title: DNase-seq from heart right ventricle (ENCSR298OIK)


title: TF ChIP-seq from HepG2 (ENCSR107DKT)

status: Public on Mar 30 2021

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
ChIP-Seq on HepG2

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 HepG2 (ENCSR843JCI)


title: TF ChIP-seq from HepG2 (ENCSR490AMH)


title: DNase-seq from heart left ventricle (ENCSR299QGI)

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: TF ChIP-seq from HepG2 (ENCSR298DSB)


title: TF ChIP-seq from HepG2 (ENCSR842SRB)


title: DNase-seq from head of caudate nucleus (ENCSR305WAA)


title: TF ChIP-seq from K562 (ENCSR297CGF)

summary:
eGFP-KLF6 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: DNase-seq from cardiac muscle cell (ENCSR842KCP)


title: DNase-seq from tibial artery (ENCSR102RSU)


title: TF ChIP-seq from HepG2 (ENCSR487LUQ)


title: TF ChIP-seq from HepG2 (ENCSR108MKR)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR839RAJ)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR490UQP)


title: DNase-seq from head of caudate nucleus (ENCSR101HFF)


title: DNase-seq from CD8-positive naive resting alpha-beta T cell (ENCSR296TFH)


title: DNase-seq from suprapubic skin (ENCSR101QXF)


title: TF ChIP-seq from HepG2 (ENCSR291MJH)


title: DNase-seq from T-cell (ENCSR837ZSS)


title: DNase-seq from posterior cingulate gyrus (ENCSR098ISE)


title: TF ChIP-seq from HepG2 (ENCSR843QIL)


title: TF ChIP-seq from HepG2 (ENCSR837GLU)


title: DNase-seq from head of caudate nucleus (ENCSR839GHA)


title: TF ChIP-seq from HepG2 (ENCSR839AJZ)


title: DNase-seq from T-cell (ENCSR299BQG)


title: DNase-seq from T follicular helper cell (ENCSR486KKY)


title: TF ChIP-seq from HepG2 (ENCSR099FCQ)


title: TF ChIP-seq from HepG2 (ENCSR832PID)


title: ATAC-seq from HepG2 (ENCSR291GJU)

summary:
ATAC-seq on human cell line HepG2

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: ATAC-seq from GM12878 (ENCSR095QNB)


title: DNase-seq from NCI-H929 (ENCSR090SMP)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR832IQN)


title: DNase-seq from placenta (ENCSR831QMZ)


title: TF ChIP-seq from HepG2 (ENCSR486JYI)


title: DNase-seq from tibial artery (ENCSR090IDV)


title: DNase-seq from right cardiac atrium (ENCSR485UQY)


title: TF ChIP-seq from HepG2 (ENCSR830FJY)


title: DNase-seq from T-cell (ENCSR290NGL)


title: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR097AMI)


title: TF ChIP-seq from HepG2 (ENCSR289PSX)


title: Screening and Identification of Key Microenvironment-Related Genes in Non-Functioning Pituitary Adenoma

city: Beijing

first: Chuzhong

last: Li

address: 119 South Fourth Ring West Road, Fengtai

country: China

institute: Beijing Neurosurgical Institute

summary: To further identify microenvironment-related genes in Non-functioning pituitary adenoma (NFPAs) and assess their prognostic value, we collected 73 NFPA tumor samples  and transcriptional expression profiles were obtained through microarray analysis. The immune and stromal scores of each sample were calculated through the ESTIMATE algorithm, and the patients were divided into high and low immune/stromal score groups. Intersection differentially expressed genes (DEGs) were then obtained to construct a protein-protein interaction (PPI) network. Potential functions and pathways of intersection DEGs were then analyzed through Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. The prognostic value of these genes was evaluated. Quantitative The quantitative real-time polymerase chain reaction in another set of NFPA samples was used to confirm the credibility of the bioinformatics analysis. The immune/stromal scores were significantly correlated with cavernous sinus (CS) invasion.

overall_design: Based on microarray expression matrix data, immune and matrix scores were calculated and differentially expressed genes were obtained. We then investigated the relationship between tumor microenvironment (TME) and tumor invasiveness, and screened out essential TME-related genes in NFPA.

first: Yazhuo

last: Zhang


title: TF ChIP-seq from MCF-7 (ENCSR829WBA)

summary:
eGFP-OVOL1 ChIP-seq on human MCF-7

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: DNase-seq from body of pancreas (ENCSR828FVZ)

status: Public on Mar 29 2021


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR819GAF)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR289GZQ)


title: MeRIP-seq analysis of the spinal cord in the mice chronic constriction injury model of neuropathic pain

city: Hangzhou

first: Longfei

last: Ma

address: 88 Jiefang Road

institute: The Second Affiliated Hospital of Zhejiang University School of Medicine

type: Methylation profiling by high throughput sequencing

summary: To search for novel m6A-modified transcripts that are involved in the genesis of neuropathic pain, We collected the ipsilateral spinal cord at 7 days after chronic constriction injury and performed m6A peak profiling using MeRIP-seq

overall_design: The m6A peak profiles of the transcripts in spinal cord from the chronic constriction injury group mice and sham group mice were measured at 7 days after operation

first: Bao-Chun

last: Jiang

first: Min

last: Yan


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR824YLD)


title: DNase-seq from T-cell (ENCSR815DWW)


title: ATAC-seq from GM23338 (ENCSR485TLP)

summary:
ATAC-seq on human cell line PGP1

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: DNase-seq from dorsolateral prefrontal cortex (ENCSR832XVZ)


title: TF ChIP-seq from SU-DHL-6 (ENCSR088HZI)


title: DNase-seq from head of caudate nucleus (ENCSR814DYF)


title: TF ChIP-seq from HepG2 (ENCSR286LPH)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR811OUF)


title: DNase-seq from tibial nerve (ENCSR484UAU)


title: DNase-seq from CD8-positive naive resting alpha-beta T cell (ENCSR283TME)


title: TF ChIP-seq from HepG2 (ENCSR813QEO)


title: TF ChIP-seq from HepG2 (ENCSR481QLH)


title: DNase-seq from left colon (ENCSR279SXQ)


title: DNase-seq from T-cell (ENCSR283MZJ)


title: TF ChIP-seq from HepG2 (ENCSR803IYP)


title: DNase-seq from heart left ventricle (ENCSR805EGZ)


title: DNase-seq from femur (ENCSR805XIF)


title: ATAC-seq from K562 (ENCSR483RKN)


title: TF ChIP-seq from HepG2 (ENCSR280SCF)


title: DNase-seq from CD14-positive monocyte (ENCSR277ZHX)


title: DNase-seq from T-cell (ENCSR803JVQ)


title: TF ChIP-seq from HepG2 (ENCSR279NEA)


title: The transcriptome of human immortalized control chondrogenic progenitor cells (CPCs) and CPCs carrying a homozygous RAB5C knock-out during chondrogenic differentiation in 3D alginate on days 0, 3 and 28

city: Goettingen

first: Gabriela

last: Salinas

state: Lower-Saxony

address: Kreuzbergring 57

department: Department of Pathology

country: Germany

institute: Universitaetsmedizin Goettingen

type: Expression profiling by high throughput sequencing

summary: The goal of this study was to investigate differences in the transcriptome of control CPCs and CPCs carrying a homozygous deletion of RAB5C upon induction of chondrogenesis by in vitro 3D alginate culture. CPCs samples were taken on day 0 in 2D culture, and on days 3 and 28 of chondrogenic differentiation in 3D alginate culture.

overall_design: Total RNA profile of CPCs and CPCs RAB5CKO on day 0 and chondrogenic differentiated in 3D alginate on days 3 and 28

first: Jerome

middle: N

last: Janssen

first: Valerio

last: Izzi

first: Elvira

last: Henze

first: Gökhan

last: Cingöz

first: Florian

last: Lowen

first: David

last: Küttner

first: Ruth

last: Neumann

first: Christof

last: Lenz

first: Vicki

last: Rosen

first: Nicolai

last: Miosge


title: TF ChIP-seq from K562 (ENCSR087TYG)

first: ENCODE

last: DCC

summary:
ChIP-Seq on 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: TF ChIP-seq from HepG2 (ENCSR481AIK)


title: DNase-seq from left lobe of liver (ENCSR802ZYE)


title: TF ChIP-seq from HepG2 (ENCSR087NSZ)


title: TF ChIP-seq from K562 (ENCSR802AHH)

summary:
eGFP-BCL6 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: TF ChIP-seq from HepG2 (ENCSR087HFN)


title: TF ChIP-seq from HepG2 (ENCSR801SNX)


title: TF ChIP-seq from HepG2 (ENCSR479WQX)


title: DNase-seq from head of caudate nucleus (ENCSR085XKS)


title: TF ChIP-seq from HepG2 (ENCSR479RZV)


title: TF ChIP-seq from HepG2 (ENCSR277VXX)


title: DNase-seq from posterior cingulate gyrus (ENCSR086PIL)


title: TF ChIP-seq from HepG2 (ENCSR277VIC)


title: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR086FTP)


title: ATAC-seq from cerebellum (ENCSR802GEV)

summary:
human UMB4727 cerebellum

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 HepG2 (ENCSR479PRL)


title: TF ChIP-seq from K562 (ENCSR801JWB)

summary:
eGFP-HOMEZ 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: DNase-seq from tibial artery (ENCSR080ISA)


title: DNase-seq from psoas muscle (ENCSR082PDJ)


title: TF ChIP-seq from HepG2 (ENCSR080UEM)


title: DNase-seq from posterior cingulate gyrus (ENCSR083HYP)


title: TF ChIP-seq from HepG2 (ENCSR082QGT)


title: ATAC-seq from thyroid gland (ENCSR474XFV)

summary:
ATAC-seq on human thyroid gland

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 HepG2 (ENCSR474YDA)


title: TF ChIP-seq from HepG2 (ENCSR801GJU)


title: DNase-seq from adrenal gland (ENCSR277KRY)


title: DNase-seq from T-cell (ENCSR473LSX)


title: TF ChIP-seq from HepG2 (ENCSR080EKH)


title: TF ChIP-seq from HepG2 (ENCSR471VAY)


title: DNase-seq from retina (ENCSR474GZQ)


title: TF ChIP-seq from HepG2 (ENCSR076KLJ)


title: TF ChIP-seq from HepG2 (ENCSR800JRG)


title: TF ChIP-seq from HepG2 (ENCSR800ASH)


title: DNase-seq from right forelimb (ENCSR274SDO)


title: TF ChIP-seq from HepG2 (ENCSR469GZL)


title: TF ChIP-seq from HepG2 (ENCSR075BAS)


title: TF ChIP-seq from HepG2 (ENCSR076SHT)


title: TF ChIP-seq from HepG2 (ENCSR469FBY)


title: DNase-seq from upper lobe of left lung (ENCSR800ADR)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR800MBE)


title: TF ChIP-seq from K562 (ENCSR276RQG)

summary:
eGFP-ZNF696 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: TF ChIP-seq from HepG2 (ENCSR799FCZ)


title: Iso-Seq analysis of barley CI 16151 and fast-neutron-derived, immune-compromised mutants infected with the powdery mildew fungus (Blumeria graminis f. sp. hordei; isolate 5874)

city: Ames

first: Roger

last: Wise

state: IA

address: Department of Plant Pathology, Entomology, and Microbiology, Iowa State University, 1344 Advanced Teaching & Research Bldg., 2213 Pammel Dr.

department: CICGRU

institute: USDA/ARS

summary: Purpose: The powdery mildew fungus, Blumeria graminis, is an obligate biotrophic pathogen of cereals and has significant impact on food security (Dean et al., 2012. Molecular Plant Pathology 13 (4): 414-430. DOI: 10.1111/j.1364-3703.2011.00783.x). Blumeria graminis f. sp. hordei (Bgh) is the causal agent of powdery mildew on barley (Hordeum vulgare L.). We sought to discover novel transcripts expressed following barley infection with blumeria.

sample_organism:
Hordeum vulgare
Blumeria hordei

platform_organism:
Hordeum vulgare
Blumeria hordei

overall_design: 90 pooled samples analyzed = 5 genotypes * 6 time points * 3 replications. The pooled sample (90 experimental units) was SAGE-ELF size selected to generate 6 PacBio cDNA Iso‐Seq Library Preparations [fragment sizes: 1) non-fractionated 2) 1000-1500 nt 3) 1500-2000 nt 4) 2000-3000 nt 5) 3000-5000 nt 6) > 5000 nt].  The non-fractionated as well as the three smallest fragment libraries were each loaded onto 3 SMRT cells, and the two largest fragment libraries were each loaded onto 2 SMRT cells for a total of 16 SMRT cells. Four error-correcting programs (HECIL, LorDEC, HALC, COLORMAP) were explored to fix indels in the long PacBio reads. Each of these programs aligns short-reads directly to the erroneous PacBio long reads and uses the pile-up to correct insertions, deletions, and mismatches. Error-corrected long reads were mapped back to the Morex genome and the number of mismatches and indels were recorded. For each long read, the software that produced the best mapping quality was retained. Note: This experiment used the identical split-plot design, tissue, and source RNA as GEO submission # GSE101304 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101304). Gene counts were also obtained from short-reads generated from GEO submission # 101304 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101304). These transcripts will be used as a reference gold standard annotation to compare results from different gene annotation pipelines.  The short reads were not re-aligned to the new fasta files.

first: Sagnik

last: Banerjee

first: Gregory

last: Fuerst

middle: P


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR800KVI)


title: DNase-seq from body of pancreas (ENCSR464TKV)


title: DNase-seq from B cell (ENCSR468AKF)


title: DNase-seq from T-cell (ENCSR467MSP)


title: DNase-seq from sigmoid colon (ENCSR276ITP)


title: DNase-seq from head of caudate nucleus (ENCSR276MDV)


title: TF ChIP-seq from HepG2 (ENCSR272TOJ)


title: DNase-seq from H9 (ENCSR275ICP)


title: DNase-seq from ovary (ENCSR798XLO)


title: TF ChIP-seq from HepG2 (ENCSR271XMW)


title: TF ChIP-seq from HepG2 (ENCSR069JKP)


title: TF ChIP-seq from MCF-7 (ENCSR463GOT)

summary:
eGFP-ESR1 ChIP-seq on human MCF-7

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 (ENCSR798MFW)


title: TF ChIP-seq from HepG2 (ENCSR798KXG)

summary:
ChIP-Seq on HepG2

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: DNase-seq from head of caudate nucleus (ENCSR797FIM)

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: TF ChIP-seq from HepG2 (ENCSR463DPV)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR060ZXQ)


title: TF ChIP-seq from HepG2 (ENCSR068ZQR)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR796YOJ)


title: DNase-seq from coronary artery (ENCSR060HPL)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR060MJY)


title: DNase-seq from posterior cingulate gyrus (ENCSR060UPU)


title: DNase-seq from T-cell (ENCSR270JQK)


title: DNase-seq from adrenal gland (ENCSR458AOS)


title: TF ChIP-seq from HepG2 (ENCSR794LVK)


title: TF ChIP-seq from HepG2 (ENCSR795CKZ)


title: TF ChIP-seq from K562 (ENCSR271RRH)

summary:
eGFP-ZNF253 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: DNase-seq from head of caudate nucleus (ENCSR271QID)


title: TF ChIP-seq from HepG2 (ENCSR460YAM)


title: DNase-seq from heart right ventricle (ENCSR792QQE)


title: DNase-seq from breast epithelium (ENCSR788IZL)


title: DNase-seq from kidney (ENCSR792ZXA)


title: DNase-seq from upper lobe of left lung (ENCSR058VBM)


title: DNase-seq from T-helper 1 cell (ENCSR058ELM)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR059NIN)


title: DNase-seq from head of caudate nucleus (ENCSR057GPV)


title: TF ChIP-seq from HepG2 (ENCSR793EHQ)


title: TF ChIP-seq from HepG2 (ENCSR269DQN)


title: DNase-seq from CD4-positive naive resting alpha-beta T cell (ENCSR787ERP)


title: TF ChIP-seq from K562 (ENCSR056VYW)

summary:
eGFP-ZNF174 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: TF ChIP-seq from K562 (ENCSR459FUE)

summary:
eGFP-ERF 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: TF ChIP-seq from HepG2 (ENCSR269MEF)


title: DNase-seq from T-helper 1 cell (ENCSR453RFW)


title: TF ChIP-seq from HepG2 (ENCSR452UFJ)


title: DNase-seq from T-cell (ENCSR788SKJ)


title: DNase-seq from T-cell (ENCSR457RVC)


title: DNase-seq from pancreas (ENCSR056PFI)


title: DNase-seq from Peyer's patch (ENCSR455GUW)


title: DNase-seq from posterior cingulate gyrus (ENCSR789FJF)


title: DNase-seq from placenta (ENCSR267UFM)


title: DNase-seq from gastrocnemius medialis (ENCSR791BHE)


title: DNase-seq from head of caudate nucleus (ENCSR268GBM)


title: TF ChIP-seq from HepG2 (ENCSR267NVP)


title: TF ChIP-seq from K562 (ENCSR454SCH)


title: TF ChIP-seq from HepG2 (ENCSR788SXN)


title: TF ChIP-seq from K562 (ENCSR056VMR)


title: DNase-seq from T-cell (ENCSR785RIM)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR785MXI)


title: TF ChIP-seq from HepG2 (ENCSR266HHO)


title: TF ChIP-seq from HepG2 (ENCSR055ZIA)


title: TF ChIP-seq from HepG2 (ENCSR055FQB)


title: TF ChIP-seq from HepG2 (ENCSR264SRY)


title: DNase-seq from thyroid gland (ENCSR450PWF)


title: DNase-seq from T-cell (ENCSR784RMA)


title: DNase-seq from posterior cingulate gyrus (ENCSR784GVR)


title: DNase-seq from adrenal gland (ENCSR053ZKP)


title: TF ChIP-seq from K562 (ENCSR054JMQ)

summary:
eGFP-REST 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: TF ChIP-seq from K562 (ENCSR264LYE)

summary:
eGFP-ESRRB 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: DNase-seq from lower lobe of right lung (ENCSR785JXR)


title: DNase-seq from T-cell (ENCSR051CYH)


title: TF ChIP-seq from HepG2 (ENCSR052FXA)


title: TF ChIP-seq from HepG2 (ENCSR264LQX)


title: DNase-seq from adrenal gland (ENCSR259GYP)


title: TF ChIP-seq from Loucy (ENCSR783QUL)


title: DNase-seq from head of caudate nucleus (ENCSR775KLH)


title: TF ChIP-seq from HepG2 (ENCSR780OXL)


title: TF ChIP-seq from HepG2 (ENCSR050KWL)


title: TF ChIP-seq from HepG2 (ENCSR046DIG)


title: TF ChIP-seq from K562 (ENCSR783EPA)

summary:
eGFP-TBPL1 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: DNase-seq from posterior cingulate gyrus (ENCSR258POP)


title: DNase-seq from T-helper 1 cell (ENCSR260UJJ)


title: TF ChIP-seq from HepG2 (ENCSR261UIH)


title: TF ChIP-seq from HepG2 (ENCSR048WVW)


title: TF ChIP-seq from HepG2 (ENCSR775YXE)


title: ATAC-seq from gastrocnemius medialis (ENCSR258JCL)

summary:
ATAC-seq on human gastrocnemius medialis

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: DNase-seq from right hindlimb (ENCSR449HOQ)


title: DNase-seq from left ventricle myocardium inferior (ENCSR770OTB)


title: TF ChIP-seq from K562 (ENCSR258PSN)

summary:
ChIP-Seq on 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: TF ChIP-seq from A549 (ENCSR448TVS)

summary:
A549 immortalized cell line stably expressing C-terminal eGFP-FOSL2 fusion protein.

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 HepG2 (ENCSR043VRG)


title: TF ChIP-seq from K562 (ENCSR257RKC)


title: TF ChIP-seq from K562 (ENCSR044IXA)

summary:
eGFP-ZNF354B 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: TF ChIP-seq from HepG2 (ENCSR769CWW)


title: DNase-seq from regulatory T cell (ENCSR042WQA)


title: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR254BCA)


title: TF ChIP-seq from HepG2 (ENCSR263XFO)


title: DNase-seq from posterior cingulate gyrus (ENCSR770JCP)


title: TF ChIP-seq from HepG2 (ENCSR251XFX)


title: TF ChIP-seq from K562 (ENCSR257AFV)

summary:
eGFP-ZNF76 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: TF ChIP-seq from K562 (ENCSR775EQV)

summary:
eGFP-ZNF583 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: TF ChIP-seq from HepG2 (ENCSR767HDQ)


title: DNase-seq from Peyer's patch (ENCSR261RWJ)


title: DNase-seq from MG63 (ENCSR443YJP)


title: DNase-seq from T-cell (ENCSR442GKD)


title: TF ChIP-seq from HepG2 (ENCSR766TSU)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR769OIG)


title: DNase-seq from T-cell (ENCSR251INE)


title: TF ChIP-seq from A549 (ENCSR445FHB)

summary:
eGFP-FOXF2 ChIP-seq on human A549

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 HepG2 (ENCSR042BQZ)


title: ATAC-seq from body of pancreas (ENCSR765MXG)

summary:
ATAC-seq on human body of pancreas

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: ATAC-seq from HepG2 (ENCSR042AWH)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR763XBU)


title: DNase-seq from transverse colon (ENCSR763AKE)


title: TF ChIP-seq from HepG2 (ENCSR764ZBK)


title: TF ChIP-seq from K562 (ENCSR041YBR)


title: TF ChIP-seq from HepG2 (ENCSR041RCS)

summary:
eGFP-SOX13 ChIP-seq on human HepG2

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 HepG2 (ENCSR249EYB)

summary:
ChIP-Seq on HepG2

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 (ENCSR250WFW)

summary:
eGFP-RREB1 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: TF ChIP-seq from HepG2 (ENCSR759KXQ)


title: TF ChIP-seq from HepG2 (ENCSR248WAU)


title: TF ChIP-seq from HepG2 (ENCSR436RQS)


title: DNase-seq from lower lobe of left lung (ENCSR757NJT)

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: TF ChIP-seq from HepG2 (ENCSR435ARI)


title: DNase-seq from T-cell (ENCSR041PCL)


title: DNase-seq from head of caudate nucleus (ENCSR440BPA)


title: TF ChIP-seq from HepG2 (ENCSR248BVU)


title: TF ChIP-seq from K562 (ENCSR758PLU)

summary:
eGFP-ZNF408 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: TF ChIP-seq from HepG2 (ENCSR434ZNS)


title: DNase-seq from pancreas (ENCSR242RPQ)


title: DNase-seq from posterior cingulate gyrus (ENCSR249RFY)


title: TF ChIP-seq from HepG2 (ENCSR039CUX)


title: TF ChIP-seq from HepG2 (ENCSR756SZU)


title: TF ChIP-seq from HepG2 (ENCSR436PIH)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR240TZG)


title: TF ChIP-seq from HepG2 (ENCSR757HBB)


title: DNase-seq from head of caudate nucleus (ENCSR432QFU)


title: DNase-seq from CD14-positive monocyte (ENCSR241BNZ)


title: DNase-seq from posterior cingulate gyrus (ENCSR037PIU)


title: DNase-seq from head of caudate nucleus (ENCSR239MQN)


title: DNase-seq from heart right ventricle (ENCSR238FMP)


title: DNase-seq from heart right ventricle (ENCSR246VSO)


title: DNase-seq from left hindlimb (ENCSR431UEM)


title: DNase-seq from CD4-positive, alpha-beta memory T cell (ENCSR239XNU)


title: TF ChIP-seq from HepG2 (ENCSR755ZAY)


title: TF ChIP-seq from HepG2 (ENCSR432QMW)


title: TF ChIP-seq from HepG2 (ENCSR750OWO)


title: DNase-seq from HCEC 1CT (ENCSR038XTK)


title: TF ChIP-seq from MCF-7 (ENCSR042GSX)

summary:
eGFP-SPDEF ChIP-seq on human MCF-7

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 HepG2 (ENCSR754KCC)


title: DNase-seq from thyroid gland (ENCSR749MUH)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR749WVO)


title: DNase-seq from head of caudate nucleus (ENCSR756FQD)


title: TF ChIP-seq from HepG2 (ENCSR753KZY)


title: DNase-seq from pancreas (ENCSR236KPK)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR751VMX)


title: TF ChIP-seq from HepG2 (ENCSR237RPW)


title: TF ChIP-seq from HepG2 (ENCSR431FOF)


title: TF ChIP-seq from HepG2 (ENCSR036RHV)


title: DNase-seq from CD8-positive naive resting alpha-beta T cell (ENCSR237BOF)


title: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR235OZX)


title: DNase-seq from T-helper 1 cell (ENCSR035SZE)


title: TF ChIP-seq from GM12878 (ENCSR748SQL)

summary:
GM12878 immortalized cell line stably expressing C-terminal eGFP-PRDM15 fusion protein.

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: DNase-seq from head of caudate nucleus (ENCSR234VLI)


title: TF ChIP-seq from K562 (ENCSR235PYI)

summary:
eGFP-ZNF41 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: TF ChIP-seq from HepG2 (ENCSR428LOB)


title: TF ChIP-seq from A549 (ENCSR748HJZ)

summary:
eGFP-HOXB5 ChIP-seq on human A549

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 (ENCSR036QIR)

summary:
eGFP-E2F3 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: DNase-seq from T-helper 17 cell (ENCSR747RGR)


title: TF ChIP-seq from HepG2 (ENCSR747VUU)


title: DNase-seq from heart right ventricle (ENCSR746RDJ)


title: TF ChIP-seq from HepG2 (ENCSR233FJO)


title: TF ChIP-seq from K562 (ENCSR236JZN)

summary:
eGFP-ZNF586 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: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR744UQK)


title: DNase-seq from head of caudate nucleus (ENCSR742HBK)


title: TF ChIP-seq from HepG2 (ENCSR422VAG)


title: TF ChIP-seq from HepG2 (ENCSR232LLP)


title: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR036ELY)


title: TF ChIP-seq from HepG2 (ENCSR735VJE)


title: DNase-seq from left cardiac atrium (ENCSR032NNU)


title: TF ChIP-seq from HepG2 (ENCSR232AAR)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR428ZCP)


title: ATAC-seq from A549 (ENCSR032RGS)

summary:
ATAC-seq on human cell line A549

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: DNase-seq from heart left ventricle (ENCSR735NTV)


title: TF ChIP-seq from HepG2 (ENCSR032LZZ)


title: DNase-seq from Caco-2 (ENCSR030HFV)


title: DNase-seq from heart left ventricle (ENCSR747SEU)


title: ATAC-seq from MCF-7 (ENCSR422SUG)


title: DNase-seq from ascending aorta (ENCSR422IIZ)


title: TF ChIP-seq from HepG2 (ENCSR421DAO)


title: TF ChIP-seq from K562 (ENCSR231PDA)

summary:
eGFP-ZNF319 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: DNase-seq from CD8-positive, alpha-beta T cell (ENCSR424JPH)


title: TF ChIP-seq from K562 (ENCSR231ZVN)

summary:
eGFP-FOXA3 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: DNase-seq from brain (ENCSR420RWU)


title: TF ChIP-seq from K562 (ENCSR026KKZ)

summary:
eGFP-ZBTB17 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: TF ChIP-seq from HepG2 (ENCSR756UNW)


title: TF ChIP-seq from HepG2 (ENCSR029ARE)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR426KLJ)


title: TF ChIP-seq from HepG2 (ENCSR734WFB)


title: TF ChIP-seq from HepG2 (ENCSR026GSW)


title: DNase-seq from posterior cingulate gyrus (ENCSR730IHD)


title: DNase-seq from T-cell (ENCSR420HOT)


title: TF ChIP-seq from HepG2 (ENCSR228ZYW)


title: TF ChIP-seq from A549 (ENCSR419VVI)

summary:
eGFP-ZNF624 ChIP-seq on human A549

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 HepG2 (ENCSR731UPJ)


title: TF ChIP-seq from HepG2 (ENCSR731LZB)


title: TF ChIP-seq from K562 (ENCSR228OQM)

summary:
eGFP-CLOCK 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: DNase-seq from T-cell (ENCSR025EYJ)


title: DNase-seq from T-cell (ENCSR419OAR)


title: DNase-seq from posterior cingulate gyrus (ENCSR729TYE)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR419KXU)


title: TF ChIP-seq from HepG2 (ENCSR025EXJ)


title: TF ChIP-seq from HepG2 (ENCSR734CRN)


title: TF ChIP-seq from HepG2 (ENCSR730DZO)


title: DNase-seq from ovary (ENCSR732RIC)


title: TF ChIP-seq from HepG2 (ENCSR725QZQ)


title: DNase-seq from effector memory CD4-positive, alpha-beta T cell (ENCSR724INK)


title: ATAC-seq from posterior cingulate cortex (ENCSR729FNL)

summary:
human UMB4727 posterior cingulate cortex

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: DNase-seq from left lung (ENCSR723VNG)


title: TF ChIP-seq from HepG2 (ENCSR024ZIS)

summary:
ChIP-Seq on HepG2

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 HepG2 (ENCSR419KSZ)


title: TF ChIP-seq from HepG2 (ENCSR227MRE)


title: DNase-seq from head of caudate nucleus (ENCSR722HJG)


title: DNase-seq from inflammatory macrophage (ENCSR721XAP)


title: DNase-seq from head of caudate nucleus (ENCSR024BXN)


title: TF ChIP-seq from HepG2 (ENCSR722TRY)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR022UVL)


title: TF ChIP-seq from HepG2 (ENCSR720PDY)


title: TF ChIP-seq from HepG2 (ENCSR020CLV)


title: TF ChIP-seq from HepG2 (ENCSR417EWD)


title: DNase-seq from head of caudate nucleus (ENCSR417LPB)


title: TF ChIP-seq from HepG2 (ENCSR225SLE)


title: TF ChIP-seq from HepG2 (ENCSR017XHZ)


title: TF ChIP-seq from HepG2 (ENCSR224NQI)


title: TF ChIP-seq from HepG2 (ENCSR717ZZW)


title: TF ChIP-seq from HepG2 (ENCSR416HDG)


title: TF ChIP-seq from K562 (ENCSR017EJY)

summary:
eGFP-DLX4 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: DNase-seq from CD8-positive, alpha-beta memory T cell (ENCSR025BWH)

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: DNase-seq from dorsolateral prefrontal cortex (ENCSR720FVJ)


title: TF ChIP-seq from HepG2 (ENCSR227PHM)


title: TF ChIP-seq from HepG2 (ENCSR413AJG)


title: DNase-seq from head of caudate nucleus (ENCSR717BBR)


title: DNase-seq from islet precursor cell (ENCSR224FOA)


title: TF ChIP-seq from K562 (ENCSR023OOE)

summary:
eGFP-ZNF764 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: DNase-seq from T-cell (ENCSR715TMH)


title: TF ChIP-seq from HepG2 (ENCSR717QSS)


title: DNase-seq from heart left ventricle (ENCSR222CLC)


title: TF ChIP-seq from HepG2 (ENCSR016OHL)


title: TF ChIP-seq from K562 (ENCSR222TVA)

summary:
eGFP-ZNF785 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: DNase-seq from left cardiac atrium (ENCSR412NMI)


title: TF ChIP-seq from K562 (ENCSR712KVZ)

summary:
eGFP-ZNF324 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: DNase-seq from T-cell (ENCSR410IYF)


title: TF ChIP-seq from HepG2 (ENCSR014HQD)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR221ROM)


title: TF ChIP-seq from HepG2 (ENCSR410FEH)


title: DNase-seq from suppressor macrophage (ENCSR711AQM)


title: TF ChIP-seq from HepG2 (ENCSR220AQM)


title: DNase-seq from head of caudate nucleus (ENCSR721DFB)


title: DNase-seq from WERI-Rb-1 (ENCSR218FSP)


title: TF ChIP-seq from HepG2 (ENCSR409PMR)


title: TF ChIP-seq from HepG2 (ENCSR711KBM)


title: DNase-seq from T-cell (ENCSR217PZP)


title: DNase-seq from T-helper 17 cell (ENCSR709YRE)


title: DNase-seq from T-cell (ENCSR218FJD)


title: TF ChIP-seq from HepG2 (ENCSR013DKM)


title: DNase-seq from suprapubic skin (ENCSR709IYR)


title: DNase-seq from head of caudate nucleus (ENCSR217OHA)


title: TF ChIP-seq from HepG2 (ENCSR013RNH)


title: TF ChIP-seq from HepG2 (ENCSR215XSZ)


title: TF ChIP-seq from HepG2 (ENCSR708KAA)


title: DNase-seq from mucosa of gallbladder (ENCSR011SAG)


title: TF ChIP-seq from HepG2 (ENCSR011INW)


title: TF ChIP-seq from HepG2 (ENCSR407BPU)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR014GTH)


title: DNase-seq from body of pancreas (ENCSR405YLV)


title: TF ChIP-seq from HepG2 (ENCSR707RKU)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR215DXT)


title: TF ChIP-seq from GM23338 (ENCSR214ZAV)

summary:
eGFP-CREB1 ChIP-seq on human GM23338

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 (ENCSR405KTQ)

summary:
eGFP-HEY1 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: DNase-seq from BE2C (ENCSR009KWQ)


title: TF ChIP-seq from HepG2 (ENCSR009LIA)


title: TF ChIP-seq from SK-N-SH (ENCSR706VOO)

summary:
ChIP-Seq on 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: DNase-seq from CD8-positive, alpha-beta memory T cell (ENCSR705GCU)


title: DNase-seq from mucosa of descending colon (ENCSR404TSP)


title: TF ChIP-seq from HepG2 (ENCSR704ENT)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR006MAW)


title: ATAC-seq from transverse colon (ENCSR404LLJ)

summary:
ATAC-seq on human transverse colon

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: DNase-seq from T-cell (ENCSR213WNV)


title: DNase-seq from stomach (ENCSR006IMH)


title: DNase-seq from posterior cingulate gyrus (ENCSR006XFA)


title: DNase-seq from placenta (ENCSR212VEN)


title: DNase-seq from brain microvascular endothelial cell (ENCSR006DKF)


title: TF ChIP-seq from HepG2 (ENCSR403MJY)


title: DNase-seq from heart right ventricle (ENCSR211SUT)


title: TF ChIP-seq from HepG2 (ENCSR005GZH)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR210ESN)


title: TF ChIP-seq from K562 (ENCSR002ZGC)

summary:
eGFP-ZNF212 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: TF ChIP-seq from HepG2 (ENCSR213QOZ)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR209ECO)


title: TF ChIP-seq from HepG2 (ENCSR402ZCY)


title: TF ChIP-seq from MM.1S (ENCSR703KWN)


title: DNase-seq from kidney (ENCSR206OJJ)


title: DNase-seq from heart right ventricle (ENCSR214NLQ)


title: TF ChIP-seq from A549 (ENCSR402OYZ)

summary:
eGFP-HOXA7 ChIP-seq on human A549

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: DNase-seq from CD4-positive, alpha-beta T cell (ENCSR206KJN)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR001QTZ)


title: TF ChIP-seq from HepG2 (ENCSR206BVQ)


title: DNase-seq from aorta (ENCSR713KNQ)


title: DNase-seq from SK-MEL-5 (ENCSR000FEK)


title: DNase-seq from dorsolateral prefrontal cortex (ENCSR401UZL)


title: TF ChIP-seq from HepG2 (ENCSR700USV)


title: ATAC-seq from thyroid gland (ENCSR201FIW)

summary:
ATAC-seq on human thyroid gland

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 HepG2 (ENCSR701WPG)


title: DNase-seq from upper lobe of left lung (ENCSR702DPD)


title: Behavioral and Gene Expression Analysis of Stxbp6-Knockout Mice

status: Public on Mar 27 2021

city: Changsha

first: Cong

last: Liu

address: No.110 Xiangya road

institute: Central South University

summary: To investigate the impact of Stxbp6 knockout on the brain, we carried out transcriptome analysis on the cortexes of Stxbp6-null (n = 3, KO) and wildtype mice (n = 3, WT) and identified 126 differentially expressed genes (DEGs) in the KO group, of which 57 were upregulated and 69 were downregulated. RNA-seq was performed on the BGISEQ platform by MGI Technology Co., Ltd, Guangdong, China.

overall_design: Gene expression profiles between cerebral cortexes from wildtype and Stxbp6-null mice.

first: Qian

last: Hu

first: Yan

last: Chen

first: Lingqian

last: Wu

first: Xionghao

first: Desheng

last: Liang


title: DNase-seq from HT1080 (ENCSR000FDI)


title: New perspectives in different gene expression profiles for early and locally advanced non-small cell lung cancer stem cells.

city: Modena

first: Beatrice

last: Aramini

state: italy

address: via del pozzo 71, via del pozzo 71

country: Italy

institute: University Hospital of Modena

summary: No effective treatments against lung cancer for early or advanced stages have been found. Our aim is to assess whether cancer stem cells (CSC) do show over expression of genes, which were previously identified for adenocarcinoma recurrence, in patients with early and locally advanced non-small cell lung cancer (NSCLC) stages.

overall_design: This is a cross-sectional study. The mRNA expression of 31 recurrence-related target genes in aldehyde dehydrogenase ALDH-high (CSC) and ALDH-low (epithelial cancer cells) populations have been analyzed in surgical specimens obtained from 22 patients, 12 harboring early (I-II) and 10 harboring locally advanced (IIIA) stages of NSCLC. The mRNA expressions were available in duplicates and ALDH-low cells have been used as reference sample.

first: Valentina

last: Masciale

first: Federico

last: Banchelli

first: Giulia

last: Grisendi

first: Roberto

last: D’Amico

first: Antonino

last: Maiorana

first: Alessandro

last: Stefani

first: Uliano

last: Morandi

first: Massimo

last: Dominici


title: DNase-seq from head of caudate nucleus (ENCSR200BNM)

first: ENCODE

last: DCC


title: Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

city: Boston

first: Rakesh

last: Jain

state: MA

address: 100 Blossom Street, Cox-7

institute: Massachusetts General Hospital

summary: Immune checkpoint blockers (ICBs) have failed in all phase III glioblastoma (GBM) trials. Here, we show that regulatory T (Treg) cells play a key role in GBM resistance to ICBs in experimental gliomas. Targeting glucocorticoid-induced TNFR-related receptor (GITR) in Treg cells using an agonistic antibody (αGITR) promotes CD4 Treg cell differentiation into CD4 effector T cells, alleviates Treg cell-mediated suppression of anti-tumor immune response, and induces potent anti-tumor effector cells in GBM. The reprogrammed GBM-infiltrating Treg cells express genes associated with a Th1 response signature, produce IFNγ, and acquire cytotoxic activity against GBM tumor cells while losing their suppressive function. αGITR and αPD1 antibodies increase survival benefit in three experimental GBM models, with a fraction of cohorts exhibiting complete tumor eradication and immune memory upon tumor re-challenge. Moreover, αGITR and αPD1 synergize with the standard of care treatment for newly-diagnosed GBM, enhancing the cure rates in these GBM models.

overall_design: Treg cells were sorted from IgG (control; spleen n=7; tumor n=5) or aGITR+aPD1 (treated; spleen n=9; tumor=7) treated GBM-bearing mice. Each individual spleen or tumor sample was harvested from different mice, respectively.

first: Zoreh

last: Amoozgar

first: Jonas

last: Kloepper

first: Jun

last: Ren

first: Rong

last: Tay

first: Samuel

middle: W

last: Kazer

first: Evgeny

last: Kiner

first: Shanmugarajan

last: Krishnan

first: Jessica

last: Possada

first: Mitrajit

last: Ghosh

first: Emilie

last: Mamessier

first: Christina

last: Wong

first: Gino

last: Ferraro

first: Ana

last: Batista

first: Nancy

last: Wang

first: Mark

last: Badeaux

first: Sylvie

last: Roberge

first: Lei

last: Xu

first: Peigen

last: Huang

first: Alex

last: Shalek

first: Dai

last: Fukumura

first: Hye-Jung

last: Kim


title: Dynamic Expression of Imprinted Genes in the Developing and Postnatal Pituitary Gland

status: Public on Mar 26 2021

city: London

first: Ruben

last: Esse

address: Guy's Hospital, Great Maze Pond

department: Department of Medical and Molecular Genetics

country: United Kingdom

institute: King’s College London

summary: In mammals, imprinted genes regulate many critical endocrine processes such as growth, the onset of puberty and maternal reproductive behaviour. Human imprinting disorders (IDs) are caused by genetic and epigenetic mechanisms that alter the expression dosage of imprinted genes. Due to improvements in diagnosis, increasing numbers of patients with IDs are now identified and monitored across their lifetimes. Seminal work has revealed that IDs have a strong endocrine component, yet the contribution of imprinted gene products in the develop-ment and function of the hypothalamo-pituitary axis are not well defined. Postnatal endocrine processes are dependent upon the production of hormones from the pituitary gland. While the actions of a few imprinted genes in pituitary development and function have been described, to date there has been no attempt to link the expression of these genes as a class to the formation and function of this essential organ. This is important because IDs show considerable overlap, and imprinted genes are known to define a transcriptional network related to organ growth. This knowledge deficit is partly due to technical difficulties in obtaining useful transcriptomic data from the pituitary gland, namely, its small size during development and cellular complex-ity in maturity. Here we utilise high-sensitivity RNA sequencing at the embryonic stages, and single-cell RNA sequencing data to describe the imprinted transcriptome of the pituitary gland. In concert, we provide a comprehensive literature review of the current knowledge of the role of imprinted genes in pituitary hormonal pathways and how these relate to IDs. We present new data that implicate imprinted gene networks in the development of the gland and in the stem cell compartment. Furthermore, we suggest novel roles for individual imprinted genes in the aetiology of IDs. Finally, we describe the dynamic regulation of imprinted genes in the pituitary gland of the pregnant mother, with implications for the regulation of maternal metabolic adap-tations to pregnancy.

overall_design: Rathke’s pouch was dissected from 7 Sox2Egfp/+ e13.5 embryos. The whole pituitary gland was dissected from 2 adult mice at postnatal week 8 and the posterior lobe was removed. The samples were processed for expression profiling by RNAseq.

first: Marika

last: Charalambous


title: TF ChIP-seq from HepG2 (ENCSR700PNE)

first: ENCODE

last: DCC

summary:
ChIP-Seq on HepG2

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 HepG2 (ENCSR400JHG)


title: Single-cell TCR sequencing reveals the dynamics of T cell repertoire profiling during Pneumocystis infection

first: Zhaohui

last: Tong

state: Beijing

address: NO. 8, Gong Ti South Road

department: Department of Respiratory and Critical Care Medicine

institute: Beijing Chaoyang Hospital

summary: T cell response exert critical roles in the host adaptive immunity against Pneumocystis. However, the dynamics and diversity of T cell immune repertoire in HIV-negative Pneumocystis remains unknown. In this study, single-cell RNA and T cell receptor (TCR) sequencing were applied on cells sorted from lung tissues of mice infected with Pneumocystis from 0 to 4 weeks. Our data demonstrated clonally CD4+ T cells and CD8+ T cells expanded in response to Pneumocystis, which marked by highly expressed genes associated with T cell activation and cytotoxicity. The length distribution of CDR3 AA and gene usage variability were similar between Pneumocystis infected mice and control group. We tracked the transcriptome and TCR immune repertoires profiles of expanded lymphocyte clones during Pneumocystis infection, which demonstrate a reconstitution of the TCR immune repertoire after Pneumocystis infection.

overall_design: Single-cell TCR profiles of wild type (WT) and mices infected with Pneumocystis 1-4 weeks.

first: Zhao-Hui

first: Kan

last: Zhai

first: Hu-qin

last: Yang

first: Han

last: Sun


title: ZFTA-RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

city: Memphis

first: Stephen

middle: C

last: Mack

state: Tennessee

address: 262 Danny Thomas Place

institute: St. Jude Children’s Research Hospital

summary: Over 60% of supratentorial (ST) ependymomas harbor a ZFTA-RELA (ZRfus) gene fusion (formerly C11orf95-RELA). To study the biology of ZRfus, we developed an autochthonous mouse tumor model using in utero electroporation (IUE) of the embryonic mouse brain. Integrative epigenomic and transcriptomic mapping was performed on IUE driven ZRfus tumors by CUT&RUN, ChIP, ATAC, and RNA sequencing and compared to human ZRfus driven ependymoma. In addition to direct canonical NF-kB pathway activation, ZRfus dictates a neoplastic transcriptional program and binds to thousands of unique sites across the genome that are enriched with Plagl family transcription factor (TF) motifs. ZRfus activates gene expression programs through recruitment of transcriptional co-activators (Brd4, Ep300, Cbp, Pol2) that are amenable to pharmacologic inhibition. Downstream ZRfus target genes converge on developmental programs marked by Plagl transcription factor proteins, and activate neoplastic programs enriched in Mapk, focal adhesion, and gene imprinting networks.

overall_design: CUT&RUN


title: Single cell RNA sequencing of the lung pre-metastatic niche in a syngeneic mouse model of rhabdomyosarcoma

city: Bethesda

first: Michael

last: Kelly

state: MD

address: 41 Center Drive

department: Center for Cancer Research

institute: NCI

summary: C57BL/6 mice were injected orthotopically with M3-9-M ffluc-mCherry rhabdomyosarcoma tumor cells in the gastrocnemius muscle of the leg. Mice were treated with 8E6 IL12-secreting genetically engineered myeloid cells (IL12-GEMys) on day 12 post tumor inoculation. Lungs were harvested 3 days post IL12-GEMy treatment, 15 days post primary tumor inoculation. 3' single cell RNA-Seq was performed on isolated cells.

overall_design: Single cell 3' RNA-Seq from lung tissue of naive mice, primary tumor-bearing pre-metastatic mice, and primary tumor-bearing pre-metastatic mice treated with IL12-GEMys.

first: Rosandra

last: Kaplan

first: Sabina

last: Kaczanowska

first: Zachary

last: Rae

first: Vishaka

last: Gopalan


title: Gene expression analysis to investigate role of tumor-intrinsic hypoxia and tumor secretome in collective migration

city: Pittsburgh

first: Shilpa

last: Sant

state: PA

address: 700 Technology Drive

department: Pharmaceutical Sciences

institute: University of Pittsburgh

summary:
We investigated two microenvironmental factors, tumor-intrinsic hypoxia, and tumor-secreted factors (secretome) as triggers of collective migration using a three-dimensional (3D) discrete-sized microtumor models that recapitulate hallmarks of Ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) transition. These two factors induced two distinct modes of collective migration: directional and radial migration in the 3D microtumors generated from the same breast cancer cell line model, T47D. Without external stimulus, large (>500µm) T47D microtumors exhibited tumor-intrinsic hypoxia and directional collective migration while small (<150 µm), non-hypoxic microtumors exhibited radial collective migration only when exposed to secretome of large microtumors. To investigate the differences in the underlying mechanism  present between hypoxia- and secretome-induced directional versus radial migration modes, we performed differential gene expression analysis of hypoxia- and secretome-induced migratory microtumors vs.  non-hypoxic, non-migratory small microtumors as controls.
We used microarrays to detail the global programme of gene expression profiling to study tumor intrinsic hypoxia induced directional migration and secretom induced radial migrartion in large 600µm microtumors with small 150μm microtumors as controls in three dimensional (3D) breast microtumor model

overall_design: To understand the mechanism of two distinct directional and radial collective migratory phenotypes using our 3D microtumor models with controlled microenvironments we carried out RNA expression profiling using Affymetrix platform. To investigate mRNA expression changes induced by tumor-intrinsic hypoxia and secretome as two microenvironmental factors and also to understand the size effect and temporal effect over 6 day period. To that end, we harvested  size specific microtumors at four time-points: i.e. small 150μm microtumors (day 6), large 600µm microtumors (day 1 and day 6) and secretome induced CM150μm microtumors(day 6).

first: Manjulata

last: Singh

first: Catalina

last: Ardila

first: Vaishali

last: Aggarwal


title: Deletion of a non-canonical regulatory sequence causes loss of Scn1a expression and epileptic phenotypes in mice II

city: Davis

first: Alex

last: Nord

address: 1544 Newton Court

department: Neurobiology, Physiology, & Behavior

institute: University of California, Davis

summary: Background: Genes with multiple co-active promoters appear common in brain, yet little is known about functional requirements for these potentially redundant genomic regulatory elements. SCN1A, which encodes the NaV1.1 sodium channel alpha subunit, is one such gene with two co-active promoters. Mutations in SCN1A are associated with epilepsy, including Dravet Syndrome (DS). The majority of DS patients harbor coding mutations causing SCN1A haploinsufficiency, however putative causal non-coding promoter mutations have been identified. Methods: To determine the functional role of one of these potentially redundant Scn1a promoters, we focused on the non-coding Scn1a 1b regulatory region, previously described as a non-canonical alternative transcriptional start site. We bred a transgenic mouse line with deletion of the extended evolutionarily-conserved 1b non-coding interval and characterized changes in gene and protein expression, and assessed seizure activity and alteration in behavior. Results: Mice harboring a deletion of the 1b non-coding interval exhibited surprisingly severe reductions of Scn1a and NaV1.1 expression throughout the brain. This was accompanied by electroencephalographic and thermal-evoked seizures, and some behavioral deficits. Conclusions: This work contributes to functional dissection of the regulatory wiring of a major epilepsy risk gene, SCN1A. We identified the 1b region as a critical disease-relevant regulatory element and provide evidence

overall_design: Characterization of differential gene expression changes with Scn1a heterozygous and homozygous knockout.

first: Jessica

middle: L

last: Haigh

first: Anna

last: Adhikari

first: Nycole

middle: A

last: Copping

first: Tyler

last: Stradleigh

first: Alexandria

last: Wade

first: Rinaldo

last: Catta-Preta

first: Linda

last: Su-Feher

first: Iva

last: Zdilar

first: Sarah

last: Morse

first: Timothy

last: Fenton

first: Anh

last: Nguyen

first: Diana

last: Quintero

first: Samrawit

last: Agezew

last: Sramek

first: Ellie

middle: J

last: Kreun

first: Jasmine

last: Carter

first: Andrea

last: Gompers

first: Jason

last: Lambert

first: Cesar

last: Canales

first: Len

last: Pennacchio

first: Axel

last: Visel

first: Diane

middle: E

last: Dickel

first: Jill

last: Silverman

middle: S


title: ATAC-seq from IMR-90 (ENCSR200OML)

first: ENCODE

last: DCC

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: Transcriptome analysis of the seed weight plasticity in Brassica napus

status: Public on Mar 25 2021

city: Valdivia

first: Javier

state: Los Ríos

address: Campus Isla Teja s/n

department: Instituto de Bioquimica y Microbiologia

country: Chile

institute: Universidad Austral de Chile

summary: A critical barrier for improving crops yield is the compensatory effect between seed weight (SW) and seed number (SN), which has been widely reported in several crops including Brassica napus. Despite the agronomic relevance of this issue, the molecular factors involved in the interaction between SW and SN are largely unknown in crops. In this work, we performed a detailed transcriptomic analysis of 48 seed samples obtained from two rapeseed spring genotypes subjected to different source-sink (S-S) ratios in order to modify the relationship between SW and SN under field conditions.

overall_design: Seed samples were collected from 5 plants per plot (25 siliques per plant from the bottom of the main raceme) in two development stages: 7 and 14 after the beginning of the shading treatment in three replicates across the different factors analyzed (genotypes, S-S ratio and sowing dates)


title: Genome-wide gene expression analysis for CRISPRi targeting a human SFTPB locus bound by NKX2-1

city: Cincinnati

first: Minzhe

last: Guo

state: OH

address: 3333 BURNET AVENUE

department: Pulmonary Biology

institute: Cincinnati Children's Hospital Medical Center

summary: RNA-seq was performed to identify genes affected by CRISPRi (dCas9-KRAB) with sgRNA (sgSFTPB#2) targeting the first intronic region of human SFTPB bound by NKX2-1 in an unbiased genome-wide fashion using A549 lung carcinoma cells that constitutively express dCas9-KRAB and NKX2-1.

overall_design: Expression of genes in A549 cells stably expressing dCas9-KRAB and NKX2-1 with the sgRNA targeting the SFTPB locus was compared with those stably expressing dCas9-KRAB and NKX2-1 with a sgRNA of non-targeting negative control.

first: Yutaka

last: Maeda


title: Rat PRDM9 shapes recombination landscapes, duration of meiosis, gametogenesis, and age of fertility

first: Kevin

last: Brick

address: 5/205 Memorial Drive

department: GBB

institute: NIDDK

summary: Vertebrate recombination concentrates in meiotic chromatin regions (hotspots) that are opened in some species by the DNA-sequence-specific-binding histone H3 trimethyltransferase PRDM9, while other species recombine in regions with already opened chromatin and other function. Inactivation of the mouse Prdm9 gene induces the shift of hotspots to functional regions, gross fertility reduction in males, and sterility in females. In contrast, the other  vertebrate species lacking PRDM9 remain fertile. To resolve this discrepancy, we generated Prdm9 deletions in the Rattus norvegicus genome and generated the first rat genome-wide maps of recombination-initiating double-strand break hotspots. Rat strains carrying the same wild-type Prdm9 allele shared 88% hotspots but strains with different Prdm9 alleles only 3%. After Prdm9 deletion, rat hotspots relocated to functional regions, 40% to positions corresponding to Prdm9-independent mouse hotspots. Despite of hotspot relocation and of decreased fertility, Prdm9-deficient rats of the SHR/OlaIpcv strain produced apparently normal offspring. Rat PRDM9 thus makes recombination landscape unique, but it is unnecessary for recombination. This peculiarity is likely similar for human PRDM9 and may resolve the paradox between the apparently species-specific functions. PRDM9 is known to play a role in speciation, as it causes mouse hybrid sterility via meiotic asynapsis. Besides the expected mild meiotic arrest, we also detected apoptosis of postmeiotic spermatids, suggesting that PRDM9 has an additional role during spermatogenesis and perhaps also in speciation.

overall_design: DSB hotspots were mapped in three wild-type rat strains and in rats either hemi-zygous or homozygous for loss of functional Prdm9. H3K4me3 ChIP-Seq was also performed to study the histone marks made by the Prdm9 protein.

first: Ondrej

last: Mihola

first: Vladimir

last: Landa

first: Florencia

last: Pratto

first: Fatima

last: Smagulova

first: Tatyana

last: Kobets

first: Petr

last: Flachs

first: Vaclav

last: Gergelits

first: Karel

last: Tresnak

first: Jan

last: Silhavy

last: Mlejnek

first: Rafael

middle: D

last: Camerini-Otero

first: Michal

last: Pravenec

first: Petukhova

last: Galina

first: Zdenek

last: Trachtulec


title: Deletion of a non-canonical regulatory sequence causes loss of Scn1a expression and epileptic phenotypes in mice

first: Alex

last: Nord

first: Jessica

last: Haigh

first: Anna

last: Adhikari

first: Nycole

last: Copping

first: Tyler

last: Stradleigh

first: Alexandria

last: Wade

first: Rinaldo

last: Catta-Preta

first: Linda

last: Su-Feher

first: Iva

last: Zdilar

first: Sarah

last: Morse

first: Timothy

last: Fenton

first: Anh

last: Nguyen

first: Diana

last: Quintero

first: Samrawit

last: Agezew

first: Michael

last: Sramek

first: Ellie

last: Kreun

first: Jasmine

last: Carter

first: Andrea

last: Gompers

first: Jason

last: Lambert

first: Cesar

last: Canales

first: Len

last: Pennacchio

first: Axel

last: Visel

first: Diane

last: Dickel

first: Jill

last: Silverman


title: Epigenetic differences between transgenes and endogenous genes promote transgene silencing in plants

city: Versailles

first: Filipe

last: Borges

address: Route de St-Cyr (RD10)

country: France

institute: Institut Jean-Pierre Bourgin - INRAE

summary: Transgene loci that spontaneously undergo RNA silencing have been instrumental to decipher RNA silencing pathways in plants. In contrast, transgene loci that are stably expressed have been poorly characterized. Here we show that stably expressed transgene loci epigenetically differ from endogenous genes. Impairing the histone H3K4me3 demethylase JMJ14 increases DNA methylation at stably expressed transgene loci but not at endogenous genes, whereas impairing the histone H3K9me2 demethylase IBM1 increases DNA methylation at endogenous genes, but decreases DNA methylation at stably expressed transgene loci. Moreover, impairing IBM1 promotes post-transcriptional gene silencing (PTGS) at stably expressed transgene loci, whereas impairing JMJ14 prevents PTGS induced systemically by grafting onto silenced rootstocks. Given that impairing DNA methylation suppresses the effect of impairing JMJ14 and restores transgene capacity to undergo graft-induced PTGS, we propose that transgene DNA methylation prevents PTGS, likely by limiting the transcription of aberrant RNA by-products that are transformed into dsRNA by cellular RNA-dependent RNA polymerases to activate PTGS.

overall_design: Genomic DNA from leaf samples analyzed by whole-genome bisulfite sequencing. Experiment 1: Leaf samples from 5-week-old plants carrying the 6b4 transgene in wild type Col-0 (6b4-1) and in mutants (6b4 jmj14, 6b4 jmj14 drm2 cmt3 and 6b4 drm2 cmt3). Experiment 2: Leaf samples of 8-week-old plants carrying the 6b4 transgene in wild type Col-0 (6b4-2) and mutants (6b4 nac50 nac52 and 6b4 ibm1).

first: Hervé

last: Vaucheret


title: DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (Dnase-Seq)

city: SEATTLE

first: John

last: Stamatoyannopoulos

state: WA

address: 2211 Elliott Avenue, 6th Floor

department: Genome Sciences

institute: Altius Institute / University of Washington

summary: Using the Notch signaling pathway, hematopoietic stem and progenitor cells (HSPC) sense and respond to the surrounding microenvironment to regulate cell fate outcome. Our previous studies have indicated that quantitative differences in Notch signal strength mediate cell-fate decisions during hematopoiesis. Low signal strength favors HSPC self-renewal, along with inhibition of myelopoiesis, whereas high signal strength promotes T cell differentiation. The basis for target gene selectivity in response to quantitative differences in Notch signal strength is unknown. Focusing on the high dose dependent induction of the T cell lineage, we found that targets essential for T cell commitment, including IL2ra, CD3 and Rag1, establish promoter DNA accessibility only upon exposure to high levels of Notch signaling.  We further find that low promoter CpG content is a feature capable of maintaining the ground state DNA inaccessibility of these lineage determining genes. Our results suggest that DNA inaccessibility at the promoters of essential T cell commitment genes, mediated in part through low CpG content, provides robust protection against stochastic activation in inappropriate Notch signaling contexts, ensuring the maintenance of HSPC developmental plasticity.

overall_design: DNase-seq data was collected across different stages of T cell development (LSK, DN1, DN2a, DN2b) and negative control (IgG), where each stage has 2 to 3 replicates. To find the accessible regions genome-wide, a peak calling approach hotspot2 was applied on each stage respectively, and in total ~170,000 DHSs regions was identified with peaks.

first: Suzanne

last: Furuyama

first: Richard

last: Sandstrom


title: DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression

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

overall_design: Refer to individual Series


title: Discovery of Klf2 Interactors in Mouse Embryonic Stem Cells by Immunoprecipitation-Mass Spectrometry Utilizing Exogenously Expressed Bait

status: Public on Mar 24 2021

city: Daejeon

first: Lin

last: Seo

address: Basic Science Bld Rm414, 291 Daehak-ro, Yuseong-gu, KAIST

department: Department of Biological Sciences

country: South Korea

institute: KAIST

summary: We report the RNA-seq data of Klf2 knockdowned cells and Snd1 knockdowned cells from mouse embryonic stem cells. Samples were lysed with total RNA prep kit.

overall_design: Two biological replicates were analyzed. RNA-seq samples in wild-type (WT) and Klf2 knockdown were treated with Snd1 knockdown in mouse embryonic stem cells (E14TG2a).

first: Jaehoon

last: Kim

first: J

last: Lee


title: Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction

city: Rehovot

first: Noa

last: Novershtern

address: Weizmann Institute

department: Molecular Genetics

country: Israel

institute: Weizmann Institute of Science


title: Molecular regulation of melatonin biosynthesis pathway in unipolar and bipolar depression

city: POZNAN

first: MONIKA

last: WEGLARZ

address: FREDRY 10

country: Poland

institute: POZNAN UNIVERSITY OF MEDICAL SCIENCES

summary: Melatonin is a neurohormone that maintains the circadian rhythms of the body. Although we know the pathway of melatonin action in the brain, we lack comprehensive cross-sectional studies on the periphery of depressed patients.

sample_organism:
Homo sapiens
Mus musculus

overall_design: This study aims to analyze genes uniquely altered after agomelatine treatment in a clinical model and melatonin treatment in a cell culture model.

first: Monika

last: Dmitrzak-Weglarz

first: Ewa

last: Banach

first: Karolina

last: Bilska

first: Beata

last: Narozna

first: Aleksandra

last: Szczepankiewicz

first: Edyta

last: Reszka

last: Jablonska

first: Pawel

last: Kapelski

first: Maria

last: Skibinska

first: Joanna

last: Pawlak


title: The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation

city: Los Angeles

first: Colette

last: Picard

state: California

address: 610 Charles E Young Dr East, Room 4045

department: Molecular, Cell and Developmental Biology

institute: University of California - Los Angeles

summary: In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create an h2a.w null mutant via CRISPR-Cas9, h2a.w-2, to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.

overall_design: ChIP-seq of a large number of modified and unmodified histones (H2A, H2A.Z, H2A.X, H3, H3K9me1, H3K9me2, H3K27me1, H1) in (WT) and triple H2A.W-null (h2a.w-2) plants to examine how the chromatin environment is perturbed upon loss of H2A.W. This was used in conjunction with ATAC-seq and bisulfite-seq of WT, h2a.w-2, double H1-null (h1) and quintuple H1 and H2A.W null (h1 h2a.w-2) to examine the relationship between H1 and H2A.W in regulating heterochromatin. Total (rRNA-depleted) RNA was also sequenced in WT and h2a.w-2 to identify any changes in gene or TE expression. Two replicates of ChIP-seq, ATAC-seq and bisulfite-see experiments were performed, while RNA-seq was done in triplicate. The h2a.w-2 line used in this study is a newly generated triple hta6 hta7 hta12 H2A.W null line. RNA-seq was also performed in h2a.w-1, the triple mutant generated in Yelagandula et al 2014, for comparison.

first: Pierre

last: Bourguet

first: Ramesh

last: Yelagandula

first: Thierry

last: Pélissier

first: Zdravko

last: Lorković

first: Suhua

last: Feng

first: Marie-Noëlle

last: Pouch-Pélissier

first: Anna

last: Schmücker

first: Steven

last: Jacobsen

first: Frédéric

last: Berger

first: Olivier

last: Mathieu


title: DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (RNA-Seq)

first: John

last: Stamatoyannopoulos

overall_design: Total RNA was extracted with the RNeasy Plus Mini Kit (Qiagen) according to the manufacturer's instructions. RNA was quantified by Nanodrop. RNA quality was assessed using either the Agilent Bioanalyzer or Tapestation. Samples with RIN values of > 8 were submitted to the High Throughput Genomics Center (www.htseq.org) or the Fred Hutchinson Cancer Research Center Genomic Shared Resource for Illumina library preparation and sequencing on a Hi-Seq2000 machine

first: Suzanne

last: Furuyama

first: Richard

last: Sandstrom


title: Expansions of adaptive-like NK cells with a tissue-resident phenotype in human lung and blood

city: Stockholm

first: Jakob

last: Michaelsson

address: Alfred Nobels allé 8, ANA Futura, level 7

department: Department of Medicine

country: Sweden

institute: Karolinska Institutet

summary: Characterisation of NKG2C+KIR+ tissue-resident NK cells in human lung and CD49a+ CD56bright NK cells in human blood.

overall_design: Two biological replicates were analyzed for each subset and from each donor


title: Chromatin accessibility of xeno-free and feeder-cultured human extended pluripotent stem cells by ATAC-seq

city: Beijing

first: Hongkui

last: Deng

address: Summer Palace Road No. 5

institute: Peking University

summary: Extended pluripotent stem (EPS) cells have shown great applicative potentials in generating synthetic embryos, directed differentiation and disease modeling. However, the lack of a xenofree culture condition has significantly limited their wide applications. We developed a chemically defined and xeno-free culture condition for culturing and deriving human EPS cells, which can be long-term stably propagated in vitro, as well as preserve their embryonic and extraembryonic developmental potentials.

overall_design: Total of 3 bilogical samples were analyzed by ATAC-seq, which included xeno-free human EPS cells, feeder-cultured human EPS cells and mTESR1-cultured human PSCs.

first: Bei

last: Liu

first: Shi

last: Chen

first: Yaxing

last: Xu

first: Yulin

last: Lyu


title: Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages

city: Ann Arbor

first: Marina

last: Pasca di Magliano

state: Michigan

address: 1500 E Medical Center Drive

department: Surgery

institute: University of Michigan

summary: We utilized biomaterial scaffolds to identify a unique gene expression signature of immune cells in tumor-bearing mice. Single cell RNA sequencing analysis then revealed two distinct macrophage populations that exist at both the primary tumor and systemically in both mice and pancreatic cancer patients, marked by the expression of C1qa, C1qb, and Trem2.

platform_organism:
Homo sapiens
Mus musculus

overall_design: This 10X Genomics single cell RNA sequencing repository includes raw and processed data files from biomaterial scaffolds from control (n=2) and tumor-bearingmice using an orthotopic model of pancreatic cancer (PDA) (n=1) and the iKras* p53* (n=1) genetically engineered model of PDA, mouse orthotopic pancreatic tumors (n=2), mouse normal pancreas samples (n=2), mouse iKras* p53* tumors (n=2), and human liver metastasis samples (n=5). Orthotopic tumors were formed from implantation of the 7940b cell line derived from the KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre (KPC) model of pancreatic cancer. Single-cell cDNA libraries were  prepared  and  sequenced  at  the  University  of  Michigan  Sequencing  Core  using  the  10x Genomics  Platform.  Samples  were run  using  paired  end  50  cycle  reads  on  HiSeq  4000  or the NovaSeq 6000 (Illumina) to a depth of 100,000 reads. The raw data were processed and aligned by the University of Michigan DNA Sequencing Core. Cellranger count version 2.2.0, 3.0.0, or 3.1.0 with default settings was used, with an initial expected cell count of 10,000.

last: di Magliano

first: Howard

last: Crawford

first: Samantha

middle: B

last: Kemp


title: Gene Expression Profile in Peripheral Blood Nuclear Cells of Small Ruminant Lentivirus-Seropositive and Seronegative Dairy Goats in Their First Lactation

city: Warszawa

first: Joanna

last: Pławińska-Czarnak

address: Nowoursynowska 159

institute: WULS-SGGW

summary:
The study investigated differences in gene expression profiles of peripheral blood nuclear cells sampled from healthy and infected with SRLV goats, belonging to two breeds. Due to the nature of the lentiviral infection we hypothesized that the virus could induce genes expression regulation.
We put forward the hypothesis that if gene expression differences exist, they should be revealed in studies conducted on custom-made Capra hircus Gene Expression Array. The results revealed that SRLV infection results in regulation of several genes in goat’s peripheral blood nuclear cells.

overall_design: The experiment was performed on 8 transcriptomic goat microarray using a common reference design. The common reference comprised a pool of equal amounts of RNA from 7 healthy goats in 4th lactation from both Polish breeds (PWI n=4 and PFI n=3). Samples were taken after finishing of lactation period. Experimental samples were collected from healthy goats and infected SRLV in the peak of 1st lactation (Healthy-goat n=4, SRLV - goatnn=4) and RNA was isolated from perypheriar nuclear blood cells.

first: Alicja

last: Majewska

first: Emilia

last: Bagnicka

first: Jarosław

last: Kaba


title: Global transcriptional analysis of xeno-free and feeder-cultured human extended pluripotent stem cells by RNA-seq

overall_design: Total of 7 samples were analyzed by RNA-seq, which included xeno-free human EPS cells and  feeder-cultured human EPS cells.


title: Microbiota are dispensable for early stages of de novo regulatory T cell induction within mesenteric lymph nodes

city: Lausanne

first: Joern

last: Pezoldt

address: Station 19, SV 3818.A

department: SV

country: Switzerland

institute: EPFL

summary: Intestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players for tolerance towards microbiota-derived and food-borne antigens, and compelling evidence suggests that intestinal microbiota modulate their differentiation and maintenance. Selected bacterial species and microbiota-derived metabolites such as short-chain fatty acids (SCFAs) have been reported to foster Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites of de novo Treg induction, and we could previously show that mLN stromal cells contribute to this process. Yet, it is not fully elucidated which direct role microbiota and their metabolites play for the early stages of de novo Treg induction and in shaping the Treg transcriptome already during the initial priming within mLNs. Here, we show that neither dysbiotic microbiota nor dietary SCFA supplementation impact de novo induction of Foxp3+ Tregs within mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent frequencies of de novo induced Foxp3+ Tregs within mLNs. Further dissection of the accessible chromatin and transcriptome revealed that microbiota indeed have a limited impact on fostering the establishment of peripherally induced Tregs and do not contribute to the initialization of the epigenetic landscape for an extensive Treg signature. Viewed as a whole, our data suggest that microbiota are dispensable for the early stages of de novo Treg induction within mLNs, while being required to foster further Treg differentiation and homeostasis at later stages within the intestinal lamina propria.

overall_design: ATAC-seq with 2-4 replicates per condition for regulatory or conventional T cells ex vivo isolated.

first: Carolin

last: Wiechers

first: Mangge

last: Zou

first: Eric

last: Galvez

first: Michael

last: Beckstette

first: Maria

last: Ebel

first: Till

last: Strowig

first: Jochen

last: Huehn


title: Global transcriptional analysis of xeno-free and feeder-cultured human extended pluripotent stem cells by single cell RNA-seq

last: Lyu

address: No.5 Yiheyuan Road Haidian District

department: School of Life Sciences

overall_design: Total of 3 samples were analyzed by single cell RNA-seq, which included xeno-free human EPS cells, feeder-cultured human EPS cells and primed PSCs.

first: Bei

last: Liu

first: Shi

last: Chen

first: Yaxing

last: Xu

first: Hongkui

last: Deng


title: RNA-Seq data for 35 controls using total RNA extracted using RNAZol

status: Public on Mar 23 2021

city: Madison

first: Hamid R.

middle: R

last: Eghbalnia

state: WI

address: 433 Babcock

institute: University of Wisconsin-Madison

summary: Methods routinely used to analyze RNA sequencing data focus on statistical significance and the detection gene differential expression changes that meet a two-fold minimum change between groups.  Due to the unique expression variability present in RNA sequencing data, this strategy may potentially overlook or obscure the detection of valuable information as a result of large expression variability in specific genes in certain samples. This paper develops tools and methods that apply variance and dispersion estimates to intra-group data in order to identify genes with expression values that diverge from the group envelope.  STRING database analysis of the genes identified with this analysis characterize gene affiliations involved in physiological regulatory networks that are associated to biological variability. Samples or genes identified as divergent can be judiciously evaluated prior to any standard differential analysis. A three-step process is presented for evaluating biological variability within a group in RNA sequencing data in which gene counts were: (1) scaled to minimize heteroscedasticity; (2) rank-ordered to potentially divergent “trendlines” for every gene in the data set; and (3) tested with the STRING database to identify statistically significant pathway associations among the genes displaying marked trendline variability and dispersion.   This approach was used to identify and portray the “trendline” profile of every gene in three test data sets.  Control data from an in-house data set and two archived samples revealed that 65-70 % of the sequenced genes displayed trendlines with minimal variation and dispersion across the sample group after rank-ordering the samples; this is referred to as linear trendline.  Nonlinear trendlines refer to all cases where the trendline is not linear. Smaller subsets of genes within the three data sets displayed markedly skewed trendlines, wide dispersion, and variability. STRING database analysis of these genes identified interferon-mediated response networks in 11-20 % of the individuals sampled at the time of blood collection.  For example, in the three control data sets, 14 to 26 genes in the defense response to virus pathway were identified in 7 individuals at false discovery rates ≤ 1.92 E-15.  Gene clusters involving leukocyte and neutrophil activation and degranulation pathways were also detected.

overall_design: 35 control samples were analyzed with several measures of variability both at the level of individual expression and at the level of joint expression relative to pathway-connected genes.

first: William

last: Wilfinger

first: Robert

last: Miller

first: Hamid

first: Karol

last: Mackey

first: Piotr

last: Chomczynski


title: Next-generation interaction screening to discover Mla6aa1-161 related protein-protein interactions regulating barley powdery mildew disease immunity and susceptibility.

city: Ames

first: Roger

last: Wise

address: Department of Plant Pathology, Entomology, and Microbiology, Iowa State University, 1344 Advanced Teaching & Research Bldg., 2213 Pammel Dr.

department: CICGRU

institute: USDA/ARS

summary: The barley R gene (Mla6aa1-161) dataset was part of a larger Y2H screen (GEO GSE150396) to identify novel proteins involved in barley immune responses. Yeast-two-hybrid (Y2H) screening was coupled with next-generation sequencing to identify and quantify interacting proteins. The Mla6aa1-161 bait was mated to a cDNA prey library derived from a 0-48 hour time course of infected leaf tissue. Screens were performed in batch liquid culture to enrich yeast populations for cells expressing positive interactions. After two rounds of enrichment under selective (Histidine absent) and non-selective (Histidine present) conditions, yeast cells were collected. Y2H plasmids were extracted and prey cDNA amplicons were generated via low-cycle PCR. Fragmented amplicons were used as input to generate sequencing libraries and processed on the HiSeq 3000 platform. Reads were mapped to the barley and Blumeria graminis genomes and read counts were analyzed using a custom data processing and scoring pipeline. Putative interactors were cloned and binary Y2H was used to confirm interactions.

overall_design: Y2H screening of a cDNA library was coupled to next-generation sequencing to identify and rank positive protein-protein interactions. Screening for the Mla6aa1-161 bait was conducted in triplicate with yeast cells grown in selective and non-selective conditions. NuGEN’s AnyDeplete technology was used to deplete HORVU3Hr1G072260 (zinc finger protein) from the samples. Two constructs of luciferase were used as bait negative controls. Samples were run on three lanes of Illumina’s HiSeq 3000.

first: Sagnik

last: Banerjee

first: Valeria

last: Velasquez-Zapata

first: James

middle: M

last: Elmore

first: Gregory

last: Fuerst


title: Genome wide DNA methylation and Hydroxymethylation of F1 mouse lung prenatally exposed to house dust mite

city: Pittsburgh

first: wan-yee

last: tang

address: 130 De Soto Street, PUBHL 4129

department: Dept of Environmental and Occupational Health

institute: University of Pittsburgh

summary: We used a mouse model of allergic lung disease to examine the effects of pre- and perinatal house dust mite (HDM) allergen exposure on offspring lung phenotypic and transcriptional outcomes. We showed that maternal HDM exposure (F0) acts synergistically with adult HDM exposure, leading to enhanced airway hyperresponsiveness (AHR) and lung inflammation when compared to mice exposed solely in adulthood. To examine the role of epigenetic inheritance of asthma susceptibility induced by maternal HDM exposure, we utilized a genome-wide MeDIP-seq and hMeDIP-seq analysis to identify genes differentially methylated (DMG) and hydroxymethylated (DHG), and their association with the enhanced AHR. In addition, we validated the relationship between DNA methylation and mRNA expression of the DMGs and DHGs in the male progenies.

overall_design: We compared the lung DNA methylation and hydroxymethylation patterns from F1 progenies from dams exposed to saline or HDM (F0-Saline_F1-HDM or F0-HDM_F1-HDM) when compared to their counterparts who did not received HDM challenges in their adulthood (F0-Saline_F1-Saline or F0-HDM_F1-Saline). Genomic DNA from each treatment group (pooled from mice of 3 individual dams) was subject for MeDIP-seq and hMeDIP-seq. Validation of airway responsiveness, cell counts and relative gene expression were performed on six mice per treatment group.

first: Wan-yee

last: Tang

middle: Y

last: Cheng

first: Jairus

last: Pulczinski


title: The microbiota is dispensable for the early stages of peripheral regulatory T cell induction within mesenteric lymph nodes

city: Braunschweig

first: Carolin

last: Wiechers

state: Niedersachsen

address: Inhoffenstraße 7

department: Experimental Immunology

institute: Helmholtz Centre for Infection Research

summary: Intestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players in tolerance to microbiota-derived and food-borne antigens, and compelling evidence suggests that the intestinal microbiota modulates their generation, functional specialization, and maintenance. Selected bacterial species and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs), have been reported to promote Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites for the generation of peripherally induced Tregs (pTregs). Despite this knowledge, the direct role of the microbiota and their metabolites in the early stages of pTreg induction within mLNs is not fully elucidated. Here, using an adoptive transfer-based pTreg induction system, we demonstrate that neither transfer of a dysbiotic microbiota nor dietary SCFA supplementation modulated the pTreg induction capacity of mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent pTreg induction within mLNs. Further molecular characterization of these de novo induced pTregs from mLNs by dissection of their transcriptomes and accessible chromatin regions revealed that the microbiota indeed has a limited impact and does not contribute to the initialization of the Treg-specific epigenetic landscape. Overall, our data suggest that the microbiota is dispensable for the early stages of pTreg induction within mLNs.

overall_design: RNA-seq with 3-4 replicates per condition for regulatory or conventional T cells ex vivo isolated.

first: Mangge

last: Zou

first: Eric

last: Galvez

first: Michael

last: Beckstette

first: Maria

last: Ebel

first: Till

last: Strowig

first: Jochen

last: Huehn

first: Joern

last: Pezoldt


title: Conserved DNA sequence features underlie pervasive RNA polymerase pausing

city: Berlin

first: Andreas

last: Mayer

address: Ihnestraße 63-73

institute: Max Planck Institute for Molecular Genetics

summary: This study reveals widespread Pol II pausing at single-nucleotide resolution across the human genome with the majority of Pol II pauses occur outside of promoter-proximal gene regions primarily along the gene-body of transcribed genes. We show DNA sequence properties underlying widespread transcriptional pausing including a new pause motif. The study indicates pervasive sequence-induced transcriptional pausing in human cells.

overall_design: Nested NET-seq measurements for HeLa cells (two biological replicate measurements) and NET-seq measurements for HEK293 cells (two technicalal replicate measurements).

first: Martyna

last: Gajos

first: Olga

last: Jasnovidova

first: Alena

last: van Bömmel

first: Susanne

last: Freier

first: Martin

last: Vingron


title: Aging-associated deficit in CCR7 is linked to worsened glymphatic function, cognition and amyloid beta pathology

status: Public on Mar 22 2021

city: Saint Louis

first: Jonathan

last: Kipnis

state: MO

address: 4515 McKinley Ave

department: Pathology and Immunology

institute: Washington University in Saint Louis

summary: Aging leads to a progressive deterioration in brain function, which will eventually result in cognitive decline and can develop into a dementia. The mechanisms underlying pathological cognitive decline in aging are still poorly understood. The peripheral immune system, as well as the meningeal lymphatic vasculature and the immune cells residing in the brain and meninges, are all affected by aging. Moreover, recent studies have linked the dysfunction of the meningeal lymphatic system and peripheral immunity to accelerated brain aging. We hypothesized that an age-related reduction in CCR7-dependent immune cell egress through the lymphatic vasculature mediates some aspects of aging-associated brain dysfunction, leading to cognitive decline and potentially exacerbating neurodegenerative diseases. Here, we report a reduction in CCR7 expression by meningeal T cells in aged mice and its associated increase in meningeal T-regulatory cells. Hematopoietic CCR7 deficiency mimicked the aging-associated changes in meningeal T cells and led to cognitive impairment. Interestingly, CCR7-deficient mice also presented impaired brain glymphatic function and showed increased amyloid beta (A) deposition when crossed with the 5xFAD transgenic mouse model of Alzheimer’s disease (AD). These results show that the aging-associated decrease in CCR7 expression impacts meningeal immunity, affects different aspects of brain function and exacerbates brain A pathology, highlighting its potential as a pathogenic mechanism for cognitive decline in aging and AD.

overall_design: Brain cells were isolated from 5 months old male 5xFAD mice, deficient for CCR7 (5xFAD::CCR7-/-, n=3) or age-matched control littermates (5xFAD, n=3). Brain cell suspensions were obtained by enzymatic and mechanic digestion of right brain hemisphere tissue, stained for surface markers and enriched for specific populations (microglia/macrophages - live CD45+CD11b+Ly6G–, and blood endothelial cells - live CD45–CD11b–CD13–CD31+) by FACS sorting. Each individual sample used in this single-cell RNA sequencing experiment resulted from brain cells pooled from 3 mice.

first: Sandro

last: DaMesquita

first: Taitea

last: Dykstra


title: Mapping H3K27ac in human MAIT cells

city: Tampa

first: Dorina

last: Avram

state: Fl

address: 12902 Magnolia Drive, MRC4

department: Department of Immunology

institute: Moffitt Cancer Center

summary: Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.

overall_design: Examination of H3K27ac in human MAIT cells from peripheral blood

first: Theodore

last: Drashansky

last: Helm

first: Zhiguang

last: Huo


title: Mapping Bcl11b binding in human MAIT cells

overall_design: Examination of Bcl11b binding in human MAIT cells from peripheral blood

first: Eric


title: Global RNA profiles show target selectivity and physiological effects of peptide-delivered antisense antibiotics

status: Public on Mar 19 2021

city: Würzburg

first: Jakob

middle: Jeremias

last: Jung

state: Bayern

address: Josef-Schneider-Str. 2/Bau D15

department: Institute of Molecular Infection Biology (IMIB)

institute: University of Würzburg

summary: Antisense peptide nucleic acids (PNAs) inhibiting mRNAs of essential genes provide a straight-forward way to repurpose our knowledge of bacterial regulatory RNAs for development of programmable species-specific antibiotics. While there is ample proof of PNA efficacy, their target selectivity and impact on bacterial physiology are poorly understood. Moreover, while antibacterial PNAs are typically designed to block mRNA translation, effects on target mRNA levels are not well-investigated. Here, we pioneer the use of global RNA-seq analysis to decipher PNA activity in a transcriptome-wide manner. We find that PNA-based antisense oligomer conjugates robustly decrease mRNA levels of the widely-used target gene, acpP, in Salmonella enterica, with limited off-target effects. Systematic analysis of several different PNA-carrier peptides attached not only shows different bactericidal efficiency, but also activation of stress pathways. In particular, KFF-, RXR- and Tat-PNA conjugates especially induce the PhoP/Q response, whereas the latter two additionally trigger several distinct pathways. We show that constitutive activation of the PhoP/Q response can lead to Tat-PNA resistance, illustrating the utility of RNA-seq for understanding PNA antibacterial activity. In sum, our study establishes an experimental framework for the design and assessment of PNA antimicrobials in the long-term quest to use these for precision editing of microbiota.

sample_organism: Salmonella enterica subsp. enterica serovar Typhimurium

overall_design: Transcriptome profile of Salmonella enterica in response to three different carrier peptide-PNA conjugates  with three replicates per sample. Total of 30 samples (3 carrier peptides*3 conditions*3 replicates + 3 Water controls).

first: Linda

last: Popella

first: Lars

last: Barquist

first: Jörg

last: Vogel

first: Kristina

last: Popova

first: Svetlana

last: Durica-Mitić


title: Transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

overall_design: Examination of changes to transcriptome resulting from removal of Bcl11b in MAIT cells