6-month follow up were algorithmically matched to IMM responders. Baseline blood e-miRNA expression levels of the matched patients were measured using next generation sequencing
Results: a  total   of 122 e-miRNAs were isolated from blood samples of 10 non-responders and 11 responders. Thirteen e-miRNAs predicted IMM failure with 90% sensitivity and 100% specificity. Ingenuity pathway analysis (IPA) determined 10 of the 13 e-miRNAs were significantly associated with angiogenesis-related biological functions (p < 0.025) and angiogenic factors that have been associated with recurrent ischemic events in ICAD. These e-miRNAs included miR-122-5p, miR-192-5p, miR-27b-3p, miR-16-5p, miR-486-5p, miR-30c-5p, miR-10b-5p, miR-10a-5p, miR-101-3p, and miR-24-3p. As predicted by IPA, the specific expression profiles of these 10 e-miRNAs in non-responders had a net result of inhibition of the angiogenesis-related functions and up expression of the antiangiogenic factors
conclusion: This study revealed distinct expression profiles of circulating e-miRNAs in refractory ICAD, suggesting an antiangiogenic mechanism underlying IMM failure.

overall_design: survey of intracranial atherosclerosis patients receiving IMM to associate the e-miRNA expression profile with recurrent ischemic events despite treatment.

first: Nestor

last: Gonzalez

first: Hao

last: Jiang

first: Juan

last: Toscano

first: Shlee

last: Song

first: Konrad

last: Schlick

first: Oana

last: Dumitrascu

first: Jianwei

last: Pan

first: Patric

middle: D

last: Leyden

first: Jeffrey

last: Saver


title: Mitochondrial mistranslation is modulated by metabolic stress

city: Perth

first: Stefan

middle: J

last: Siira

state: Western Australia

address: 15 Hospital Ave, Nedlands

department: Precision Health

country: Australia

institute: The Kids Research Institute Australia

summary: Changes in the rate and fidelity of mitochondrial protein synthesis impact the metabolic and physiological roles of mitochondria. Here we explored how environmental stress in the form of a high-fat diet modulates mitochondrial translation using mutant mice with error-prone (Mrps12ep/ep) or hyper-accurate (Mrps12ha/ha) mitochondrial ribosomes. Intriguingly, although both mutations are metabolically beneficial in reducing body weight, decreasing circulating insulin and increasing glucose tolerance during a high-fat diet, they manifest divergent (either deleterious or beneficial) outcomes in a tissue-specific manner. In two distinct organ types that are commonly affected by metabolic disease, the heart and the liver, Mrps12ep/ep mice were protected against heart defects but sensitive towards lipid accumulation in the liver, activating genes involved in steroid and amino acid metabolism. In contrast, enhanced translational accuracy in Mrps12ha/ha mice protected the liver from a high-fat diet through activation of liver proliferation programs, but enhanced the development of severe hypertrophic cardiomyopathy. While these findings reflect the complex transcriptional and cell signalling responses that differ between post-mitotic (heart) and highly proliferative (liver) tissues, they also suggest that trade-offs between the rate and fidelity of mitochondrial protein synthesis dictate tissue-specific outcomes toward commonly encountered stressful environmental conditions.

overall_design: Total RNA differential gene expression of Mrps12ep/ep and Mrps12ha/ha in mouse heart and liver tissue, relative to Mrps12+/+, in triplicate (biological & technical)

first: Tara

middle: R

last: Richman

first: Judith

middle: A

last: Ermer

first: Irina

last: Kuznetsova

first: Chris

last: Brosnan

first: Guilia

last: Rossetti

first: Jessica

last: Baker

first: Kara

last: Perks

first: Henrietta

last: Szappanos

first: Helena

middle: M

last: Viola

first: Nicola

last: Whiley

first: Livia

last: Hool

first: Steven

last: Zuryn

first: Olicer

last: Rackham

first: Aleksandra

last: Filipovska


title: RNAseq of human SNc and VTA midbrain dopamine neurons isolated from post mortem material of control subjects and Parkinson's Disease patients using laser capture microdisection.

city: Stockholm

first: Eva

last: Hedlund

address: Svante Arrhenius v. 16C

department: Department of Biochemistry and Biophysics

country: Sweden

institute: Stockholm University

summary: Defining the transcriptional profiles of SNc and VTA dopamine neurons could reveal mechanisms underlying their differential susceptibilities in Parkinson’s disease. To conclusively identify genes stably enriched in either VTA or SNc dopamine neurons we conducted transcriptomic profiling across 18 human subjects and revealed novel genes in human that stably define dopamine neuron subtypes by random pooling algorithm.

overall_design: A total of 50 samples were analyzed. Each sample consists of approximately 50-120 laser-captured motor neurons from post-mortem human tissue. Samples are divided in 4 groups (Control SNc, n=26; Control VTA, n=17; PD SNc, n=5; PD VTA, n=4). For cases having more than 1 replicate per group, corresponding samples were averaged before analysis so that  each Case have only 1 SNc and 1 VTA.

first: Julio

last: Benitez

first: Shangli

last: Cheng

first: Menghan

last: Wang

first: Qiaolin

last: Deng


title: A small RNA regulates pprM, a modulator of pleiotropic proteins promoting DNA repair, in Deinococcus radiodurans under ionizing radiation

city: Austin

first: Lydia

last: Contreras

state: Texas

address: 200 E Dean Keeton St

institute: University of Texas at Austin

summary: This study explores the regulatory network of a sRNA named PprS (previously Dsr2) in Deinococcus radiodurans R1. We compared the transcriptomes of two strains with and without exposure to 10 kGy acute ionizing radiation (IR): D. radiodurans  R1 (wild-type) and a PprS knockdown mutant (PprSKD) that expresses ~2-fold less PprS compared to WT levels. Analysis of this RNAseq dataset demonstrated significant differential expression of several transcripts in both WT (34) and PprSKD (61) strains during recovery from IR. However, we did not observe any significantly differentially expressed transcripts between the two strains during recovery from IR. 31 transcripts were signficantly differentially expressed when comparing the two strains under unirradiated conditions. To determine the regulatory network that this sRNA, PprS could regulate we performed a MAPS (MS2-affinity purification followed by RNAsequencing) experiment in which a MS2-binding domain tagged PprS was expressed from a constutive promoter from a plasmid (pRADgro) in D. radiodurans R1. A control plasmid (containing only the MS2-binding domain) was also expressed and differential enrichment was compared to this control. MAPS suggested ~130 potential interacting transcripts with PprS and we were able to validate the binding and stabilization of one specific transcript, pprM, for PprS.

overall_design: RNAseq of D. radiodurans R1 (WT) and PprSKD strains after recovery from 0kGy or 10 kGy IR and MAPS of MS2BD-PprS

first: Jordan

middle: K

last: Villa

first: Runhua

last: Han

first: Chen-Hsun

last: Tsai

first: Angela

last: Chen

first: Philip

last: Sweet

first: Gabriela

last: Franco

first: Respina

last: Vaezian

first: Rok

last: Tkavc

first: Michael

last: Daly


title: Maternal Cold Exposure Enhances Fetal Brown Adipose Tissue Development

city: Baton Rouge

first: Ji Suk

last: Chang

state: LA

address: 6400 Perkins Rd.

department: Gene Regulation and Metabolism

institute: Pennington Biomedical Research Center

summary: Brown adipose tissue (BAT) is specialized for dissipating energy in the form of heat. BAT-mediated heat production is critical for effective adaption of newborns to the extrauterine environment. However, very little is known about whether and how fetal BAT development is modulated in-utero in response to changes in maternal thermal environment during pregnancy. The present study aims at determining whether maternal cold exposure influences fetal BAT development via placental remodeling. BL6 female mice were acclimated at 28C or 18C for 7 days prior to mating with male mice and maintained at their respective temperature until embryonic day 18.5. Placental and fetal BAT samples were collected for transcriptome analysis.

overall_design: Examination of placenta and fetal BAT mRNA profiles of mice housed at 28°C or at 18°C during gestation

first: Sujoy

last: Ghosh

first: Richard

last: Carmouche

first: Susan

last: Newman

first: Chul-Hong

last: Park

first: Jisu

last: Lee

first: Nathan

first: Rui

last: Zhang

first: Clara

last: Huesing

first: Dorien

last: Reijnders

first: Jennifer

last: Sones

first: Heike

last: Münzberg


title: Next-generation sequencing to characterize the molecular basis for the differentiation of ES cells into testicular somatic cell-like cells and germ cell-like cells

city: Aberdeen

first: Ryohei

last: Sekido

address: Foresterhill

department: Institute of Medical Sciences

institute: University of Aberdeen

summary: Taking advantage of the tesco-cfp transgenic mouse line in which CFP is exclusively expressed in Sertoli cells under the control of a testis-specific enhancer (tesco), we established an embryonic stem cell from the mouse line (i.e. tcESC). We also created tcESC constitutively expressing mouse Sf1 transgene (tc;Sf1ESC). When we induced the differentiation of the two ESC lines into testicular somatic cell-like cells (TesLCs), tc;Sf1ESCs efficiently developed seminiferous tubule-like structures with the appearance of CFP-positive Setoli cell-like cells (SCLCs) in the tubules. On the other hand, epiblast-like cells (EpiLCs) were generated from ESCs having a germ cell-specific Prdm1-gfp transgene. Co-culture of tc;Sf1TesLCs with Prdm1-gfp EpiLCs resulted in self-organised aggregates, or testicular organoids. In the organoid, the EpiLCs differentiated into GFP-positive PGCLCs or gonocyte-like cells that were enclosed within a seminiferous tubule-like structure composed of CFP-positive SCLCs.

overall_design: SCLCs and PGCLCs were isolated by flow cytometry from day 12 of TesLC culture and day 6 of testicular organoids, respectively. Then RNA was extracted from these cells, as well as tcESCs and tc;Sf1ESCs. All samples were in biologically duplicate. Hight-throughput sequencing was performed on Illimina HiSeq4000 platform.

first: Rore

last: Holly

first: Nicholas

last: Owen


title: MCF-7 cells treated with p300 KAT inhibitor A-485

status: Public on Jun 16 2021

city: Gainesville

first: Daiqing

last: Liao

state: Florida

address: 2033 Mowry Road

department: Anatomy and Cell Biology

institute: University of Florida

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Expression data from MCF-7 cells treated with p300 KAT inhibitor A-485

summary: Transcriptome analysis of MCF-7 (Estrogen receptor positive breast cancer) cells treated with p300 KAT inhibitor A-485 using Affymetrix GeneChip Human Transcriptome Array 2.0.

overall_design: MCF-7 cells were treated with A-485 (3 µM) for 24 hours. RNA was extracted and gene expression was analyzed using the Affymetrix GeneChip Human Transcriptome Array 2.0.

first: Aaron

last: Waddell

first: Haocheng

last: Ding

first: Zhiguang

last: Huo


title: miRNA profiling in human precision-cut lung slices (PCLS)

city: Hannover

first: Stella Marie

last: Reamon-Buettner

address: Nikolai-Fuchs Strasse1

department: Preclinical Pharmacology & In Vitro Toxicology

country: Germany

institute: Fraunhofer-ITEM

type:
Non-coding RNA profiling by array
Third-party reanalysis

summary:
Transcriptome analysis revealed miRNA profiles from PCLS of tumor-free tissue comparable to normal lung tissue
Suitability of human PCLS as a model for lung-specific miRNA investigations by RTqPCR and microarray analyses

overall_design: miRNA profiles from human PCLS of tumor-free tissues in n = 10 donors were obtained by GeneChip™ miRNA 4.0 Arrays. To determine their use for gene expression analysis, the miRNA profiles (tumor-free tissues) were compared to miRNA profiles (also obtained by GeneChip™ miRNA 4.0 Arrays) of n = 9 human PCLS treated with low dose (LD) 0.1 mM; medium dose (MD) 0.3 mM; and high dose (HD) 1 mM of methyl acrylate. To determine whether the expression levels of certain lung-disease associated miRNAs expressed in the human PCLS of tumor-free tissue comparable to miRNA expression levels in ‘healthy’ lung, we searched for published miRNA data from human lungs. CEL Files from GSE81203 obtained by GeneChip™ miRNA 3.0 Array were downloaded from GEO and were re-analyzed TAC 4.0, using Affymetrix default settings and RMA normalization. Lung disease-related miRNAs with average signal (log2) intensity > 6 in the human PCLS of tumor-free tissues were compared manually to corresponding average signal (log2) intensity in the ‘healthy’ lung samples (GSE81203).

first: Stella

first: Monika

last: Niehof


title: Differential Ezh1/2 regulation of hemogenic fate and hematopoietic stem and progenitor cell formation from arterial endothelium

status: Public on Jun 17 2021

first: Mohamad Ali

last: Najia

address: 1 Blackfan Circle

department: Hematology/Oncology

institute: Boston Children's Hospital

summary: Across species, hematopoietic stem and progenitor cells (HSPCs) arise during embryogenesis from a specialized arterial population, termed hemogenic endothelium. Here, we describe a mechanistic role for the epigenetic regulator, Enhancer of zeste homolog-1 (Ezh1) in vertebrate HSPC production via regulation of hemogenic commitment. Loss of ezh1 in zebrafish embryos favored acquisition of hemogenic (gata2b) and HSPC (runx1) fate at the expense of the arterial program (ephrinb2a, dll4). In contrast, ezh1 overexpression blocked hematopoietic progression via maintenance of arterial gene expression. The related polycomb group subunit, Ezh2, functioned in a non-redundant, sequential manner, whereby inhibition had no impact on arterial identity, but was capable of blocking ezh1-knockdown associated HSPC expansion. Single-cell RNA-seq across ezh1 genotypes revealed a dropout of ezh1+/- cells among arterial endothelium associated with positive regulation of gene transcription. Exploitation of Ezh1/2 modulation has potential functional relevance for improving in vitro HSPC differentiation from induced pluripotent stem cell sources.

overall_design: Single-cell RNA-sequencing of kdrl:GFP reporter positive FACS sorted cells from EZH1 WT, HET and KO zebrafish 30 hours post-fertilization

first: Mohamad

first: Rebecca

last: Soto

first: Trista

last: North


title: Genome-wide H3K27ac deposition in MCF-7 cells treated with p300 KAT inhibitor A-485

summary: MCF-7 (Estrogen receptor positive breast cancer) cells were treated with p300 KAT inhibitor A-485 and genome wide H3K27ac deposition was measured by ChIP-seq.

overall_design: MCF-7 cells were treated with A-485 (3 µM) for 24 hours. Chromatin was extracted, sonicated, and histones enriched with H3K27ac were immunoprecipitated. Purified DNA was used for library construction and ChIP-sequencing.


title: Single-nuclear transcriptomics reveals a diversity of proximal tubule cell states in a dynamic response to acute kidney injury.

first: Kari

middle: Ann

last: Koppitch

address: 1425 San Pablo Street, BCC 312

department: Stem Cell

institute: USC

summary: We performed a mild-to-moderate ischemia reperfusion injury (IRI) to model injury responses reflective of kidney injury in a variety of clinical settings. Single-nuclear RNA-sequencing (snRNA-seq) of genetically labeled injured PTCs at 7-days (“early”) and 28-days (“late”) time points post-IRI identified specific gene and pathway activity in the injury-repair transition. In particular, we identified Vcam1+/Ccl2+ proximal tubule cells at a late injury stage distinguished by marked activation of NF-kB-, TNF- and AP-1-signaling pathways. This population of PTCs showed features of a senescence-associated secretory phenotype but did not exhibit G2/M cell cycle arrest. These pro-inflammatory, pro-fibrotic proximal tubule cells are likely triggers for chronic disease progression.

overall_design: Krt20 was previously identified as a marker of injured proximal tubule cells (Liu et al., JCI Insight, 2017). We generated a Krt20T2A-CE; INTACTnuGFP/+ mouse line to enable the isolation and tracing of Krt20+ cells in acute kidney injury. A reporter mouse expressing GFP linked to the histone protein H2B in all nephron cells was used as control (Legouis et al., Nature Metabolism, 2020). In total nine samples were processed for snRNA-seq: two Krt20T2A-CE; INTACTnuGFP/+ samples collected on day 7 after IRI, three Krt20T2A-CE; INTACTnuGFP/+ samples collected on day 28 after IRI and four control samples (three sham surgery mice and one non-surgery mouse).

first: Louisa

last: Gerhardt

first: Jing

last: Liu

first: Pietro

middle: E

last: Cippà

first: Andrew

middle: P

last: McMahon


title: Nuclear barrier induction as a new modality of cellular senescence

city: Daejeon

first: Ji-Hwan

last: Park

address: 125 Gwahak-ro, Yuseong-gu

institute: Korea Research Institute of Bioscience and Biotechnology (KRIBB)

summary: Blocking of nucleocytoplasmic trafficking is an essential feature of replicative senescence (RS). However, whether nuclear barrier per se causes cellular senescence still remains elusive. Here, we show that nuclear barrier induced by blocking nucleocytoplasmic trafficking, especially nuclear export, elicits RS-like changes in SA-β-gal activity, DNA damage, and expression of cell cycle regulators. Comparative transcriptome analysis revealed that nuclear barrier-induced senescence (NBIS) was most similar in gene expression changes to RS compared to senescence induced by stresses (oxidative stress, DNA damage and oncogene), implying that nuclear barrier induces RS-like physiological senescence-associated changes. Shared senescence-related processes between NBIS and RS included lysosomal degradation, nuclear transport, and translation, resulting in coordinated reduction in transmission of extrinsic signals to nucleus and intracellular protein supply from nucleus. Notably, these processes were conserved in yeast aging. Therefore, we propose NBIS as a novel modality of cellular senescence, representing the fundamental nature of physiological aging in eukaryotes.

overall_design: We performed seven comparisons as follows: 1) RS HDFs (n=3; passage=53) versus young (n=3; passage=12) HDFs (RS/Young); 2) WGA-treated HDFs (n=3) versus young HDFs (n=3) (WGA/Young); 3) LMB-treated HDFs (n=3) versus young HDFs (n=3) (LMB/Young); 4) RCC1 shRNA-treated (n=3) versus control shRNA-treated HDFs (n=3) (RCC1-KD/Control); 5) HDFs overexpressing RasV12 (n=3) versus control ORF (n=3) (RasV12/Control ORF); 6) H2O2-treated HDFs (n=3) versus young HDFs (n=2) (H2O2/Young); and 7) doxorubicin-treated HDFs (n=3) versus young HDFs (n=2) (Doxorubicin/Young), where n indicates the number of replicates for each condition. The comparison 1-3 used the samples of young HDFs in batch 1 as the controls, and the comparison 6-7 used those in batch 3 (see description and characteristics: batch).

first: Sung-Jin

last: Ryu

first: ByungJu

last: Kim

first: Chi-Hyun

first: Hyo

last: Choi

first: Eun-Jin

last: Jang

first: Young-Yon

last: Kwon

first: Cheol-Koo

last: Lee

first: Jeong

last: Han

first: Kyung

last: Cho

first: Daehee

last: Hwang

first: Young-Sam

first: Sang-Chul


title: Dnmt1 has global de novo methylation activity and is specifically targeted to transposable elements

city: Berlin

first: Helene

last: Kretzmer

address: Ihnestraße 63

department: Genome Regulation

institute: Max Planck Institute for Molecular Genetics

type: Methylation profiling by high throughput sequencing

summary: DNA methylation plays a critical role in development, particularly in silencing transposable elements. Conserved across mammals, the methylation landscape is dependent on the combined activities of the canonical maintenance enzyme Dnmt1 and the de novo Dnmts 3a and 3b. Here we demonstrate that Dnmt1 displays clear de novo activity in vitro and in vivo and is specifically directed to IAP retrotransposons. We provide an indepth characterization using whole genome bisulfite sequencing and long-read Nanopore sequencing in genetically engineered methylation depleted embryonic stem cells. Further using additional knockout and MassSpec experiments we show that Dnmt1’s de novo methylation activity is dependent on Uhrf1 and its genomic targeting linked to Trim28 and H3K9 trimethylation. Our data suggest that Dnmt1 is essential for adding and maintaining DNA methylation especially at IAPs and that this mechanism may be of physiological relevance for retrotransposon repression during certain phases of development.

overall_design: Analysis of Dnmt1 de novo activity in DNA methylation depleted ES cells and during development.

first: Chuck

last: Haggerty

first: Christina

last: Riemenschneider

first: Abhishek

last: Sampath Kumar

first: Raha

last: Weigert

first: Nina

last: Bailly

first: Alexandra

last: Mattei

first: Pay

last: Gießelmann

first: Björn

last: Brändl

last: Galonska

first: Bernd

last: Timmermann

first: David

last: Meierhofer

first: Alexander

last: Meissner


title: RNAseq data from WT and FOXO1-GFP null (KO) cytotoxic T lymphocytes (CTL) untreated or treated with PI3Kp110δ inhibitor for 24hr

city: Dundee

first: Laura

last: Spinelli

address: Dow Street

department: Cell Signalling and Immunology

institute: University of Dundee

summary: Phosphatidylinositol-3-kinase p110 delta (PI3Kp110δ) is pivotal for CD8+ T cell immune responses. To inform how PI3Kp110δ directs CD8+ T cell fate the current study focuses on PI3Kp110δ controlled transcriptional programs and reveals how PI3Kp110δ selectively induces and represses expression of key genes that create a cytotoxic T cell (CTL). The data identify differences in PI3Kp110δ regulated transcriptional programs between naïve and effector cytotoxic T cells including differential control of cytolytic effector molecules, costimulatory receptors and the critical inhibitory receptors CTLA4 and SLAMF6. However, common to both naïve and effector cells is PI3Kp110δ control of the production of chemokines and cytokines that orchestrate communication between the adaptive and innate immune system. The study provides a comprehensive resource for understanding how PI3Kp110δ uses multiple processes  mediated by Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.

overall_design: mRNA profile of CTL from WT or FOXO1-GFP KO mice untreated or treated with PI3Kp110δ inhibitor IC87114 for 24hr. 3 biological replicates for each condition.

first: Julia

last: Marchingo

first: Aneela

last: Nomura

first: Marcos

last: Damasio

first: Doreen

last: Cantrell


title: RNA-sequencing analysis of VEGFR2 knocking down in retinal pigment epithelial (RPE) cells upon glucose depletion.

city: guangzhou

first: Ruiqiang

last: Yan

address: 黄埔大道西601号

country: China

institute: Jinan University

summary: RNA-sequencing analysis was utilized to investigate the impact of VEGFR2 knockdown via siRNA on transcriptome profiling in primary human RPE cells under the glucose depletion condition compared to the control siRNA.

overall_design: Expression of VEGFR2 was downregulated via siVEGFR2 followed by glcuose starvation. RNA-sequencing analysis was carried out to compare the transcriptome profiling between the siVEGFR2- and siControl-treated RPE cells under the same condition.

first: Bohan

last: Xu

first: Linbin

last: Zhou

first: Qishan

last: Chen

first: Jianing

last: Zhang

first: Lijuan

last: Huang

first: Shasha

last: Wang

first: Zhimin

last: Ye

first: Xiangrong

last: Ren

first: Yu

last: Cai

first: Weirong

first: Xuri

last: Li

first: Rong

last: Ju


title: RNAseq data from unstimulated or TCR retriggered (4hr) cytotoxic T lymphocytes (CTL) in the presence or absence of PI3Kp110δ or MEK inhibitors

first: Laura

last: Spinelli

overall_design: mRNA profile of CTL unstimulated or TCR retriggerd 4hr  in the presence or absence of PI3Kp110δ inhibitor IC87114 or MEK inhibitor PD184252. 3 biological replicates for each condition. Please note that BR stands for Biological Replicate.

first: Julia


title: Spinal astrocytes RNA-sequencing

city: Toulouse

first: David

last: OHAYON

state: Haute-Garonne

address: Université Paul Sabatier 118 Route de Narbonne

country: France

institute: CNRS

summary: We have identified an unidentified sub-population of astrocytes (Olig2-AS) in the mouse spinal cord that can be distinguished from other astrocyte populations by the expression of Olig2, a transcription factor currently recognized as a hallmark of oligodendrocytes (Ohayon et al., 2019 Glia). The present project aims at characterizing further this new sub-type of astrocytes and at elucidating their function in the physiological CNS by performing a RNA-seq.

overall_design: Glial cells mRNA profiles of 7 day old Aldh1L1-GFP/Olig2-tdTomato mice

last: Ohayon


title: The landscape of human brain immune response in patients with severe COVID-19

city: New York

first: Panos

last: Roussos

state: NY

address: 1470 Madison Ave

department: Psychiatry

institute: Icahn School of Medicine at Mount Sinai

summary: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has been associated with neurological and neuropsychiatric illness in many individuals. We sought to further our understanding of the relationship between brain tropism, neuro-inflammation and host immune response in acute COVID-19 cases. 3 brain regions (dorsolateral prefrontal cortex, medulla oblongata and choroid plexus) from 5 patients with severe COVID-19 and 4 controls were examined. The presence of virus was assessed by western blot against viral spike protein, as well as viral transcriptome analysis covering >99% of SARS-CoV-2 genome and all potential serotypes. Droplet-based single-nucleus RNA sequencing (snRNA-seq) was performed in the same samples to examine the impact of COVID-19 on transcription in individual cells of the brain. Quantification of viral spike S1 protein and viral transcripts did not detect SARS-CoV-2 in the postmortem brain tissue. However, analysis of 68,557 single-nucleus transcriptomes from three distinct regions of the brain identified an increased proportion of stromal cells, monocytes and macrophages in the choroid plexus of COVID-19 patients. Furthermore, differential gene expression, pseudo-temporal trajectory and gene regulatory network analyses revealed transcriptional changes in cortical microglia associated with a range of biological processes, including cellular activation, mobility and phagocytosis. Despite the absence of detectable SARS-CoV-2 in the brain at time of death, the findings suggest significant and persistent neuroinflammation in patients with acute COVID-19.

overall_design: Single-nucleus transcriptome analysis of human brain tissue from patients with coronavirus disease 2019 amd controls

first: John

middle: F

last: Fullard

first: Hao-Chih

last: Lee


title: High-depth spatial transcriptome analysis by photo-isolation chemistry

city: Kyoto

first: Shinya

last: Oki

address: 53 Kawahara-cho, Shogoin

institute: Kyoto University

summary: We established a transcriptome profiling method coupled with photo-isolation chemistry (PIC) that allows the determination of expression profiles specifically from photo-irradiated regions of interest.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: We performed PIC to isolate expression profiles from small domain of the E14.5 mouse neural tube. We performed PIC to isolate expression profiles from small domain of HeLa cells or NIH3T3 cells. We performed PIC to isolate expression profiles from each of the major hippocmpal [CA1, CA2 and dentate gyrus (DG) ] in 8 weeks male mice.

first: Mizuki

last: Honda

first: Ryuichi

last: Kimura

first: Akihito

last: Harada

first: Kazumitsu

last: Maehara

first: Kaori

last: Tanaka

first: Chikara

last: Meno

first: Yasuyuki

last: Ohkawa


title: CRISPR RNA-seq from HepG2 (ENCSR999MAE)

status: Public on Jun 15 2021

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against EIF4A3. (EIF4A3-BGHcLV16)

For 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


title: CRISPR RNA-seq from K562 (ENCSR999DVK)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against NIPBL. (NIPBL-BGKcLV08)

For 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


title: total RNA-seq from macrophage (ENCSR998WNE)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 10 minute.

For 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


title: RNAseq data for ex vivo Naïve CD8+ T cells and TCR activated 24hr in the presence or absence of PI3Kp110δ inhibitor

overall_design: mRNA profile of ex vivo CD8+ T cells, 24hr activated in the presence or absence of PI3Kp110δ inhibitor IC87114. 3 biological replicates for each condition.The dataset includes also a group of 6 samples (number 10 to 15) which were run on the same RNAseq lane but are not part of the manuscript.

last: Marchingo

first: Aneela

last: Nomura

first: Marcos

last: Damasio

first: Doreen

last: Cantrell


title: The Exon Junction Complex Core Represses Cancer-specific Mature mRNA Re-splicing: A Potential Key Role in Terminating Splicing

city: Toyoake

first: Akila

last: Mayeda

state: Aichi

address: 1-98 Dengakugakubo, Kutsukake-cho

department: Institute for Comprehensive Medical Science

institute: Fujita Health University

summary: Using the TSG101 pre-mRNA, we previously discovered cancer-specific re-splicing of mature mRNA that generates aberrant transcripts/proteins.  The fact that mRNA is aberrantly re-spliced in various cancer cells implies there must be an important mechanism to prevent deleterious re-splicing on the spliced mRNA in normal cells.  We thus postulated that the mRNA re-splicing is controlled by specific repressors and we searched for repressor candidates by siRNA-based screening for mRNA re-splicing activity.  We found that knock-down of EIF4A3, which is a core component of the exon junction complex (EJC), significantly promoted mRNA re-splicing.  Remarkably, we could recapitulate cancer-specific mRNA re-splicing in normal cells by knock-down of any of the core EJC proteins, EIF4A3, MAGOH or RBM8A (Y14), implicating the EJC core as the repressor of mRNA re-splicing often observed in cancer cells.  We propose that the EJC core is a critical mRNA quality control factor to prevent over-splicing of mature mRNA.

overall_design:
Previously, it was demonstrated that the induction and overexpression of the tumor suppressor gene TP53 (p53) prevents cancer-specific aberrant splicing of TSG101 pre-mRNA, i.e., generation of the re-spliced TSG101Δ154-1054 mRNA.  Therefore, this mRNA re-splicing event is under the control of TP53, presumably indirectly through other regulators; i.e., upregulation of an mRNA re-splicing repressor and/or downregulation of an mRNA re-splicing activator.  To identify such repressor or activator candidates, we activated TP53, using highly selective MDM2 inhibitor RG7388 to repress aberrant re-splicing, and searched for up- or down-regulated genes on a microarray.  This microarray data were deposited in this GEO database.
Using siRNA-based screening for mRNA re-splicing activity, we have identified EIF4A3, one of core factors of EJC, as the repressor of mRNA re-splicing (see above Summary), however, EIF4A3 expression was not up-regulated, but rather down-regulated, under the RG7388-mediated activation of TP53.  Therefore, EIF4A3 was not a TP53-dependent repressor of mRNA re-splicing.  There could be another unidentified regulator of mRNA re-splicing, which is under the control of the tumor suppressor gene TP53.
Reference:  bioRxiv 2021.04.01.438154; doi: https://doi.org/10.1101/2021.04.01.438154

first: Yuta

last: Otani

first: Ken-ichi

last: Fujita

first: Toshiki

last: Kameyama


title: shRNA RNA-seq from HepG2 (ENCSR997HCQ)

summary:
Control shRNA against no target in HepG2 cells followed by RNA-seq. (NT_BGHLV37)

For 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


title: CRISPR RNA-seq from K562 (ENCSR997ACY)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against RPL23A. (RPL23A-BGKcLV08)

For 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


title: CRISPR RNA-seq from K562 (ENCSR994EWL)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against ADAT3. (ADAT3-BGKcLV23)

For 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


title: BruChase-seq from GM12878 (ENCSR993ASV)

summary: For 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


title: eCLIP from K562 (ENCSR999YGP)

summary:
eCLIP experiment on K562 against GRWD1

For 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


title: Control eCLIP from HepG2 (ENCSR991LWQ)

summary:
eCLIP control experiment on HepG2 against DDX52

For 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


title: CRISPR RNA-seq from K562 (ENCSR990DKW)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against MORC2. (MORC2-BGKcLV19)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR991XFO)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against DROSHA. (DROSHA_BGHcLV05)

For 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


title: CRISPR RNA-seq from K562 (ENCSR989ZNZ)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against APEX1. (APEX1-BGKcLV13)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR989GNV)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against SMYD3. (SMYD3-BGHcLV20)

For 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


title: total RNA-seq from placenta (ENCSR899OKE)

summary:
Stam Placenta 11008

For 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


title: total RNA-seq from macrophage (ENCSR992IIX)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 40 minute.

For 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


title: microRNA-seq from activated CD4-positive, alpha-beta T cell (ENCSR898GHF)

summary:
RNA Evaluation human CD4+ T cells (activated day 7) microRNA-seq from Mortazavi

For 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


title: shRNA RNA-seq from K562 (ENCSR898ABR)

summary:
Control shRNA against no target in K562 cells followed by RNA-seq. (NT-BGKLV36-D)

For 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


title: total RNA-seq from macrophage (ENCSR896LKP)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 15 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR898KNS)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against STAU2. (STAU2-BGKcLV11)

For 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


title: CRISPR RNA-seq from K562 (ENCSR897BYR)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against RBM25. (RBM25-BGKcLV11)

For 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


title: microRNA-seq from right lobe of liver (ENCSR895DRP)

summary:
RNA Evaluation human tissue W61 right lobe liver microRNA-seq from Mortazavi

For 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


title: eCLIP from K562 (ENCSR891RIC)

summary:
eCLIP experiment on K562 against NIPBL

For 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


title: CRISPR RNA-seq from K562 (ENCSR889MBF)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against TRNAU1AP. (TRNAU1AP-BGKcLV06)

For 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


title: Control eCLIP from HepG2 (ENCSR986HXA)

summary:
eCLIP control experiment on HepG2 against FUS

For 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


title: CRISPR RNA-seq from K562 (ENCSR982XTO)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against NSUN5. (NSUN5-BGKcLV19)

For 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


title: TF ChIP-seq from K562 (ENCSR987KYK)

summary:
eGFP-ZNF717 ChIP-seq on human K562

For 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


title: CRISPR RNA-seq from K562 (ENCSR883MTV)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against DDX39B. (DDX39B-BGKcLV17)

For 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


title: total RNA-seq from macrophage (ENCSR982MXJ)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 25 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR978MMZ)

summary:
Control CRISPR gRNA against no target in K562 cells followed by RNA-seq. (NT-BGKcLV19)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR884REL)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against METTL3. (METTL3-BGHcLV22)

For 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


title: total RNA-seq from F121-9 (ENCSR982PLD)

summary:
LRGASP_mouse ES

For 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


title: polyA plus RNA-seq from macrophage (ENCSR879BNI)

summary:
mRNA-seq on whole cell extract RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for30 minutes.

For 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


title: microRNA-seq from lower lobe of left lung (ENCSR877HZT)

summary:
RNA Evaluation human tissue W78 lower lobe of left lung microRNA-seq from Mortazavi

For 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


title: BruChase-seq from MCF-7 (ENCSR874VJT)

summary: For 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


title: eCLIP from HepG2 (ENCSR876EYA)

summary:
eCLIP experiment on HepG2 against BCLAF1

For 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


title: TF ChIP-seq from K562 (ENCSR879HUU)

summary:
eGFP-GABPB2 ChIP-seq on human K562

For 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


title: CRISPR RNA-seq from K562 (ENCSR877JEM)

summary:
Control CRISPR gRNA against no target in K562 cells followed by RNA-seq. (NT-BGKcLV23)

For 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


title: eCLIP from HepG2 (ENCSR979EWD)

summary:
eCLIP experiment on HepG2 against STAU2

For 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


title: Bru-seq from IMR-90 (ENCSR873ZUO)


title: CRISPR RNA-seq from HepG2 (ENCSR977NJB)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against KPNB1. (KPNB1-BGHcLV14)

For 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


title: eCLIP from HepG2 (ENCSR977OXG)

summary:
eCLIP experiment on HepG2 against PRPF4

For 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


title: CRISPR RNA-seq from K562 (ENCSR975NHV)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against EIF6. (EIF6-BGKcLV23)

For 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


title: total RNA-seq from macrophage (ENCSR868ZAZ)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 75 minute.

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR865WQR)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against CACTIN. (CACTIN-BGHcLV22)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR871XPX)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against CTCF. (CTCF-BGHcLV18)

For 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


title: Bru-seq from HepG2 (ENCSR974AQD)


title: total RNA-seq from macrophage (ENCSR864RGP)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 90 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR865UKM)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against RPS3. (RPS3-BGKcLV04-C)

For 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


title: Control eCLIP from K562 (ENCSR864XNB)

summary:
eCLIP control experiment on K562 against DDX52

For 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


title: CRISPR RNA-seq from K562 (ENCSR974RYS)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against ZNF800. (ZNF800-BGKcLV06)

For 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


title: eCLIP from HepG2 (ENCSR973HOJ)

summary:
eCLIP experiment on HepG2 against FXR2

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR862BCF)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against ANXA2. (ANXA2-BGHcLV12)

For 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


title: CRISPR RNA-seq from K562 (ENCSR972AZD)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against SRSF9. (SRSF9-BGKcLV06)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR861BRA)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against TAF9. (TAF9-BGHcLV20)

For 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


title: CRISPR RNA-seq from K562 (ENCSR854OFV)

summary:
Control CRISPR gRNA against no target in K562 cells followed by RNA-seq. (NT-BGKcLV21)

For 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


title: Control eCLIP from K562 (ENCSR857ORY)

summary:
eCLIP control experiment on K562 against ABCF1

For 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


title: total RNA-seq from macrophage (ENCSR857KZU)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 120 minute.

For 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


title: eCLIP from HepG2 (ENCSR970FEW)

summary:
eCLIP experiment on HepG2 against DDX52

For 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


title: CRISPR RNA-seq from K562 (ENCSR965MSX)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against SMAD4. (SMAD4-BGKcLV17)

For 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


title: shRNA RNA-seq from K562 (ENCSR967QNT)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against GPKOW. (GPKOW_BGKLV36)

For 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


title: total RNA-seq from macrophage (ENCSR965WQM)

summary:
Ribo depletion RNA-seq on nucleoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 25 minute.

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR853AOV)

summary:
Control CRISPR gRNA against no target in HepG2 cells followed by RNA-seq. (NT-BGHcLV05-B)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR964HKT)

summary:
Control CRISPR gRNA against no target in HepG2 cells followed by RNA-seq. (NT-BGHcLV16)

For 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


title: CRISPR RNA-seq from K562 (ENCSR854MSP)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against CPSF4. (CPSF4-BGKcLV21)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR964YLV)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against EIF3H. (EIF3H-BGHcLV05-B)

For 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


title: eCLIP from K562 (ENCSR964VOX)

summary:
eCLIP experiment on K562 against UTP18

For 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


title: polyA plus RNA-seq from A549 (ENCSR964GKZ)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 15 mins.

For 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


title: Control eCLIP from K562 (ENCSR960OKV)

summary:
eCLIP control experiment on K562 against HNRNPC

For 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


title: CRISPR RNA-seq from K562 (ENCSR963JFM)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against POLR2A. (POLR2A-BGKcLV13)

For 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


title: CRISPR RNA-seq from K562 (ENCSR867XAL)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against DDX20. (DDX20-BGKcLV08)

For 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


title: shRNA RNA-seq from K562 (ENCSR953IQF)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against NUP35. (NUP35-BGKLV38-C)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR959HPB)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against NOLC1. (NOLC1-BGHcLV07)

For 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


title: microRNA-seq from ovary (ENCSR957UVO)

summary:
RNA Evaluation human tissue W80 ovary microRNA-seq from Mortazavi

For 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


title: CRISPR RNA-seq from K562 (ENCSR846OQD)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against G3BP1. (G3BP1-BGKcLV11)

For 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


title: eCLIP from K562 (ENCSR958FKZ)

summary:
eCLIP experiment on K562 against PABPC4

For 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


title: shRNA RNA-seq from K562 (ENCSR949RMX)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against XRN1. (XRN1-BGKLV38-C)

For 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


title: shRNA RNA-seq from K562 (ENCSR952OOP)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against CKAP4. (CKAP4-BGKLV36-B)

For 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


title: Control eCLIP from K562 (ENCSR952RGL)

summary:
eCLIP control experiment on K562 against AQR

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR845MNM)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against SRSF7. (SRSF7_BGHcLV03)

For 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


title: CRISPR RNA-seq from K562 (ENCSR949QWR)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against DUS3L. (DUS3L-BGKcLV17)

For 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


title: shRNA RNA-seq from K562 (ENCSR952QDQ)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against METAP2. (METAP2_BGKLV36)

For 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


title: total RNA-seq from macrophage (ENCSR842HHZ)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 35 minute.

For 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


title: total RNA-seq from macrophage (ENCSR959OQW)

summary:
Ribo depletion RNA-seq on nucleoplasmic fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 75 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR840JRU)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against SNRPC. (SNRPC-BGKcLV23)

For 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


title: shRNA RNA-seq from HepG2 (ENCSR840QOH)

summary:
RNA-seq on HepG2 cells treated with an shRNA knockdown against ETF1. (ETF1_BGHLV37)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR836XZH)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against CNOT7. (CNOT7-BGHcLV10)

For 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


title: total RNA-seq from placenta (ENCSR942YMN)

summary:
Stam Placenta 11010

For 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


title: CRISPR RNA-seq from K562 (ENCSR939BTN)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against SRSF4. (SRSF4-BGKcLV04-C)

For 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


title: TF ChIP-seq from SK-N-SH (ENCSR835VBH)

summary:
CSRNP3 ChIP-seq on human SK-N-SH

For 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


title: shRNA RNA-seq from K562 (ENCSR940GIC)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against CKAP4. (CKAP4-BGKLV36-D)

For 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


title: total RNA-seq from macrophage (ENCSR940IMN)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 10 minute.

For 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


title: total RNA-seq from macrophage (ENCSR839HSB)

summary:
Ribo depletion RNA-seq on cytoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 60 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR943CXG)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against MDM2. (MDM2-BGKcLV19)

For 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


title: total RNA-seq from macrophage (ENCSR839GBV)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 35 minute.

For 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


title: CRISPR RNA-seq from K562 (ENCSR832XLB)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against FYTTD1. (FYTTD1-BGKcLV21)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR834IFU)

summary:
Control CRISPR gRNA against no target in HepG2 cells followed by RNA-seq. (NT-BGHcLV05-C)

For 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


title: polyA plus RNA-seq from macrophage (ENCSR938LWT)

summary:
mRNA-seq on whole cell extract RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for120 minutes.

For 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


title: total RNA-seq from macrophage (ENCSR837DAP)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 0 minute.

For 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


title: eCLIP from HepG2 (ENCSR834YLD)

summary:
eCLIP experiment on HepG2 against DROSHA

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR940FIN)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against GNL3. (GNL3-BGHcLV05-E)

For 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


title: polyA plus RNA-seq from A549 (ENCSR937WIG)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 0 mins.

For 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


title: Control eCLIP from HepG2 (ENCSR831WYG)

summary:
eCLIP control experiment on HepG2 against EXOSC5

For 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


title: polyA plus RNA-seq from A549 (ENCSR831FZM)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 20 mins.

For 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


title: CRISPR RNA-seq from K562 (ENCSR828YEB)

summary:
Control CRISPR gRNA against no target in K562 cells followed by RNA-seq. (NT_BGKcLV04)

For 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


title: Control eCLIP from K562 (ENCSR832DWW)

summary:
eCLIP control experiment on K562 against PUM1

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR932GTJ)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against PAN2. (PAN2-BGHcLV22)

For 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


title: microRNA-seq from progenitor cell of endocrine pancreas (ENCSR931OFX)

summary:
RNA Evaluation H9 derived pancreatic progenitor cells microRNA-seq from Mortazavi

For 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


title: TF ChIP-seq from K562 (ENCSR934RJP)

summary:
ZNF3 ChIP-seq on human K562

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR929EIP)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against SRPK2. (SRPK2-BGHcLV12)

For 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


title: CRISPR RNA-seq from K562 (ENCSR928MEW)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against RPLP0. (RPLP0-BGKcLV11)

For 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


title: Control eCLIP from K562 (ENCSR925ZRV)

summary:
eCLIP control experiment on K562 against WRN

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR827PII)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against NT. (NT-BGHcLV12)

For 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


title: total RNA-seq from macrophage (ENCSR924IHS)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 0 minute.

For 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


title: Control eCLIP from HepG2 (ENCSR825FTY)

summary:
eCLIP control experiment on HepG2 against PCBP1

For 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


title: CRISPR RNA-seq from K562 (ENCSR825EPB)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against BAZ1A. (BAZ1A-BGKcLV17)

For 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


title: CRISPR RNA-seq from HepG2 (ENCSR925OFV)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against RPL23A. (RPL23A-BGHcLV09)

For 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


title: eCLIP from HepG2 (ENCSR820WHR)

summary:
eCLIP experiment on HepG2 against POLR2G

For 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


title: total RNA-seq from macrophage (ENCSR820OHO)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 60 minute.

For 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


title: eCLIP from HepG2 (ENCSR820UYE)

summary:
eCLIP experiment on HepG2 against PABPN1

For 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


title: CRISPR RNA-seq from K562 (ENCSR921RQX)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against THOC1. (THOC1-BGKcLV15)

For 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


title: TF ChIP-seq from SK-N-SH (ENCSR922RFY)

summary:
eGFP-TCF4 ChIP-seq on human SK-N-SH

For 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


title: shRNA RNA-seq from K562 (ENCSR818TZM)

summary:
RNA-seq on K562 cells treated with an shRNA knockdown against UTP3. (UTP3-BGKLV38-B)

For 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


title: CRISPR RNA-seq from K562 (ENCSR816LHY)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against RPL11. (RPL11-BGKcLV15)

For 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


title: eCLIP from HepG2 (ENCSR916XIV)

summary:
eCLIP experiment on HepG2 against EIF3H

For 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


title: polyA plus RNA-seq from macrophage (ENCSR917CGF)

summary:
mRNA-seq on whole cell extract RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 0 minutes.

For 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


title: CRISPR RNA-seq from K562 (ENCSR916PCG)

summary:
RNA-seq on K562 cells treated with a CRISPR gRNA against E4F1. (E4F1-BGKcLV17)

For 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


title: Bru-seq from PC-3 (ENCSR916VGW)

summary: For 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


title: total RNA-seq from macrophage (ENCSR911EZW)

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for 15 minute.

For 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


title: polyA plus RNA-seq from macrophage (ENCSR822FMG)

summary:
mRNA-seq on whole cell extract RNA which is part of BMDM cell, stimulated with 100 ng/ml Lipid A for180 minutes.

For 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


title: Control eCLIP from K562 (ENCSR816NVJ)

summary:
eCLIP control experiment on K562 against NIPBL

For 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


title: eCLIP from K562 (ENCSR922WJV)

summary:
eCLIP experiment on K562 against PCBP1

For 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


title: total RNA-seq from macrophage (ENCSR811YTU)

summary:
Ribo depletion RNA-seq on nucleoplasmic fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 60 minute.

For 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


title: BruChase-seq from IMR-90 (ENCSR809IJG)


title: CRISPR RNA-seq from HepG2 (ENCSR821GQN)

summary:
RNA-seq on HepG2 cells treated with a CRISPR gRNA against ZNF574. (ZNF574-BGHcLV18)

For 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


title: microRNA-seq from endodermal cell (ENCSR820BMF)

summary:
RNA Evaluation H1-derived endodermal cells microRNA-seq from Mortazavi

For 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


title: eCLIP from K562 (ENCSR819XBT)

summary:
eCLIP experiment on K562 against AATF

For 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


title: eCLIP from K562 (ENCSR906ZJF)

summary:
eCLIP experiment on K562 against SDAD1

For 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


title: Mint-ChIP-seq from immature natural killer cell (ENCSR806HUT)

summary:
H3K4me1 Mint-ChIP-seq on human immature natural killer cell

For 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


title: eCLIP from HepG2 (ENCSR907GUB)

summary:
eCLIP experiment on HepG2 against ZC3H11A

For 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