title: Histone ChIP-seq from pancreas (ENCSR211SBE)

summary:
H3K4me3 ChIP-seq on pancreas female adult (61 years)

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: Histone ChIP-seq from lower lobe of left lung (ENCSR875OQJ)

status: Public on Feb 27 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:
H3K27ac ChIP-seq on lower lobe of left lung male adult (60 years)

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: Histone ChIP-seq from SJSA1 (ENCSR214NMO)

summary:
H3K4me3 ChIP-seq on human SJSA1

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: Histone ChIP-seq from spleen (ENCSR593INW)

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: Histone ChIP-seq from BE2C (ENCSR874NDX)

summary:
H3K4me1 ChIP-seq on human BE2C

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: Histone ChIP-seq from skin epidermis (ENCSR156MYA)

summary:
H3K27ac ChIP-seq of skin epidermis male adult (65 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from skin epidermis (ENCSR194KGO)

summary:
H3K27ac ChIP-seq of skin epidermis female adult (66 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from left lung (ENCSR157JGF)

summary:
H3K9me3 ChIP-seq on left lung male adult (40 years)

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: Histone ChIP-seq from Caco-2 (ENCSR401WUV)

summary:
H3K9me3 ChIP-seq on human Caco-2

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: Histone ChIP-seq from lower lobe of left lung (ENCSR155EOT)

summary:
H3K4me1 ChIP-seq on lower lobe of left lung female adult (59 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from spleen (ENCSR200QAA)

summary:
Control ChIP-seq on spleen male adult (26 years)

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: Histone ChIP-seq from pancreas (ENCSR868ZOR)

summary:
H3K27ac ChIP-seq on pancreas female adult (59 years)

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: Histone ChIP-seq from uterus (ENCSR216EVK)


title: Histone ChIP-seq from lower lobe of left lung (ENCSR152VOJ)

summary:
H3K36me3 ChIP-seq on lower lobe of left lung female adult (59 years)

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: Histone ChIP-seq from pancreas (ENCSR137ZID)

summary:
H3K27ac ChIP-seq on pancreas female adult (41 years)

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: Histone ChIP-seq from heart left ventricle (ENCSR863BVD)

summary:
H3K27ac ChIP-seq on heart left ventricle female adult (46 years)

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: Histone ChIP-seq from skin epidermis (ENCSR207ABA)

summary:
H3K27ac ChIP-seq of keratinocyte basal cell carcinoma male adult (67 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from heart left ventricle (ENCSR848BXL)

summary:
H3K4me1 ChIP-seq on heart left ventricle female adult (46 years)

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: Histone ChIP-seq from HAP-1 (ENCSR131DVD)

summary:
H3K27ac ChIP-seq on human HAP-1

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: Histone ChIP-seq from spleen (ENCSR401KZW)

summary:
H3K27ac ChIP-seq on spleen male adult (26 years)

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: Histone ChIP-seq from left lung (ENCSR864ECD)

summary:
H3K4me3 ChIP-seq on left lung male adult (40 years)

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: Histone ChIP-seq from skin epidermis (ENCSR397NQK)

summary:
H3K27ac ChIP-seq of keratinocyte basal cell carcinoma male adult (65 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from lower lobe of left lung (ENCSR846VGG)

summary:
Control ChIP-seq on lower lobe of left lung female adult (59 years)

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: Histone ChIP-seq from lower lobe of left lung (ENCSR842LST)

summary:
H3K27me3 ChIP-seq on lower lobe of left lung male adult (60 years)

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: Histone ChIP-seq from pancreas (ENCSR847FTJ)

summary:
H3K36me3 ChIP-seq on pancreas female adult (41 years)

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: Histone ChIP-seq from skin epidermis (ENCSR386CKJ)

summary:
H3K27ac ChIP-seq of skin epidermis male adult (75 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from SJSA1 (ENCSR590ZSL)

summary:
H3K4me1 ChIP-seq on human SJSA1

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from heart right ventricle (ENCSR839VEU)

summary:
Control ChIP-seq on heart right ventricle male adult (40 years)

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: Histone ChIP-seq from skin epidermis (ENCSR835YED)

summary:
H3K4me3 ChIP-seq of skin epidermis male adult (77 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from MG63 (ENCSR380ORO)

summary:
H3K36me3 ChIP-seq on human MG63

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from pancreas (ENCSR130HAG)

summary:
Control ChIP-seq on pancreas female adult (61 years)

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: Histone ChIP-seq from spleen (ENCSR123ASL)

summary:
H3K27me3 ChIP-seq on spleen female adult (41 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from heart left ventricle (ENCSR120ITZ)

summary:
Control ChIP-seq on heart left ventricle female adult (59 years)

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: Histone ChIP-seq from RWPE2 (ENCSR115IRD)

summary:
H3K36me3 ChIP-seq on human RWPE2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR126UEY)

summary:
Control ChIP-seq of skin epidermis female adult (71 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR111ZAD)

summary:
Control ChIP-seq of keratinocyte basal cell carcinoma female adult (48 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BE2C (ENCSR377FNA)

summary:
ChIP-seq on human BE2C

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: Histone ChIP-seq from brain microvascular endothelial cell (ENCSR111QCU)

summary:
H3K27ac ChIP-seq on human brain microvascular endothelial cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from spleen (ENCSR122MPC)

summary:
H3K4me3 ChIP-seq on spleen female adult (59 years)

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: Histone ChIP-seq from HAP-1 (ENCSR121CWP)

summary:
H3K36me3 ChIP-seq on human HAP-1

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: Histone ChIP-seq from BE2C (ENCSR114YOX)

summary:
H3K36me3 ChIP-seq on human BE2C

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: Histone ChIP-seq from heart left ventricle (ENCSR371UJJ)

summary:
H3K36me3 ChIP-seq on heart left ventricle female adult (46 years)

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: Histone ChIP-seq from heart right ventricle (ENCSR370OQJ)

summary:
H3K27ac ChIP-seq on heart right ventricle male adult (40 years)

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: Histone ChIP-seq from uterus (ENCSR588FQI)

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: Histone ChIP-seq from brain microvascular endothelial cell (ENCSR587VHH)

summary:
H3K36me3 ChIP-seq on human brain microvascular endothelial cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from lower lobe of left lung (ENCSR089ZLR)

summary:
Control ChIP-seq on lower lobe of left lung male adult (60 years)

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: Histone ChIP-seq from heart left ventricle (ENCSR084UMY)

summary:
H3K36me3 ChIP-seq on heart left ventricle female adult (59 years)

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: Histone ChIP-seq from lower lobe of left lung (ENCSR368BOE)

summary:
H3K4me3 ChIP-seq on lower lobe of left lung male adult (60 years)

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: Histone ChIP-seq from NCI-H929 (ENCSR368CYW)

summary:
H3K27ac ChIP-seq on human NCI-H929

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: Histone ChIP-seq from spleen (ENCSR377ILM)


title: Histone ChIP-seq from gastroesophageal sphincter (ENCSR364YAY)


title: Histone ChIP-seq from gastrocnemius medialis (ENCSR098OLN)


title: Histone ChIP-seq from tibial artery (ENCSR360UUM)


title: Histone ChIP-seq from spleen (ENCSR589DBF)


title: Control ChIP-seq from skin epidermis (ENCSR583XAM)

summary:
Control ChIP-seq of keratinocyte squamous cell carcinoma male adult (84 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from spleen (ENCSR826MTK)


title: Histone ChIP-seq from skin epidermis (ENCSR822EOS)

summary:
H3K4me3 ChIP-seq of keratinocyte squamous cell carcinoma female adult (80 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from spleen (ENCSR831EDZ)


title: Histone ChIP-seq from MG63 (ENCSR804JFU)

summary:
H3K27me3 ChIP-seq on human MG63

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR360NJD)

summary:
Control ChIP-seq of skin epidermis male adult (78 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR568JFZ)

summary:
Control ChIP-seq of skin epidermis male adult (67 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from spleen (ENCSR564WJA)

summary:
H3K27ac ChIP-seq on spleen female adult (59 years)

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: Histone ChIP-seq from spleen (ENCSR080JPX)


title: Histone ChIP-seq from heart left ventricle (ENCSR564QBS)

summary:
H3K4me1 ChIP-seq on heart left ventricle male adult (40 years)

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: Histone ChIP-seq from spleen (ENCSR801KDK)

summary:
H3K36me3 ChIP-seq on spleen female adult (59 years)

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: Histone ChIP-seq from skin epidermis (ENCSR869TDT)

summary:
H3K27ac ChIP-seq of keratinocyte squamous cell carcinoma female adult (80 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from WERI-Rb-1 (ENCSR354XIL)

summary:
H3K36me3 ChIP-seq on human WERI-Rb-1

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: Histone ChIP-seq from NCI-H929 (ENCSR359BGB)

summary:
H3K27me3 ChIP-seq on human NCI-H929

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: Histone ChIP-seq from heart right ventricle (ENCSR350GZX)

summary:
H3K4me1 ChIP-seq on heart right ventricle male adult (40 years)

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: Histone ChIP-seq from SJSA1 (ENCSR564OSQ)

summary:
H3K27me3 ChIP-seq on human SJSA1

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: Histone ChIP-seq from MG63 (ENCSR579SNM)

summary:
H3K4me3 ChIP-seq on human MG63

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: Histone ChIP-seq from sigmoid colon (ENCSR793IKH)

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: Control ChIP-seq from skin epidermis (ENCSR564GJK)

summary:
Control ChIP-seq of keratinocyte basal cell carcinoma male adult (58 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from skin epidermis (ENCSR560BEL)

summary:
H3K27ac ChIP-seq of keratinocyte basal cell carcinoma female adult (48 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from heart right ventricle (ENCSR519UXW)

summary:
Control ChIP-seq on heart right ventricle female adult (46 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR529OPX)

summary:
Control ChIP-seq of keratinocyte squamous cell carcinoma female adult (71 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from SJSA1 (ENCSR349VAW)

summary:
H3K27ac ChIP-seq on human SJSA1

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR785LQK)

summary:
Control ChIP-seq of keratinocyte basal cell carcinoma male adult (65 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from lower lobe of left lung (ENCSR791BWS)

summary:
H3K4me3 ChIP-seq on lower lobe of left lung female adult (59 years)

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: Histone ChIP-seq from SJCRH30 (ENCSR782BWI)

summary:
H3K9me3 ChIP-seq on human SJCRH30

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: Histone ChIP-seq from heart right ventricle (ENCSR519DSV)

summary:
H3K9me3 ChIP-seq on heart right ventricle male adult (40 years)

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: Histone ChIP-seq from heart right ventricle (ENCSR783LKF)

summary:
H3K9me3 ChIP-seq on heart right ventricle female adult (46 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR071DPR)

summary:
Control ChIP-seq of keratinocyte squamous cell carcinoma male adult (75 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from esophagus muscularis mucosa (ENCSR077HGR)


title: Histone ChIP-seq from spleen (ENCSR343DFX)

summary:
H3K27ac ChIP-seq on spleen female adult (41 years)

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: Histone ChIP-seq from heart right ventricle (ENCSR345GSH)

summary:
H3K36me3 ChIP-seq on heart right ventricle male adult (40 years)

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: Histone ChIP-seq from skin epidermis (ENCSR074BEW)

summary:
H3K4me3 ChIP-seq of keratinocyte basal cell carcinoma male adult (67 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from skin epidermis (ENCSR531VWS)

summary:
H3K27ac ChIP-seq of keratinocyte basal cell carcinoma male adult (77 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from tibial artery (ENCSR342FPJ)


title: Histone ChIP-seq from stomach (ENCSR063HOI)


title: Histone ChIP-seq from brain microvascular endothelial cell (ENCSR032CAS)

summary:
H3K27me3 ChIP-seq on human brain microvascular endothelial cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BE2C (ENCSR780XZD)

summary:
H3K27me3 ChIP-seq on human BE2C

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: Histone ChIP-seq from skin epidermis (ENCSR334DRN)

summary:
H3K27ac ChIP-seq of skin epidermis male adult (67 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: Histone ChIP-seq from spleen (ENCSR341AXR)

summary:
H3K9me3 ChIP-seq on spleen female adult (59 years)

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: Histone ChIP-seq from skin epidermis (ENCSR340ZTB)

summary:
H3K27ac ChIP-seq of skin epidermis female adult (80 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR033XKQ)

summary:
Control ChIP-seq of skin epidermis female adult (66 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from HAP-1 (ENCSR771IOP)

summary:
ChIP-seq on human HAP-1

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: Histone ChIP-seq from Caco-2 (ENCSR061UOM)

summary:
H3K4me1 ChIP-seq on human Caco-2

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: Histone ChIP-seq from gastrocnemius medialis (ENCSR499VCQ)

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: Histone ChIP-seq from SJCRH30 (ENCSR769CSE)

summary:
H3K27ac ChIP-seq on human SJCRH30

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: Histone ChIP-seq from esophagus squamous epithelium (ENCSR024JJL)

summary:
H3K27me3 ChIP-seq on esophagus squamous epithelium male adult (54 years)

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: Histone ChIP-seq from skin epidermis (ENCSR339XMR)

summary:
H3K27ac ChIP-seq of keratinocyte basal cell carcinoma male adult (58 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from skin epidermis (ENCSR321KDV)

summary:
H3K27ac ChIP-seq of keratinocyte squamous cell carcinoma female adult (71 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from HL-60 (ENCSR309MYO)

summary:
ChIP-seq on human HL-60

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR306YLG)

summary:
Control ChIP-seq of keratinocyte squamous cell carcinoma male adult (78 years). Note that tissue excised from donor is cancerous.

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: Histone ChIP-seq from lower lobe of left lung (ENCSR313CEH)

summary:
H3K27ac ChIP-seq on lower lobe of left lung female adult (59 years)

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: Histone ChIP-seq from left lung (ENCSR494WCX)

summary:
H3K27ac ChIP-seq on left lung male adult (40 years)

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: Histone ChIP-seq from skin epidermis (ENCSR291PVS)

summary:
H3K4me3 ChIP-seq of keratinocyte squamous cell carcinoma male adult (78 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from MG63 (ENCSR302CFJ)

summary:
ChIP-seq on human MG63

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: Histone ChIP-seq from skin epidermis (ENCSR011KBS)

summary:
H3K4me3 ChIP-seq of keratinocyte squamous cell carcinoma male adult (84 years). Note that tissue excised from donor is cancerous.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from brain microvascular endothelial cell (ENCSR000JGO)

summary:
ChIP-seq on human brain microvascular endothelial cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Brain Genexpession of a mouse modle of Sepsis-associated encephalopathy (SAE)

city: Villingen-Schwenningen

first: Markus

last: Blaess

address: Jakob-Kienzle-Strasse 17

department: Institute of Precision Medicine

country: Germany

institute: Furtwangen University

summary: Sepsis-associated encephalopathy (SAE) is a major and frequent complication in patients with sepsis resulting in delirium and premature death. Sepsis survivors commonly suffer from long-term cognitive impairment causing immense burden on patients, caregivers, and economic health systems. Underlying pathophysiology of SAE related cognitive deficits  is  largely unresolved, Thus treatment options are missing.  We report that experimental polymicrobial sepsis in mice induces synaptic pathology in the central nervous system underlying defective long-term potentiation and cognitive dysfunction. Analysis of differentially expressed  genes revealed severely affected downregulation of genes related to neuronal and synaptic signaling in the brain, e.g. of the activity-regulated cytoskeleton-associated protein (Arc ), of the transcription-regulatory EGR family, and of the dual-specificity phosphatase 6 (Dusp6). On the protein level, ARC expression and mitogen-activated protein (MAP) kinase signaling in the brain was disturbed during SAE. For targeted rescue of dysregulated synaptic signaling and plasticity, we overexpressed ARC in the hippocampus by bilateral in-vivo stereotactic microinjection of an adeno-associated virus containing a neuron-specific plasmid of the Arc transgene. Hereby, defective synaptic plasticity and signaling in the hippocampus were restored and memory function improved. Accordingly, synaptic plasticity, neuronal spine pathology, and memory dysfunction also improved when post-septic mice were subjected to enriched environment demonstrating the potential for activity-induced recovery of long-term cognitive dysfunction. Together, we identified synaptic pathology of neurocognitive dysfunction after severe systemic infection and provide a proof-of-concept approach to interfere with SAE pathomechanisms leading to cognitive improvement.

overall_design: In total the RNA of 16 mice was analzyed. In 8 mice an experimental polymicrobial sepsis was induced. In 4 mice the expression was analyzed  during the acute Phase 3 days after sepsis induction. Antother 4 mices survived 10 weeks. 4 and 4 mice receiving the same antibiotic treatment served as control.

first: Benedikt

last: Grünewald

first: Franziska

last: Hörhold

first: Ralf

last: Hempel

first: Rainer

last: König

first: Christian

last: Geis


title: Histone ChIP-seq from spleen (ENCSR768RIK)

summary:
H3K36me3 ChIP-seq on spleen male adult (26 years)

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: Immunomodulating effects of 13- and 16-hydroxylated docosahexaenoyl ethanolamide in LPS stimulated RAW264.7 macrophages

city: Wageningen

first: Guido

last: Hooiveld

address: HELIX, Stippeneng 4

department: Div. Human Nutrition & Health

country: Netherlands

institute: Wageningen University

summary: Docosahexaenoyl ethanolamide (DHEA), the ethanolamine conjugate of the n-3 long chain polyunsaturated fatty acid docosahexaenoic acid, is endogenously present in the human circulation and in tissues. Its immunomodulating properties have been (partly) attributed to an interaction with the cyclooxygenase-2 (COX-2) enzyme. Recently, we discovered that COX-2 converts DHEA into two oxygenated metabolites, 13- and 16-hydroxylated-DHEA (13- and 16-HDHEA, respectively). It remained unclear whether these oxygenated metabolites also display immunomodulating properties like their parent DHEA. In the current study we investigated the immunomodulating properties of 13- and 16-HDHEA in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The compounds reduced production of tumor necrosis factor alpha (TNFα), interleukin (IL)-1β and IL-1Ra, but did not affect nitric oxide (NO) and IL-6 release. Transcriptome analysis showed that the compounds inhibited the LPS-mediated induction of pro-inflammatory genes (InhbA, Ifit1) and suggested potential inhibition of regulators such as toll-like receptor 4 (TLR4), MyD88, and interferon regulatory factor 3 (IRF3), whereas anti-inflammatory genes (SerpinB2) and potential regulators IL-10, sirtuin 1 (Sirt-1), fluticasone propionate were induced. Additionally, transcriptome analysis of 13-HDHEA suggests a potential anti-angiogenic role. In contrast to the known oxylipin-lowering effects of DHEA, liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) analyses revealed that 13- and 16-HDHEA did not affect oxylipin formation. Overall, the anti-inflammatory effects of 13-HDHEA and 16-HDHEA are less pronounced compared to their parent molecule DHEA. Together, this suggests that the COX-2 metabolism of DHEA may act as a regulatory mechanism to limit the anti-inflammatory properties of DHEA.

overall_design: Microarray analysis was performed on LPS-activated RAW264.7 macrophages treated with 13-, 16-HDHEA or vehicle.

first: Ian

last: de Bus

middle: J

first: Mark

middle: V

last: Boekschoten

first: Michiel

last: Balvers


title: Investigation of the gene expression in the major surface protein deficient mutant of Treponema denticola

city: Chiyoda-ku

first: Kazuyuki

last: Ishihara

state: Tokyo

address: Misakicho 2-1-14

department: Microbiolgy

country: Japan

institute: Tokyo Dental College

summary: Treponema denticola is involved in chronic periodontitis pathogenesis. The mechanism underlying the regulation of the expression of its virulence factors, such as major surface protein (Msp) is yet to be clarified. We determined the gene expression profiles of Msp-deficient mutants of T. denticola. Gene expression profiles of T. denticola ATCC 35405 (wild type), and msp-deficient mutant, DMSP3, were determined using DNA microarray analysis. In addition to several differentially expressed genes, dentilisin expression was reduced in DMSP3. Potential repressor, TDE_0344, was elevated in DMSP3.

overall_design: Comparison of 2 strains of T. denticola.  Treponema denticola ATCC 35405 and DMSP3 were cultured in TYGVS medium for 24-48 h. Profile of gene expression of T. denticola DMSP3 was compared to that of ATCC 35405.

first: Yuki

last: Arai

first: Yuichiro

last: Kikuchi

first: Kazuko

last: Okamoto-Shibayama

first: Eitoyo

last: Kokubu

first: Seikou

last: Shintani


title: Bovine Sperm-borne miRNAs

status: Public on Feb 26 2021

city: Oxford

first: Yue

last: Du

state: Oxford

address: NDCLS, RDM, JR hospital, head

country: United Kingdom

institute: University of Oxford

type: Non-coding RNA profiling by high throughput sequencing

summary: Purpose: to construct a library of miRNAs in bovine sperm was constructed using Illumina high‐throughput sequencing technology. Result: Unique sequences that were 18–26 nucleotides in length were mapped to specific precursors in miRBase 20.0 using BLAST. A total of 951 known miRNAs and 8 novel, highly expressed miRNA candidates were identified.

overall_design: Sperm-borne miRNAs of bovine

first: Yongsheng

last: Wang


title: Histone ChIP-seq from heart right ventricle (ENCSR496TBI)

first: ENCODE

last: DCC

summary:
H3K4me1 ChIP-seq on heart right ventricle female adult (46 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from skin epidermis (ENCSR327PYZ)

summary:
Control ChIP-seq of skin epidermis female adult (48 years). Note that tissue excised from donor is adjacent epidermis from Mohs cancer removal procedure.

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: The NK cell stress response status modulates anti-tumor immunity [ATAC-seq]

city: New York

first: Kathryn

middle: Grace

last: Hockemeyer

state: New York

address: 550 1st Avenue

department: Pathology

institute: NYU Langone Health

summary: The tumor microenvironment (TME) comprises numerous forms of cellular stress, which can activate Heat Shock Factor 1 (HSF1), the master transcription factor of the proteotoxic stress response. We profiled HSF1 activity across tumor-infiltrating immune populations, revealing the highest activity in CD8+ T cells and the lowest in natural killer (NK) cells. To elucidate the mechanisms through which HSF1 regulates immune surveillance, we generated an in vivo model of augmented HSF1 activity. Tumor challenge revealed that accumulation of HSF1 dampens NK-mediated tumor immunity and impairs both cytotoxicity and production of interferon gamma (IFN-γ) in NK cells. Single-cell transcriptional profiling identified a loss of anti-tumor signaling pathways, including interferon signaling, within the HSF1-enhanced TME. In NK cells, integration of chromatin accessibility with transcriptomics revealed that HSF1 deregulates accessibility and expression of genes encoding for NK receptors, leading to an inhibitory bias.

overall_design: Single-cell RNA-sequencing was performed in tumors engrafted in wild-type (WT) controls and mice bearing serine to alanine mutations in amino acids 303 and 307 (S303/7A). Tumors from 4 mice were pooled for  Transcriptomic and epigenetic profiling of NK cells was performed by mRNA sequencing and assay for transposase-accessible chromatin (ATAC) sequencing in splenic NK cells isolated from wild-type and HSF1-enhanced mice under steady state conditions. For RNA-seq, 3 biological replicates of NK cells from WT and S303/7A were used. For ATAC-seq, 4 biological replicates of NK cells from WT and S303/7A mice were used.

first: Iannis

last: Aifantis


title: The NK cell stress response status modulates anti-tumor immunity [scRNA-seq]

type: Expression profiling by high throughput sequencing


title: ARC2 elicits a secondary metabolic response requiring afsR and afsS in Streptomyces coelicolor

city: Toronto

first: Vanessa

last: Yoon Calvelo

state: ON

address: 661 University Avenue

department: Biochemistry

country: Canada

institute: University of Toronto

summary: In this work, we demonstrate that the addition of the small molecule elicitor ARC2 to Streptomyces coelicolor cultures results in global changes in gene expression including many secondary metabolic genes. A profile of the Streptomyces coelicolor transcriptome in the absence and presence of ARC2 was performed by RNA-seq. Total RNA was extracted after 10 hours of treatment with either the DMSO solvent control or the ARC2 small molecule elicitor. A V2 rapid run mode with paired-end 2x75 bp reads on the Illumina HiSeq platform was performed for RNA sequencing.

overall_design: Examination of Streptomyces coelicolor gene expression in the absence and presence of the chemical elicitor ARC2.

middle: Y

last: Calvelo

first: Justin

middle: R

last: Nodwell


title: Influence of follicular lymphoma B cells on tumor-supportive stromal cells gene expression

city: RENNES

first: Celine

last: Pangault

address: 2, avenue du Léon Bernard

department: Medical School of Rennes

country: France

institute: Rennes University Hospital

summary: GEP on Affymetrix U133+2.0 microarrays was performed on in vitro expanded stromal cells with or without B cells priming.

overall_design: Gene expression analysis was performed on stromal cells (MSC) derived from bone marrow (BM) of healthy donors (HD). BM-MSC were primed with primary follicular lymphoma B cells (FL, n=6) or SUDHL4 cell line (SUD, n=2), and compared to untreated BM-MSC (n=6) to explore stromal modification in FL context.

first: Karin

last: Tarte

first: Erwan

last: Dumontet

first: Fabien

last: Guilloton


title: Koala methylomes reveal divergent and conserved DNA methylation signatures of X chromosome regulation

city: ATLANTA

first: Devika

last: Singh

state: Georgia

address: North Ave NW

institute: Georgia Institute of Technology

type: Methylation profiling by high throughput sequencing

summary: We examined genome-wide patterns of DNA methylation from whole genome DNA methylation maps of five tissues (brain, kidney, lung, skeletal muscle, and pancreas) from one male koala and one female koala (Phascolarctos cinereus), and present the first whole genome, multi-tissue “methylome atlas” with information on tissue- and sex-specific variation of DNA methylation for a marsupial.

overall_design: Whole genome bisulfite sequencing (WGBS) data from 5 tissues, brain, kidney, lung, skeletal muscle, and pancreas, for one male (Ben) and one female koala (PC) sequenced by the Ramaciotti Centre for Genomics for methylome sequencing using NovaSeq6000. 2 sequencing runs were performed per sample.

first: David

last: Alvarez-Ponce

first: Soojin

last: Yi

first: Dan

last: Sun

first: Rebecca

middle: N

last: Johnson

middle: E

last: Alquezar-Planas

first: Andrew

middle: G

last: King


title: Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

city: Irvine

last: Shi

state: California

address: 811 Health Sciences Rd

institute: University of California, Irvine

summary: Herpes Simplex virus-1 (HSV-1) causes widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) mainly by immediate early gene ICP27. Mechanistically, ICP27 directly binds to the essential mRNA 3’ processingfactor CPSF, induces the assembly of a dead-end 3’ processing complex, and blocks mRNA cleavage. Remarkably, ICP27 also acts as a sequence-dependent activator of mRNA 3’ processing for HSV-1 and a subset of host genes. Our results here show that the bimodal activities of ICP27 play a key role in HSV-1-induced alternative polyadenyalation.

overall_design: (1) 4SU-seq: explore the effect of ICP27 and HSV-1 on transcription termination; (2) CLIP-seq: examination of RNA binding sites of ICP27.

first: Xiuye

last: Wang


title: BRCA2 promotes DNA-RNA hybrid resolution by DDX5 helicase at DNA breaks to facilitate their repair

city: Seville

first: Andrés

last: Aguilera

address: Av. Américo Vespucio 24

department: Genome BIology

country: Spain

institute: CABIMER, Universidad de Sevilla

summary: The BRCA2 tumor suppressor is a DNA double-strand break repair factor essential to maintain genome integrity. BRCA2-deficient cells spontaneously accumulate DNA-RNA hybrids, a known source of genome instability. However, the specific role of BRCA2 on these structures remains poorly understood. Here we identified the DEAD-box RNA helicase DDX5 as a BRCA2 interacting partner. We show that DDX5 associates with DNA-RNA hybrids that form in the vicinity of DSBs and this association is enhanced by BRCA2. Notably, BRCA2 stimulates the DNA-RNA hybrid helicase activity of DDX5. Impaired BRCA2-DDX5 interaction, as observed in cells bearing the breast cancer variant BRCA2-T207A, reduces DDX5 association with DSBs, decreases the number of RPA foci upon irradiation and impairs RAD51 repair foci formation. Our findings are consistent with DNA-RNA hybrids being an impediment for the repair of DSBs by homologous recombination and reveal BRCA2 and DDX5 as active players in their removal.

overall_design: Genome-wide inspection of RNA-DNA hybrids accumulation in siC control and DDX5-depleted (siDDX5) K562 cells

first: Gaetana

last: Sessa

first: Belen

last: Gómez-González

first: Sonia

last: Silva

first: Carmen

last: Pérez-Calero

first: Romane

last: Beaurepere

last: Barroso

first: Sylvain

last: Martineau

first: Charlotte

last: Martin

first: Åsa

last: Ehlén

first: Juan

middle: S

last: Martínez

first: Bérangère

last: Lombard

first: Damarys

last: Loew

first: Stephan

last: Vagner

first: Aura

last: Carreira


title: Reorganization of 3D chromatin architecture of rice genomes during heat stress (MeDIP-Seq)

city: Beijing

first: Xiaofeng

last: Gu

address: Zhongguancun south street

country: China

institute: Chinese Academy of Agricultrual Sciences

summary:
Background: The three-dimensional spatial organization of the genome plays important roles in chromatin accessibility and gene expression in multiple biological process, and has been reported to be altered in response to environmental stress. However, the functional changes in spatial genome organization during environmental changes in crop plants are poorly understood.
Results: Here we perform Hi-C, ATAC-seq and RNA-seq in two agronomically important rice cultivars, Nipponbare (Nip; Japonica) and 93-11 (Indica), to report a comprehensive profile of nuclear dynamics during heat stress (HS). We show that heat stress affects different levels of chromosome organization, including A/B compartment transition, increase in size of topologically associated domains, and loss of short-range interactions. The chromatin architectural changes were associated with chromatin accessibility and gene expression changes. Comparative analysis revealed that 93-11 exhibited more dynamic gene expression and chromatin accessibility changes, including of HS-related genes, consistent with observed higher HS tolerance in this cultivar.
Conclusions: Our data uncovered higher-order chromatin architecture as a new layer in understanding transcriptional regulation in response to heat stress in rice.

overall_design: 6mA-IP-seq with two replicates

first: Zhe

last: Liang

first: Qian

last: Zhang

first: Qing

last: Liu

first: Changmian

last: Ji

first: Pingxian

first: Guihua

last: Hu

first: Yifan


title: TFEB promotes prostate cancer progression via regulating ABCA2-dependent lysosomal biogenesis

status: Public on Feb 25 2021

city: Guangzhou

first: Yifeng

last: Luo

state: Guangdong

address: 58 Zhongshan 2nd Road

department: Institute of Respiratory Diseases of Sun Yat-sen University

institute: The First Affiliated Hospital of Sun Yat-sen University

summary: The goals of this study is to find effect of overexpression-TFEB in prostate cancer cell (DU145 cell line).

overall_design: To further explore the potential molecular mechanisms of how TFEN affects cancer cell growth and metastasis, we upregulated TFEB expression in DU145 cells which showed relatively low TFEB expression, and then performed the RNA-seq in DU145-TFEB and DU145-Vector cells.

first: Xuejin

last: Zhu

first: Weide

last: Zhong


title: Time-resolved single cell transcriptomics of an ibrutinib-treated mantle cell lymphoma cell line

city: Würzburg

first: Antoine-Emmanuel

last: Saliba

address: Josef-Schneider-Straße 2 / D15

institute: Helmholtz Institute for RNA-based Infection Research

summary: We performed a high-throughput droplet-based single-cell RNA sequencing experiment on a sensitive MCL cell line model (REC-1) treated with ibrutinib over time using the 10x Genomics platform. Two biological replicates were generated of an untreated control, 6 h, and 48 h ibrutinib-treated cells.

overall_design: REC-1 cells were cultured for 48 h, one sample stayed untreated, the second was treated with 400 nM ibrutinib for 6 h and the third for 48 h. After harvesting, the cells were stained with propidium iodide to identify the surviving cells which entered single-cell RNA sequencing.

first: Viktoria

last: Fuhr

first: Ehsan

last: Vafadarnejad

first: Oliver

last: Dietrich

first: Panagiota

last: Arampatzi

first: Angela

last: Riedel

first: Antoine

first: Andreas

last: Rosenwald

first: Hilka

last: Rauert-Wunderlich


title: Histone ChIP-seq from SJCRH30 (ENCSR022MBN)

first: ENCODE

last: DCC

summary:
H3K27me3 ChIP-seq on human SJCRH30

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: Lipid signalling enforces functional specialization of Treg cells in tumours [scRNA-seq EAE]

status: Public on Feb 24 2021

city: Memphis

first: Hongbo

last: Chi

state: TN

address: 262 Danny Thomas Place

department: Immunology

institute: St Jude Children's Research Hospital

summary: Metabolic reprogramming enforces Treg cell functional specialization in tumors by coordinating fatty acid biosynthesis and inhibitory receptor signaling pathways. These findings point to new avenues to selectively targeting intratumoral Treg cells for cancer therapy.

overall_design: We used scRNA-seq to compare Treg cells from spleen and CNS in EAE mouse model

first: Seon

middle: A

last: Lim

first: Hao

last: Shi

first: Jun

last: Wei


title: Specialization of the Reiterated Copies of the Heterodimeric Integration Host Factor Genes in Geobacter sulfurreducens

city: Mexico

first: Leticia

last: Vega

state: Mexico

address: Circuito Ext s/n

country: Mexico

institute: Universidad Nacional Autonoma de Mexico

summary: Integration host factor (IHF) is a widely distributed small heterodimeric protein member of the bacterial Nucleoid-Associated Proteins (NAPs), implicated in multiple DNA regulatory process. IHF recognizes a specific DNA sequence and induces a large bend of the nucleic acid. IHF function has been mainly linked with regulation of s54-dependent promoters, where IHF commonly recognizes a DNA sequence between the enhancer-binding region and the promoter, facilitating a close contact between the upstream bound activator and the promoter bound, RNA polymerase. In proteobacteria, the genes encoding IHF subunits (ihfA and ihfB) are found in a single copy. However, in some Deltaproteobacteria, like Geobacter sulfurreducens, those genes are duplicated. To date, the functionality of IHF reiterated encoding genes is unknown. In this work, we achieved the functional characterization of the ihfA-1, ihfA-2, ihfB-1, and ihfB-2 from G. sulfurreducens. Unlike the ΔihfA-2 or ΔihfB-1 strains, single gene deletion in ihfA-1 or ihfB-2, provokes an impairment in fumarate and Fe(III) citrate reduction. Accordingly, sqRT-PCR experiments showed that ihfA-1 and ihfB-2 were expressed at higher levels than ihfA-2 and ihfB-1. In addition, RNA-Seq analyzes of the ΔihfA-1 and ΔihfB-2 strains revealed a total of 89 and 122 differentially expressed genes, respectively. Futhermore, transcriptional changes in 25 genes were shared in both mutant strains. Among these genes, we confirmed the upregulation of the pilA-repressor, GSU1771, and downregulation of the triheme-cytochrome (pgcA) and the aconitate hydratase (acnA) genes by RT-qPCR. EMSA experiments also demonstrated the direct binding of IHF to the upstream promoter regions of GSU1771, pgcA and acnA. PilA changing in ΔihfA-1 and ΔihfB-2 strains was also verified by immunoblotting. Additionally, heme-staining of subcellular fractions in ΔihfA-1 and ΔihfB-2 strains revealed a remarkable deficit of c-type cytochromes. Overall, our data indicate that at least during fumarate and Fe(III) citrate reduction, the functional IHF regulator is likely assembled by the products of ihfA-1 and ihfB-2. Also, a role of IHF controlling expression of multiple genes (other than s54 dependent) affects G. sulfurreducens physiology and extracellular electron transfer.

overall_design: mRNA profiles of Geobacter sulfurreducens strains (DL1, DihfA-1, DihfB-2) in NBAF medium, in duplicate, using Illumina Genome Analyzer Iix

first: Andrade

last: Angel

first: Hernández-Eligio

last: Alberto

first: Tirado

last: Ana Lilia

first: Vega-Alvarado

last: Leticia

first: Olvera

last: Maricela

first: Morett

last: Enrique

first: Juárez

last: Katy


title: In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [Pofut1 ATAC-seq]

summary: The role of nutrient signaling processes in the fate decision of CD8 are incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

overall_design: We used ATAC seq to compare chromatin accessibility profiles of Pofut1 KO and Spike P14 cells from the dual-color transfer system at day 5 post-infection from spleen

first: Hongling

last: Huang

first: Yogesh

last: Dhungana


title: In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [Pofut1_microarray]

summary: The role of nutrient signaling processes in the fate decision of CD8 is incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

overall_design: We used microarrays to compare the global transcription profiles of WT or Pofut1-null P14 cells with or without NICD co-expression at day 7.5 post-infection from spleen.


title: In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [NICD_microarray]

overall_design: We used microarrays to compare the global transcription profiles of empty vector- or NICD-expressing vector-transduced P14 cells at day 7.5 post-infection from spleen.


title: Germline masculinization by Phf7 in D. melanogaster requires its evolutionarily novel C-terminus and the HP1-family protein HP1D3csd

city: Kweishan, Taoyuan

first: Shu Yuan

last: Yang

address: Wenhua 1st Rd, No. 259

country: Taiwan

institute: Chang Gung University

summary: This study is designed to investigate genes regulated by Phf7 in the embryonic germline of D. melanogaster

overall_design: Stage 17 embryonic gonads from control (vas-GFP) or Phf7-mutants (Phf7[DN18]; vasGFP) were isolate by FACS sorting, RNA was purified and sent for 3'-end cDNA library construction and high throughput sequencing

first: Shu


title: ChIPseq on H4K20me1 on TX1072 cell line at different times of Xist induction through Doxycycline.

city: Leuven

first: Aurélie

last: Bousard

address: Herestraat 49, bus 912

country: Belgium

institute: VIB/KULeuven

summary: During X chromosome inactivation (XCI), in female mammals, gene silencing is initiated by a long-noncoding RNA, called Xist. Xist RNA accumulation also allows for the deposition of specific chromatin marks. Among others, PRC2-dependent H3K27me3 and PrSet7-dependent H4K20me1 become enriched at the inactive X chromosome. However, the dynamics of this process in relation to Xist RNA accumulation remains unknown as is the molecular mechanism allowing for H4K20me1 enrichment. To follow XCI dynamics in living cells, we developed a genetically encoded, H3K27me3-specific intracellular antibody, or H3K27me3-mintbody. By combining it with live-imaging of H4K20me1, the X chromosome and Xist RNA we uncover striking similarities in the accumulation dynamics of H3K27me3 and H4K20me1. Further ChIP-seq analysis confirmed concurrent accumulation of H4K20me1 and H3K27me3 during XCI albeit with distinct genomic distributions. Xist B and C repeat mutant, which can silence the X but does not allow for H3K27me3 enrichment, also showed lack of H4K20me1 deposition. Thus, both H3K27me3 and H4K20me1 are deposited at the inactive X through a common molecular mechanism but are dispensable for the initiation of gene silencing.

overall_design: ChIPseq on H4K20me1 on TX1072 cell line at different times of Xist induction through Doxycycline (0,4,8,12,24 hours), in replicates.

first: Sjoerd

last: Tjalsma

first: Mayako

last: Hori

first: Yuko

last: Sato

first: Aurelie

first: Akito

last: Ohi

first: Ana

middle: C

last: Raposo

first: Julia

last: Roensch

first: Agnes

last: Le Saux

first: Junpei

last: Nogami

first: Kazumitsu

last: Maehara

first: Tomoya

last: Kujirai

first: Yasuyuki

last: Ohkawa

first: Hitoshi

last: Kurumizaka

first: Simão

last: Teixeira da Rocha

first: Jan

last: Żylicz

first: Hiroshi

last: Kimura

first: Edith

last: Heard


title: Reorganization of 3D chromatin architecture of rice genomes during heat stress (Bisulfite-seq)

first: Xiaofeng

last: Gu

overall_design: BS-seq with two replicates

first: Zhe

last: Liang

first: Qian

last: Zhang

first: Qing

last: Liu

first: Changmian

last: Ji

first: Pingxian

first: Guihua

last: Hu

first: Yifan

last: Wang


title: Epigenetic silencing of STAT3-targeted miR-193a, by constitutive activation of JAK/STAT signaling, leads to tumor progression through overexpression of YWHAZ in gastric cancer

city: Chia-Yi

first: Yu Ming

last: Chuang

address: 168 University Road,Min Hsiung

department: Department of Biomedical Science

institute: National Chung Cheng University

summary: To investigate aberrant JAK/STAT signalling conferred epigenetic silencing of miR-193a, leading to overexpression of YWHAZ and metastasis in gastric cancer.

overall_design: AGS gastric cancer cells were  infected with lentivirus containing shGFP or shSTAT3

first: Michael

middle: W

last: Chan

first: Pearlly

last: Yan

first: Jian-Liang

last: Chou

first: Jora

middle: M

last: Lin

first: Yu-Ming


city: Boston

first: David

last: Kozono

state: MA

address: 450 Brookline Avenue

department: Radiation Oncology

institute: Dana-Farber Cancer Institute

summary: A549 cells with FOXM1 or LIN54 sgRNA knockout, which confers resistance to the CHK1 inhibitor prexasertib, were generated. These cells and control (empty vector) cells were synchronized in S phase, released for 1 hour and treated with 100 nM prexasertib or DMSO (vehicle) for 2 hours. RNA-seq profiling was performed to identify drug-induced perturbations in gene expression in these cells.

overall_design: RNA-seq profiling of A549 cells with sgRNA knockouts that confer prexasertib resistance, compared to control A549 cells, with or without prexasertib treatment

first: Timothy

middle: B

last: Branigan

first: Amy

last: Schade

first: James

last: DeCaprio


title: Lipid signalling enforces functional specialization of Treg cells in tumours [microarray #1]

first: Hongbo

last: Chi

overall_design: In total 25 samples were analyzed: TIL Treg cells (WT, n = 7;Scap-KO, n = 3;Fasn-KO, n = 3;PD-1high WT Treg cells, n=4; PD-1low from WT Treg cells, n=4), WT Lymph node Treg from mice with no tumors (n=4).

first: Seon

last: Lim

first: Jun

last: Wei

first: Yogesh

last: Dhungana


title: Lipid signalling enforces functional specialization of Treg cells in tumours [scRNA-seq]

overall_design: We used scRNA-seq to compare CD45+ immune cells composition in B16 tumor microenvironment of wild-type mice and mice with Scap Treg-specific deletion.

first: Seon-Ah

first: Hao

last: Shi


title: Lipid signalling enforces functional specialization of Treg cells in tumours [microarray #2]

overall_design: In total 10 samples were analyzed: PLN WT Treg cells ( In vitro 0h, n=5; In vitro 8h TCR stimulation, n=5)


title: Prostate cancer-derived small extracellular vesicles promote osteoclastogenesis and cancer-induced osteolysis via miR-152-3p delivery

city: 重庆

first: Yutong

last: Wu

address: 高滩岩正街30号

institute: Third Military Medical University

summary: Extracellular vesicles (EVs) play critical roles in regulating bone metastatic microenvironment through mediating intercellular communications. Here, we report a direct regulatory mode between tumor cells and osteoclasts in osteolytic metastasis of prostate cancer via vesicular miRNAs transfer. Combined analysis of miRNAs profiles both in tumor-derived small EVs (sEVs) and osteoclasts identified miR-152-3p as a potential osteolytic molecules. Further in vitro experiments showed that sEVs were enriched in miR-152-3p, which targets osteoclastogenic regulator MAFB. Blocking miR-152-3p in sEVs upregulated the expression of MAFB and impaired osteoclastogenesis in recipient osteoclasts. In vivo xenograft mouse model found that blocking of miR-152-3p in sEVs significantly rescued the loss of trabecular architecture, while systemic inhibition of miR-152-3p using antagomiR-152-3p reduced the osteolytic lesions of cortical bone while remaining the basic trabecular architecture. Together, our findings suggest that miR-152-3p carried by prostate cancer-derived sEVs deliver osteolytic signals from tumor cells to osteoclasts, facilitating osteolytic progression in bone metastasis.

overall_design: small RNA sequencing of small extracellular vesicles secreted by three human prostate cancer cell lines.

first: Qinyu

last: Ma

first: Mengmeng

last: Liang


title: Lipid signalling enforces functional specialization of Treg cells in tumours

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

overall_design: Refer to individual Series


title: Effects of sepsis and dichloroacetate on hepatic transcriptome

status: Public on Feb 22 2021

city: Winston Salem

first: Matthew

middle: Allan

last: Quinn

state: NC

address: 575 N Patterson Ave

institute: Wake Forest School of Medicine

summary: This study was designed to capture the effects of chronic sepsis (30 hours) on hepatic gene expression. Furthermore, we characterized the effects of pharmacological targeting of the pyrruvate dehydrogenase kinase pathway via dichloroacetate treatment in septic mice.

overall_design: RNAseq for 3 conditions, 4 replicates each.

first: Jennifer

last: Martinez


title: P-selectin axis plays a key role in microglia immunophenotype and glioblastoma progression

city: Tel Aviv

first: Ronit

last: Satchi-Fainaro

address: Klatzkin 35

department: physiology and pharmacology

country: Israel

institute: Tel Aviv University

summary: We aimed to evaluated the effect of P-Selectin knockdown in glioblastoma cells on their tumorigenesis and the brain microenvironment. To that end, we have established P-Selectin knockdown GL261 glioblastoma cells by shRNA. For control, scrambled shRNA was used (NC). P-Selectin kncockdown and NC GL261 cells were inoculated intra-cranially into mice. 16-21 days post tumor cell inoculation, cancer cells and cells of the tumor microenvironment were isolated using magnetic beads cell separation.   We showed meaningful changes in gene expression and cluster distributions between the groups.

overall_design: Droplet-based single-cell RNA-Seq of glioblastoma cells, CD11b positive cells and T cells isolated by magnetic beads separation from P-Selectin knockdown GL261 tumors compared to negative control GL261 tumors.

first: Asaf

last: Madi

first: Eilam

last: Yeini


title: Rab11a-recycling endosomes function to regulate cell signaling during retinal neurogenesis in zebrafish

city: St. Louis

first: Brian

middle: Stewart

last: Clark

state: Missouri

address: 660 S Euclid Ave; Campus Box #8096

department: Ophthalmology and Visual Sciences

institute: Washington University

summary: We report the transcriptional changes associated with inhibition of recycling endosome function within the developing zebrafish retina. Recycling endosome function was inhibited through transgenic expression of a Rab11a dominant negative protein within the developing retinal progenitor cells using UAS::mCherry-Rab11aS25N; vsx2::Gal4 transgenic zebrafish. Changes in gene expression, compared to vsx2:Gal4 controls were profiled through bulk RNA-sequencing experiments of dissected zebrafish retinas. Gene expression changes resulting from inhibition of recycling endosome function were then compared to experiments in which canonical signaling pathways were modulated, including activation of Notch-signaling (over-expression of the constitutively active Notch1a intracellular domain; UAS::myc-NICD1a; vsx2::Gal4), activation of Wnt-signaling (over-expression of Wnt2b; UAS::EGFP-Wnt2b;; vsx2::Gal4), activation of Hippo-signaling (over-expression of nuclear retained YapS87A; dRED::UAS::YapS87A; vsx2::Gal4), and inhibition of mTor signaling (through treatment of zebrafish embryos with Torrin).

overall_design: 60 pooled eyes from experimental or control embryos were pooled for one sample. RNA-sequencing experiments were performed in triplicate for each experimental condition.

last: Link


title: Naked mole rat cells are protected from cellular senescence via Wnt/β-catenin-promoted cholesterol metabolism

status: Public on Feb 21 2021

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary: The naked mole rat (NMR; Heterocephalus glaber) exhibits cancer resistance and an exceptionally long lifespan of approximately 30 years. The longevity of the NMR is widely debated, as it poses challenges to theories associated with aging, cancer, and redox homeostasis. In the present study, we report unique mechanisms of cholesterol metabolism in NMR cells that could be responsible in part for their anti-senescent properties. We found that NMR fibroblasts abundantly express β-catenin, and that increased β-catenin activity is linked to increased accumulation of cholesterol-enriched lipid droplets. Either β-catenin knockdown or inhibition of cholesterol synthesis abolished lipid droplet formation, and enhanced induction of senescence-like phenotypes. Analysis of β-catenin-regulated genes revealed that β-catenin upregulated the LXR/RXR pathway and Apolipoprotein F, which are involved in cholesterol biogenesis and transport. Specifically, Apolipoprotein F is involved in the accumulation of lipid droplets, protecting NMR cells from cellular senescence. We thus suggest that increased β-catenin activity evolved in NMRs to offset senescence via the accumulation of cholesterol-enriched lipid droplets. Hence, the anti-senescence effects of the Wnt/β-catenin signaling in NMRs reveals new strategies for the development of anti-cancer and anti-aging treatments.

overall_design: To determine the mechanisms by which β-catenin induced accumulation of cholesterol-enriched lipid droplets, we performed comparative RNA-seq analysis of control and β-catenin knockdown NSFs (Naked mole rats skin fibroblasts).

first: Woei-Yaw

last: Chee

first: Okuzaki

last: Daisuke

first: Masato

last: Okada


title: Upregulation of COX4-2 via HIF-1α stabilization in COX4-1 deficiency

city: Jerusalem

first: Ann

last: Saada (Reisch)

department: Department of Genetics

institute: Hadassah Medical Center

summary: Cytochrome-c-oxidase (COX) subunit 4 (COX4) plays important roles in the function, assembly and regulation of COX (mitochondrial respiratory complex 4), the terminal electron acceptor of the oxidative phosphorylation (OXPHOS) system. The principal COX4 isoform, COX4-1, is expressed in all tissues, whereas COX4-2 is mainly expressed in the lungs, or under hypoxia and other stress conditions. We have previously described a patient with a COX4-1 defect with a relatively mild clinical presentation compared to other primary COX deficiencies, and hypothesized that this could be the result of compensatory upregulation of COX4-2. To this end, COX4-1 was downregulated using a stable expression of COX4I1-targeting shRNAs in human foreskin fibroblasts (HFF), to mirror and compare it to the primary patient's cells. COX4-1, COX4-2 and HIF-1α were detected by immunocytochemistry. The mRNA transcripts of both COX4 isoforms and HIF-1 target genes were carried out by RT-qPCR. COX activity and OXPHOS function were measured by enzymatic and oxygen consumption assays, respectively. Pathways were analyzed by CEL-Seq2 and by RT-qPCR.

overall_design: mRNA profiles of COX4I1 knockdown cells (5 plicates) vs. control (5 plicates)

first: Liza

last: Douiev

first: Chaya

last: Miller

first: Shmuel

last: Ruppo

first: Hadar

last: Benyamini

first: Bassam

last: Abu-Libdeh

last: Saada


title: ChIP-seq analysis reveals the direct targets of GltR in the P. aeruginosa genome

city: Shanghai

first: Chen

middle: Chen

last: Xu

address: No.646, Songtao Road

institute: Shanghai Institute of Materia Medica Chinese Academy Sciences

summary: we performed ChIP-seq assays to identify in vivo targets of GltR. The plasmid mini-gltR-flag-lacz was constructed and the resultant plasmid was fused to P. aeruginosa strain PAO1, yielding PAO1/mini-gltR-flag-lacz. We investigated GltR-binding to the chromosome of PAO1 during growth with glucose by ChIP-Seq. Sequence reads obtained from three independent ChIP-Seq experiments using anti-flag antibody and mapped to the P. aeruginosa PAO1 genome.Using the MACS software,we identified 55 enriched loci (q-value < 0.05) harboring GltR-binding peaks, that were enriched > 3-fold, but were absent in control sample conducted without anti-flag antibody.

overall_design: Perform a genome-wide screen for GltR binding sites.

first: Chenchen

first: Lefu

last: Lan


title: FOXO1 mitigates the SMAD3/FOXL2C134W transcriptomic effect in a model of human adult granulosa cell tumor

city: La Jolla

first: Christian

last: Secchi

address: 9500 Gilman Drive, Biomedical Science Building, Room 5045

institute: University of California, San Diego

summary: Granulosa cell tumors (GCTs) are a rare form of stromal cell malignant cancer accounting for one in twenty cases of ovarian cancer. More than 400 tumors from aGCT patients of diverse ethnicities showed one single mutation in the Forkhead box L2 transcription factor gene FOXL2: Cys134Trp (c.402C<G). In this work, seeking more comprehensive profiling of the mutant FOXL2C134W transcriptomic activity in a model of adult Granulosa Cell Tumor (aGTC), we performed an RNA-seq analysis comparing the effect of FOXL2WT/SMAD3 and FOXL2C134W/SMAD3 overexpression in presence/absence of FOXO1 in an established human GC line (HGrC1).

overall_design: To demonstrate the role of SMAD3 as a molecular partner of FOXL2C134W in aGCT progression on a genome-wide level, we carried out RNA-seq analysis in HGrC1 overexpressing FOXL2C134W together with SMAD3, compared to FOXL2WT/SMAD3 as a control. We further explored the FOXL2 antagonistic tumor-suppressive transcription factor FOXO1 to study its influence on the SMAD3/FOXL2C134W induced alterations. FOXO factors are considered as tumor suppressors for their parts in the initiation of apoptotic process and in the cell cycle arrest.

first: Paola

last: Benaglio

first: Francesca

last: Mulas

first: Martina

last: Belli

first: Dwayne

last: Stupack

first: Shunichi

last: Shimasaki


title: Transcriptomic analysis of Drosophila larval lymph glands

status: Public on Feb 20 2021

city: clermont ferrand

first: yoan

last: renaud

address: place henri dunand

institute: igred

summary: The lymph gland is one of the main larval hematopoietic organin in Drosophila melanogaster. In wnandering third instar larav, it is composed of two pairs of anterior lobes, followed by 2 to 3 pair of posterior lobes. To gain further insight into the gene expression repertoire of Drosophila blood cells, we established the gene expression profiles of third instar larva lymph glands anterior and posterior lobes.

overall_design: Drosophila lymph gland anterior and posterior lobes were dissected from third instar larvae (white1118) and their RNA were extracted for analysis by deep sequencing, in triplicate, using Illumina NextSeq sequencing platform.

first: Lucas

last: Waltzer

first: Yoan

last: Renaud


title: In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [scRNA-seq]

first: Hongbo

last: Chi

summary: The role of nutrient signaling processes in the fate decision of CD8 T cells are incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

overall_design: We used scRNA-seq to compare transcriptional heterogeneity of sgNTC (‘spike for sgPofut1’)- or sgPofut1-transduced P14 cells from the dual-color transfer system at day 7 post-infection from spleen; We used scRNA-seq to compare transcriptional heterogeneity of empty vector (‘spike for NICD’)- or NICD-expressing vector- transduced P14 cells from the dual-color transfer system at day 7 post-infection from spleen.

first: Hongling

last: Huang

first: Yogesh

last: Dhungana

first: Hao

last: Shi


title: Effect of Fzd9 knock-out on MycER-BclXl insulinoma progression

city: Barcelona

first: Mariano

middle: F

last: Zacarias-Fluck

address: Natzaret, 115-117

department: Preclinical and Translational Research Program

institute: Vall d'Hebron Institute of Oncology (VHIO)

summary:
Analysis of MycER-BclXl-induced insulinoma in Fzd9 wt and knock out mice after three days of MycER activation
Mice (n=4/genotype) were euthanized three days after tamoxifen inoculation and pancreatic islets were isolated and frozen at -80ºC until processing.

overall_design: Mice were treated with Tamoxifen i.p. to activate MycER

first: Laura

last: Soucek


title: in vivo neurogenesis based electromagnetized gold nanoparticles

status: Public on Feb 19 2021

city: Seoul

first: Jongpil

last: Kim

address: 30, Pildong-ro 1-gil

country: South Korea

institute: Dongguk university

summary: Electromagnetized gold nanopartilces can facilitate hippocampal neurogenesis.

overall_design: Male C57BL/6 mice were used. For the surgery, the mice were anesthetized with avertin and placed in a stereotaxic frame, after which the AuNPs were injected into the hippocampus at fixed coordinates [anteroposterior (AP): -2.18 mm, mediolateral (ML): ± 1.2 mm, dorsoventral (DV): -2 mm] for 4 min at a 0.5 μl min-1 rate using a 26-gauge 10 μl Hamilton syringe. The mice were then placed in the middle of a pane between two coils at 3 weeks exposure. One pair of Helmholtz coils was used for both the control and AuNPs groups with EMF exposure.

first: Yujung

last: Chang

first: Byounggook

last: Cho


title: Genome binding/occuoancy profiling by high throughout sequencing in mouse embryonic stem cells.

city: Nanjing

first: Su

last: Ting

address: No. 12, Xuefu Road, Pukou District

department: Model Animal Research Center

institute: Nanjing University

summary: We mapped the subunit of the PRC2, Rbbp4, using ChIP-seq in embryonic stem cells. We found that Rbbp4 protein binds to genome regions of mesendodermal genes and pluripotency-associated genes, and therefore reflect pluripotent cell state and lineage potential. We idetified the physiological targets of Rbbp4 in mouse ES cells.

overall_design: Embryonic Stem Cells ChIP-Seq

first: Jinzhong

last: Qin

first: Yikai

first: Ting

last: Su


title: Expression profiling of WT and the ka120 mutant in Arabidopsis [array]

city: Berkeley

first: Yangnan

last: Gu

address: 371 Koshland Hall

department: Plant and Microbial Biology

institute: University of California at Berkeley

summary: Identification of the transcriptional responses upon loss of importin-beta gene KA120 in Arabidopsis

overall_design: The entire rosette of three-week-old Col-0 WT and the ka120 mutant plants were collected. Three biological replicates were performed for each genotype.


title: KA120 negatively regulates effector-triggered immunity [RNA-seq]

summary: Purpose: To understand the autoimmune phenotype in the ka120 mutant and the suppression of ka120 phenotype by the pad4 and ndr1 mutant, we performed the whole genome transcriptome analysis on three-week-old Arabidopsis WT, ka120, ka120 pad4, and ka120 ndr1 plants (the entire rosette was sampled).

overall_design: The mRNA profiles of three-week-old plants of wild type (Col-0), ka120, ka120 pad4, and ka120 ndr1 mutants were generated by deep sequencing, in triplicate, using Illumina HiSeq PE-150.

first: Xueqi

last: Shen


title: EZH2 Dynamically Associates with Non-coding RNAs in Mouse Hearts after Acute Angiotensin II

status: Public on Feb 18 2021

city: Shenzhen

first: Zhihua

last: Wang

address: No. 12, Langshan Road, Xili Street, Nanshan District, Shenzhen

department: Shenzhen Key Laboratory of Cardiovascular Disease

institute: Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen

summary: Enhancer of zeste 2 (EZH2) governs gene reprogramming during cardiac hypertrophy through epigenetic remodeling, a process regulated by numerous non-coding RNAs (ncRNAs). However, the dynamic interaction between EZH2 and ncRNAs upon hypertrophic stimulation remains elusive. Here we performed an unbiased profiling for EZH2-associated ncRNAs in mouse hearts treated with Angiotensin II (AngII) at different time points (0, 4, and 24 h). The interactions between EZH2 and long ncRNAs (lncRNAs), Chaer, Mirt1, Hotair, and H19, were validated by PCR. RIP-seq analysis identified a total of 126 ncRNAs to be significantly associated with EZH2. These ncRNAs covers all five categories including intergenic, antisense, intron-related, promoter-related and both antisense and promoter-related. According to their changing patterns after AngII treatment, these ncRNAs were clustered into four groups, constantly enhanced, transiently enhanced, constantly suppressed and transiently suppressed. Structural prediction showed that EZH2 bound to hairpin motifs in ncRNAs including snoRNAs. Interaction strength prediction and RNA pull-down assay confirmed the direct interaction between EZH2 and Snora33. Interestingly, two antisense lncRNAs of Malat1, Gm20417, and Gm37376, displayed different binding patterns from their host gene after AngII treatment, suggesting a crucial role of this genomic locus in modulating EZH2 behavior. Our findings reveal the profile of EZH2-associated ncRNAs upon hypertrophic stimulation, and imply a dynamic regulation of EZH2 function in cardiac hypertrophy.

overall_design: Two independent RIP products from each group were mixed before reverse transcription into cDNA sequencing library using KAPA Stranded RNA-Seq Library Preparation Kit. The libraries were subjected to quality validation using the Agilent Bioanalyzer 2100, and sequenced using Illumina NextSeq 500 in DNA Link USA Inc. The reads were mapped to mouse genome (mm10) using TopHat2, and visualized on the UCSC browser (http://genome.ucsc.edu). LncRNAs were picked out according to NONCODE database. Screening criteria was set as reads >1.0; ratio of anti-EZH2 group relative to normal IgG group >2 in at least one tissue.

first: Shun

first: Ningning

last: Guo

first: Shuangling

last: Li

first: Yuan

last: He

first: Di

last: Zheng

first: Lili


title: Genome-wide shifts in histone modification patterns at early stage of rice infection with root-knot nematode Meloidogyne graminicola

status: Public on Feb 17 2021

city: Ghent

first: Bruno

last: Verstraeten

state: Oost-Vlaanderen

address: Technologiepark 71

institute: Ghent University

summary: There is mounting evidence for the role of epigenetic processes in the regulation of plant responses to a wide range of external stimuli. Despite their importance, the significance of epigenetic processes in plant-pathogen interactions remain poorly understood. So far, the role of histone modifications has not been investigated at genome wide level in plant-nematode interactions, although their expression levels are altered in nematode-induced galls. In this study, we first applied chemical inhibitors of histone modifying enzymes on rice plants. Despite theirdistinct effects on histone modifications, application of different concentrations of Niconinamide, sulfamethazine and fumaric acid lead to reduced susceptibility to nematode infection. Similarly, two overexpression lines of histone lysine methyltransferases and one histone deacetylase were analyzed in an infection assay with nematodes, showing contrasting results in susceptibility. These data indicate that histone modifications can affect plant defence against nematodes in rice. To further investigate their effect, the genome-wide level of three histone marks namely H3K9ac, H3K9me2 and H3K27me3 was studied by chromatin-immunoprecipitation (ChIP)-sequencing on nematode-induced galls in comparison with control root tips.

overall_design: Three histone marks were investigated under infected and control conditions. For H3K9me2 and H3K27me3 three samples were used for each experimental condition. For H3K9ac two samples were used for each experimental condition. For peak calling an input sample was used.

first: Mohammad

last: Atighi

first: Tim

last: De Meyer

first: Tina

last: Kyndt


title: Barley shoot and root growing in low-Pi condition

city: Poznan

first: Andrzej

last: Pacak

address: Uniwersytetu Poznanskiego 6

country: Poland

institute: Adam Mickiewicz University, Poznan

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

overall_design: Refer to individual Series


title: Identification of AGO-associated viral interfering RNAs in Zika virus infected neural stem cells

status: Public on Feb 16 2021

city: Los Angeles

first: Zhifei

last: Luo

address: 1450 Biggy Street, NRT 6514

institute: University of Southern California

summary: Viral interfering RNA (viRNA) has been identified from several viral genomes via directly deep RNA sequencing of the virus-infected cells, including zika virus (ZIKV). Once produced by endoribonuclease Dicer, viRNAs, similar to microRNAs, are loaded onto Argonaute (AGO) family proteins of the RNA-induced silencing complexes (RISCs) to pair with their RNA targets and then initiate cleavage of the target genes. However, identities of functional ZIKV viRNAs and their viral RNA targets remain largely unknown. By combining AGO-associated RNA sequencing, deep sequencing analysis in ZIKV-infected neural stem cells (NSCs), and miRanda target scanning, we have defined 29 ZIKV derived viRNA profiles in NSCs, and established the complex interaction networks between the viRNAs and their viral targets. Our recent study has shown that ZIKV capsid protein interacted with Dicer and antagonized its endoribonuclease activity depending on its histidine (H) at the 41st amino acid. Accordingly, the rescued ZIKV-H41R mutant virus, compared to wild-type ZIKV, no longer suppressed Dicer enzymatic activity and consequently failed to inhibit miRNA biogenesis in NSCs. As a result, much higher levels of viRNAs generated from the ZIKV-H41R virus-infected NSCs, suggesting Dicer-dependent viRNA production. Knockdown of individual RNAi machinery in ZIKV-infected NSCs suggests that viRNA is a limiting factor of ZIKV infection in NSCs. The mapping of viRNAs to their RNA targets is paving a way to further investigate how viRNAs play the role in anti-viral mechanisms or even other unknown biological functions.

overall_design: miRNA-seq

first: Jianxiong

last: Zeng

first: Xiaochun

last: Xie

first: Qiming

last: Liang

first: Zhen

last: Zhao


title: GATA transcription factors, SOX17 and TFAP2C, drive the human germ-cell specification program [Bisulfite-Seq]

city: Kyoto

first: Yukihiro

last: Yabuta

state: Kyoto

address: Yoshida-Konoe-cho, Sakyo-ku

department: Anatomy and Cell Biology

institute: Kyoto University, Graduate school of medicine

summary: The in vitro reconstitution of human germ-cell development provides a robust framework for clarifying key underlying mechanisms. Here, we explored transcription factors (TFs) that engender the germ-cell fate in their pluripotent precursors. Unexpectedly, SOX17, TFAP2C, and BLIMP1, which act under the BMP signaling and are indispensable for human primordial germ-cell-like cell (hPGCLC) specification, failed to induce hPGCLCs. In contrast, GATA3 or GATA2, immediate BMP effectors, combined with SOX17 and TFAP2C, generated hPGCLCs. GATA3/GATA2 knockouts dose-dependently impaired BMP-induced hPGCLC specification, whereas GATA3/GATA2 expression remained unaffected in SOX17, TFAP2C, or BLIMP1 knockouts. In cynomolgus monkeys, a key model for human development, GATA3, SOX17, and TFAP2C were co-expressed exclusively in early PGCs. Crucially, the TF-induced hPGCLCs acquired a hallmark of bona fide hPGCs to undergo epigenetic reprogramming and mature into oogonia/gonocytes in xenogeneic reconstituted ovaries. By uncovering a TF circuitry driving the germ line program, our study provides a paradigm for TF-based human gametogenesis.

overall_design: Whole Genome Bisulfite Sequence (WGBS): Overexpression of SOX17, TFAP2C, GATA3, clone_1; day77

first: Yoji

last: Kojima

first: Chika

last: Yamashiro

first: Yusuke

last: Murase

first: Ikuhiro

last: Okamoto

first: Chizuru

last: Iwatani

first: Hideaki

last: Tsuchiya

first: Masataka

last: Nakaya

first: Tomoyuki

last: Tsukiyama

first: Tomonori

last: Nakamura

first: Takuya

last: Yamamoto

first: Mitinori

last: Saitou


title: Gene expression profile of murine submandibular gland epithelial cells

city: Obu

first: Yosuke

last: Shikama

state: Aichi

address: 7-430 Morioka-cho

institute: National Center for Geriatrics and Gerontology

summary: We examined effects of aging on gene expression profile of murine submandibular gland epithelial cells

overall_design: Young or aged C57BL/6 mice (N=1 each) were used. We isolated epithelial cells from murine submandibular glands by positive selection using Miltenyi mouse CD326 (epithelial cell adhesion molecule; EpCAM) MicroBeads.


title: GATA transcription factors, SOX17 and TFAP2C, drive the human germ-cell specification program [RNA-Seq]

overall_design: 3' RNA-Seq samples of human iPSCs at different time points during PGCLC differentiation with genetic modification


title: Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [WES]

city: Daejeon

first: Hye Jin

last: Nam

email: nhj0120@gmail.com, hjnam@krict.re.kr

state: Not US or Canada

address: 141 Gajeongro, Yuseong

institute: Korea Research Institute of Chemical Technology

summary: Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

overall_design: Somatic mutations of 559T and 592T cells

first: Hye

last: J Nam

first: Heeyeong

last: Cho


title: Nerve Growth Factor neutralization promotes oligodendrogenesis by increasing miR-219a-5p levels

status: Public on Feb 15 2021

city: Roma

first: Ivan

last: Arisi

address: viale Regina Elena 295

department: Bioinformatics Facility

country: Italy

institute: European Brain Research Institute

summary: Alterations of the crosstalk between the nervous and immune systems may underlie the inflammatory and neurodegenerative changes characterizing Multiple Sclerosis (MS). Among the molecules that actively interconnect these two systems is the Nerve Growth Factor (NGF), involved in both regulating inflammation and in brain homeostasis. Additionally, NGF is known to modulate oligodendrogenesis and reduce myelination, further suggesting an involvement of NGF in MS ethiology. In this study, we find that NGF regulates oligodendrogenesis by modulating the levels of miR-219a-5p, a well-known positive regulator of oligodendrocyte (OL) differentiation. We utilized a transgenic NGF-deprivation mouse model, AD11, in which postnatal expression of an anti-NGF antibody leads to NGF neutralization and progressive neurodegeneration. Notably, we find that these mice also display increased myelination. A microRNA profiling of AD11 brain  samples (hippocampus) by Agilent microarray analysis revealed that NGF deprivation leads to an increase of miR-219a-5p levels and a downregulation of its predicted targets, compared to AD11-VH control mice. The AD11-VH controls are transgenic mice where only the heavy chain of the transgenic antibody is expressed, while in AD11 mice express the whole functional antibody (heavy + light chain)

overall_design: A transcriptomic profile of microRNA genes was obtained from the brain  hippocampus of transgenic anti-NGF AD11 mice and control mice, at 1 month of age. A total of n=8 samples were analyzed by Agilent microarray: n=4 AD11 samples and n=4 control samples.

first: Rossella

last: Brandi

first: Miriam

last: Fabiano

first: Corinna

last: Giorgi

first: Federico

last: La Regina

first: Francesca

last: Malerba

first: Sabrina

last: Turturro

first: Andrea

last: Storti

first: Flavia

last: Ricevuti

first: Susann

last: Amadio

first: Cinzia

last: Volontè

first: Raffaella

last: Scardigli

first: Mara

last: D’Onofrio

first: Antonino

last: Cattaneo


title: Azathioprine Antagonizes Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma

first: Hye Jin

last: Nam


title: Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [microarray]

summary:
Expression profiling of 559T(proneural subtype of glioblastoma), 592T(mesenchymal subtype of glioblastoma) and normal human astrocyte (NHA)
Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

overall_design: triplicate for each cell. Compare the expression of glioblastoma cells versus NHA.

first: Hye

middle: J


title: Terminally differentiated CD4+ T cells promote myocardial inflammaging

city: Würzburg

first: Tom

last: Gräfenhan

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

department: Core Unit SysMed

institute: University of Wuerzburg

summary: We generated a xenograft transplantation model in which young humanized mice were treated to harbor a senescent-like human CD4+ T cell compartment. Our data uncover a role for terminally differentiated T cells in promoting cardiac inflammaging.

overall_design: Whole transcriptome profiles of hearts of NSG-DR1 mice comparing the control condition with the condition after human CD4+ T-cell transplantation. RNA was sequenced on the NextSeq-500 platform with ~55 million reads per sample in paired-end mode with 75 nt read length

first: Murilo

last: Delgobo

first: Margarete

last: Heinrichs

first: Nils

last: Hapke

first: Diyaa

last: Ashour

first: Marc

last: Appel

first: Mugdha

last: Srivastava

first: Tobias

last: Heckel

first: Ioakim

last: Spyridopoulos

first: Ulrich

last: Hofmann

first: Stefan

last: Frantz

first: Gustavo

last: Ramos


title: Short-Term Western-Style Diet Negatively Impacts Reproductive Outcomes in Primates

city: Portland

first: Brett

last: Davis

state: Oregon

address: 3181 SW Sam Jackson Park Rd

institute: Oregon Health and Science University

summary: Consumption of a Western-style diet impairs the ovarian follicular microenvironment and preimplantation development without changes in insulin resistance and body fat percentage in non-human primates.

overall_design: A longitudinal study to assess the effect of short-term western style consumption on thesusmacaque ovairan follicular microenvironment and preimplantation development.

first: Sweta

last: Ravisankar

first: Alison

last: Ting

first: Melinda

last: Murphy

first: Nash

last: Redmayne-Titley

first: Dorothy

last: Wang

first: Carrie

last: McArthur

first: Diana

middle: L

last: Takahashi

first: Paul

last: Kievit

first: Shawn

last: Chavez

first: Jon

middle: D

last: Hennebold