title: Urinary MicroRNA-based Diagnostic Model for Central Nervous System Tumors Using Nanowire Scaffolds

city: Nagoya

first: Atsushi

last: Natume

address: 65 Tsurumai-cho

institute: Nagoya University

summary: A urinary miRNA combination could be a powerful classifier for the detection of patients with brain tumors.

overall_design: Urinary microRNA profiles of glioblastomas, lower grade gliomas, meningiomas, other brain tumors, and collected non-cancer controls.

first: Yotaro

last: Kitano

first: Kosuke

last: Aoki

first: Fumiharu

last: Ohka

first: Shintaro

last: Yamazaki

first: Kazuya

last: Motomura

first: Kuniaki

last: Tanahashi

first: Masaki

last: Hirano

first: Tsuyoshi

last: Naganawa

first: Mikiko

last: Iida

first: Yukihiro

last: Shiraki

first: Tomohide

last: Nishikawa

first: Hiroyuki

last: Shimizu

first: Junya

last: Yamaguchi

first: Sachi

last: Maeda

first: Hidenori

last: Suzuki

first: Toshihiko

last: Wakabayashi

first: Yoshinobu

last: Baba

first: Takao

last: Yasui

last: Natsume


title: Control ChIP-seq from A549 (ENCSR641LIQ)

status: Public on Mar 30 2021

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
ChIP-seq on human A549

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


title: ATAC-seq from left lobe of liver (ENCSR624ODL)

summary:
ATAC-seq on human left lobe of liver

For data usage terms and conditions, please refer to http://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 HepG2 (ENCSR693GOR)

summary:
ChIP-Seq on HepG2

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


title: Control ChIP-seq from GM23338 (ENCSR627BZD)

summary:
ChIP-seq on human GM23338

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


title: Control ChIP-seq from HepG2 (ENCSR621FPD)


title: ATAC-seq from adrenal gland (ENCSR651SOJ)

summary:
ATAC-seq on human adrenal gland

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


title: Pancreatic cancer prognosis is predicted by chromatin accessibility

status: Public on Mar 31 2021

city: New York

first: Sagar

last: Chhangawala

state: NY

address: 1300 York Ave.

department: PBSB

institute: Weill Cornell Medical College

type: Expression profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Control ChIP-seq from HepG2 (ENCSR615JHA)


title: Control ChIP-seq from K562 (ENCSR616LTS)

summary:
ChIP-seq on human K562

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


title: Control ChIP-seq from A549 (ENCSR615QEB)


title: Control ChIP-seq from MCF-7 (ENCSR646YPU)

summary:
Input control ChIP-seq on human eGFP-HBP1 tagged MCF7 cell line.

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


title: ATAC-seq from ovary (ENCSR996ZCR)

summary:
ATAC-seq on human ovary

For data usage terms and conditions, please refer to http://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 HepG2 (ENCSR592WMK)

summary:
ChIP-seq on human HepG2

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


title: Control ChIP-seq from A549 (ENCSR969KWE)


title: ATAC-seq from right lobe of liver (ENCSR685ZMP)

summary:
ATAC-seq on human right lobe of liver

For data usage terms and conditions, please refer to http://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 K562 (ENCSR653VRZ)


title: Control ChIP-seq from K562 (ENCSR606GRT)

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: ATAC-seq from heart left ventricle (ENCSR399OSE)

summary:
ATAC-seq on human heart left ventricle

For data usage terms and conditions, please refer to http://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 (ENCSR578ORB)

summary:
Control ChIP-seq of skin epidermis male adult (84 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: ATAC-seq from left colon (ENCSR600ZHS)

summary:
ATAC-seq on human left colon

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


title: Control ChIP-seq from K562 (ENCSR397ZZR)

summary:
Control ChIP-seq in K562

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


title: ATAC-seq from right lobe of liver (ENCSR607BTF)


title: Control ChIP-seq from A549 (ENCSR957URO)


title: Control ChIP-seq from nephron (ENCSR959CIX)

summary:
Control ChIP-seq on nephron female embryo (5 days)

For data usage terms and conditions, please refer to http://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 K562 (ENCSR953NJZ)

summary:
ChIP-Seq on K562

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


title: Control ChIP-seq from K562 (ENCSR596VPT)


title: Control ChIP-seq from K562 (ENCSR592PUP)


title: ATAC-seq from ovary (ENCSR392UJM)


title: Control ChIP-seq from K562 (ENCSR589YUZ)


title: DNase-seq from kidney capillary endothelial cell (ENCSR988YKR)


title: Control ChIP-seq from K562 (ENCSR965AWP)


title: ATAC-seq from lower lobe of right lung (ENCSR948MQC)

summary:
ATAC-seq on human lower lobe of right lung

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


title: ATAC-seq from left cardiac atrium (ENCSR390SLL)

summary:
ATAC-seq on human left cardiac atrium

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


title: ATAC-seq from colonic mucosa (ENCSR970UNF)

summary:
ATAC-seq on human colonic mucosa

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


title: ATAC-seq from heart right ventricle (ENCSR563ZNI)

summary:
ATAC-seq on human heart right ventricle

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


title: ATAC-seq from upper lobe of right lung (ENCSR990NNX)

summary:
ATAC-seq on human upper lobe of right lung

For data usage terms and conditions, please refer to http://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 A549 (ENCSR941GEM)

summary:
ChIP-seq on human A549

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


title: ATAC-seq from right lobe of liver (ENCSR952SPO)


title: Control ChIP-seq from K562 (ENCSR956YUD)

summary:
ChIP-seq on human K562

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


title: Control ChIP-seq from K562 (ENCSR385NZN)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-SMAD3 fusion protein.

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


title: Control ChIP-seq from K562 (ENCSR194QBX)


title: Control ChIP-seq from HepG2 (ENCSR561BTA)

summary:
Control ChIP-seq on HepG2

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


title: Control ChIP-seq from K562 (ENCSR193DQJ)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-HMG20A fusion protein.

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


title: Control ChIP-seq from type B pancreatic cell (ENCSR394CIG)

summary:
Control ChIP-seq on type B pancreatic cell originated from type B pancreatic 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 HepG2 (ENCSR388OQM)

summary:
ChIP-Seq on HepG2

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


title: Control ChIP-seq from K562 (ENCSR926XXG)


title: Control ChIP-seq from A549 (ENCSR928HJI)


title: TF ChIP-seq from heart left ventricle (ENCSR565HBN)

summary:
CTCF 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: Control ChIP-seq from HepG2 (ENCSR555EMB)


title: ATAC-seq from lower lobe of left lung (ENCSR555ZDH)

summary:
ATAC-seq on human lower lobe of left lung

For data usage terms and conditions, please refer to http://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 K562 (ENCSR185VVF)


title: Control ChIP-seq from MCF-7 (ENCSR925PLG)

summary:
MCF7 immortalized cell line stably expressing C-terminal eGFP-OVOL1 fusion protein.

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


title: ATAC-seq from heart left ventricle (ENCSR925LGW)

summary:
ATAC-seq on human heart left ventricle

For data usage terms and conditions, please refer to http://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 K562 (ENCSR182QFE)


title: Control ChIP-seq from brain (ENCSR553CWR)

summary:
Control ChIP-seq on brain female embryo (5 days)

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


title: ATAC-seq from adrenal gland (ENCSR553LAZ)

summary:
ATAC-seq on human adrenal gland

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


title: Control ChIP-seq from K562 (ENCSR918YCV)


title: ATAC-seq from pancreas (ENCSR918TVE)

summary:
ATAC-seq on human pancreas

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


title: Control ChIP-seq from A549 (ENCSR382YXI)


title: Control ChIP-seq from K562 (ENCSR177ADZ)


title: ATAC-seq from right cardiac atrium (ENCSR177JWR)

summary:
ATAC-seq on human right cardiac atrium

For data usage terms and conditions, please refer to http://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 K562 (ENCSR174APY)


title: ATAC-seq from posterior vena cava (ENCSR552QUA)

summary:
ATAC-seq on human posterior vena cava

For data usage terms and conditions, please refer to http://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 K562 (ENCSR167ONN)


title: Control ChIP-seq from HepG2 (ENCSR550ZLZ)


title: Control ChIP-seq from HepG2 (ENCSR172OXO)

summary:
ChIP-seq on human HepG2

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


title: Control ChIP-seq from K562 (ENCSR905GXX)


title: Control ChIP-seq from HepG2 (ENCSR356LLA)


title: TF ChIP-seq from heart left ventricle (ENCSR355PMV)

summary:
CTCF 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: Control ChIP-seq from K562 (ENCSR899URK)

summary:
ChIP-seq on human K562

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


title: Control ChIP-seq from A549 (ENCSR542LGX)

summary:
ChIP-seq on human A549

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


title: Control ChIP-seq from HFFc6 (ENCSR542JNY)

summary:
Control ChIP-seq on HFFc6

For data usage terms and conditions, please refer to http://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 GM23338 (ENCSR533JIB)

summary:
ChIP-seq on human GM23338

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


title: Control ChIP-seq from K562 (ENCSR532WSQ)


title: ATAC-seq from psoas muscle (ENCSR890DWH)

summary:
ATAC-seq on human psoas muscle

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


title: ATAC-seq from heart right ventricle (ENCSR157OSO)

summary:
ATAC-seq on human heart right ventricle

For data usage terms and conditions, please refer to http://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 K562 (ENCSR525VRV)


title: Control ChIP-seq from HepG2 (ENCSR152QMD)

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: ATAC-seq from pancreas (ENCSR530XBF)


title: Control ChIP-seq from A549 (ENCSR175NUT)


title: ATAC-seq from adrenal gland (ENCSR542RNG)


title: Control ChIP-seq from A549 (ENCSR348EIP)


title: Control ChIP-seq from K562 (ENCSR532KDW)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-TEAD1 fusion protein.

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


title: ATAC-seq from psoas muscle (ENCSR886VCC)


title: ATAC-seq from mucosa of urinary bladder (ENCSR153IUB)

summary:
ATAC-seq on human mucosa of urinary bladder

For data usage terms and conditions, please refer to http://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 GM23338 (ENCSR883NMO)


title: Control ChIP-seq from HepG2 (ENCSR141EZP)

summary:
Control ChIP-seq on HepG2

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


title: Control ChIP-seq from K562 (ENCSR144PFT)


title: ATAC-seq from heart right ventricle (ENCSR522FGI)


title: Control ChIP-seq from K562 (ENCSR134JXS)


title: Control ChIP-seq from HepG2 (ENCSR524BHN)

summary:
ChIP-Seq on HepG2

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


title: Control ChIP-seq from GM23338 (ENCSR518DKF)


title: ATAC-seq from left ventricle myocardium superior (ENCSR133WJY)

summary:
ATAC-seq on human left ventricle myocardium superior

For data usage terms and conditions, please refer to http://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 K562 (ENCSR516XLO)

summary:
ChIP-Seq on K562

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


title: DNase-seq from RCC (ENCSR337IRF)


title: ATAC-seq from right lobe of liver (ENCSR516CPW)

summary:
ATAC-seq on human right lobe of liver

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


title: ATAC-seq from heart right ventricle (ENCSR133CMC)


title: Control ChIP-seq from HEK293T (ENCSR128PFN)


title: Control ChIP-seq from mesothelial cell of epicardium (ENCSR333DCK)

summary:
Control ChIP-seq on epicardium (mesothelium) cells originated from epicardium (mesothelium) cells

For data usage terms and conditions, please refer to http://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 A549 (ENCSR514NTD)


title: Control ChIP-seq from GM23338 (ENCSR866FCH)

summary:
Control ChIP-seq on GM23338

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


title: Control ChIP-seq from K562 (ENCSR121UHI)


title: Control ChIP-seq from A549 (ENCSR510MWR)


title: Control ChIP-seq from K562 (ENCSR326NFX)


title: Control ChIP-seq from K562 (ENCSR328FYU)


title: Control ChIP-seq from neural crest cell (ENCSR318RRK)

summary:
Control ChIP-seq on neural crest cell originated from neural crest 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 K562 (ENCSR863VLO)

summary:
ChIP-seq on human K562

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


title: Control ChIP-seq from K562 (ENCSR116EAU)


title: Control ChIP-seq from HepG2 (ENCSR313HFF)


title: Control ChIP-seq from MCF-7 (ENCSR115CIR)

summary:
ChIP-seq on human MCF-7

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


title: ATAC-seq from left cardiac atrium (ENCSR310UDW)

summary:
ATAC-seq on human left cardiac atrium

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


title: ATAC-seq from heart left ventricle (ENCSR310RJN)

summary:
ATAC-seq on human heart left ventricle

For data usage terms and conditions, please refer to http://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 nephron (ENCSR846POB)

summary:
Control ChIP-seq on nephron female embryo (5 days)

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


title: ATAC-seq from adrenal gland (ENCSR864ADD)

summary:
ATAC-seq on human adrenal gland

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


title: ATAC-seq from sciatic nerve (ENCSR120MOY)

summary:
ATAC-seq on human sciatic nerve

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


title: ATAC-seq from esophagus mucosa (ENCSR303PWB)

summary:
ATAC-seq on human esophagus mucosa

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


title: ATAC-seq from mucosa of descending colon (ENCSR496PPU)

summary:
ATAC-seq on human mucosa of descending colon

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


title: Control ChIP-seq from K562 (ENCSR310OPP)


title: Control ChIP-seq from A549 (ENCSR308QHN)

summary:
ChIP-seq on human A549

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


title: ATAC-seq from Right ventricle myocardium inferior (ENCSR855BMI)

summary:
ATAC-seq on human right ventricle myocardium inferior

For data usage terms and conditions, please refer to http://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 K562 (ENCSR502CWG)


title: Control ChIP-seq from neural progenitor cell (ENCSR322GAX)

summary:
Control ChIP-seq on neural progenitor 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 K562 (ENCSR298RRI)


title: ATAC-seq from mucosa of descending colon (ENCSR491VXJ)


title: Control ChIP-seq from MCF-7 (ENCSR293ITU)


title: Control ChIP-seq from brain (ENCSR292BUB)

summary:
Control ChIP-seq on brain female embryo (5 days)

For data usage terms and conditions, please refer to http://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 HepG2 (ENCSR856RWG)

summary:
ChIP-Seq on HepG2

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


title: Control ChIP-seq from K562 (ENCSR833FPN)


title: Control ChIP-seq from HepG2 (ENCSR487JIM)

summary:
Control ChIP-seq on HepG2

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


title: Control ChIP-seq from K562 (ENCSR322WTB)


title: Transcription factor Ascl2 promotes geminal center B cell responses through directly regulating AID transcription

city: Beijing

first: Chen

last: Dong

address: Haidian District

department: Institute for Immunology and School of Medicine

country: China

institute: Tsinghua University

summary: During germinal center (GC) reactions, activated B cells undergo clonal expansion and functional maturation to produce high-affinity antibodies, and differentiate into plasma and memory cells, accompanied with class-switching recombination (CSR) and somatic hypermutation (SHM). Activation-induced deaminase (AID) is responsible for both CSR and SHM in GC B cells. Transcriptional mechanisms underlying AID regulation and GC B cell reactions are still not well understood. Here, we show that expression of Ascl2 transcription factor is upregulated in GC B cells. Ectopic expression of Ascl2 promotes GC B cell development and enhances antibody production as well as affinity maturation. Conversely, deletion of Ascl2 in B cells impairs the germinal center response. Genome-wide analysis reveals that Ascl2 directly regulates GC B cell-related genes, including AID; ectopic expression of AID in Ascl2-deficient B cells rescues their antibody defects. Thus, Ascl2 regulates AID transcription and promotes germinal center B cell responses.

overall_design: We constructed RVKM-Ascl2 retrovirus, and performed RNA-seq using transfected in vitro cultured activated B cells. Also, ChIP-seq of GC B cells from draining LN of KLH immunized C57BL/6 mice.

first: Lin

last: Sun

first: Xiaohong

last: Zhao

first: Xindong

last: Liu

first: Bo

last: Zhong

first: Hong

last: Tang

first: Wei

last: Jin

first: Hans

last: Clevers

first: Hui

last: Wang


title: Role of Top1 and Genome structure in SARS-CoV-2 infection

first: Sook Yuin Jessica

last: Ho

state: New York

address: 1468 Madison Avenue

department: Microbiology

institute: Icahn School of Medicine at Mount Sinai

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

sample_organism:
Homo sapiens
Mesocricetus auratus

platform_organism:
Homo sapiens
Mesocricetus auratus


title: ATAC-seq from right lobe of liver (ENCSR836FIL)

summary:
ATAC-seq on human right lobe of liver

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


title: SNRPA1 BindNSeq

city: San Francisco

first: Hani

last: Goodarzi

department: Biochemistry and Biophysics

institute: UCSF

summary: Assessing the influence of RNA structural and sequence variations on SNRPA1 binding preference in vitro

overall_design: Recombinant SNRPA1 protein was incubated with SSE RNA and SSE RNA with structural and sequence variants. The resulting RNA-protein complexes were then immunoprecipitated with an anti-SNRPA1 antibody, washed 1X, and the SNRPA1-bound RNA was isolated using acid phenol chloroform extraction. The pool of input RNA, along with two replicates of SNRPA1-bound RNA were sequenced on a NextSeq500 instrument.

first: H

first: L

last: Fish


title: Role of Top1 and 3D Genome structure in SARS-CoV-2 infection [Hi-C]

summary: The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.

overall_design: To study alterations in genome structure after SARS-CoV-2 infection, we performed Hi-C on SARS-CoV-2 infected A549-ACE2 cells at 0,8 and 24 hours post infection. Experiment was done in biological duplicate. Each biological replicate was sequenced with 4 technical replicates. To study the impact of Top1 on the inflammatory response to SARS-CoV-2, we knocked-down TOP1 expression using siRNA in A549-ACE2 cells. Cells were then left uninfected or infected with SARS-CoV-2. Cells that were not treated with siRNA (no siRNA) or scrambled siRNA (siSCR) were used as controls. The experiment was done in triplicate.

first: Jessica

middle: S

first: Bobo

middle: W

last: Mok

first: Laura

last: Campisi

first: Tristan

last: Jordan

first: Soner

last: Yildiz

first: Sreeja

last: Parameswaran

first: Joseph

middle: A

last: Wayman

first: Natasha

middle: N

last: Gaudreault

first: David

last: Meekins

first: Sabarish

middle: V

last: Indran

first: Igor

last: Morozov

first: Jessie

middle: D

last: Trujillo

first: Yesai

last: Fstkchyan

first: Raveen

last: Rathnasinghe

first: Zeyu

last: Zhu

first: Simin

last: Zheng

first: Kris

last: White

first: Helen

last: Ray-Jones

first: Valeriya

last: Malysheva

first: Michiel

middle: J

last: Thiecke

first: Siu-Ying

last: Lau

first: Honglian

first: Anna

last: Zhang

first: Andrew

middle: C

last: Lee

first: Wen-Chun

first: Teresa

last: Aydillo

first: Betsaida

last: Melo

first: Ernesto

last: Guccione

first: Robert

last: Sebra

first: Elaine

last: Shum

first: Jan

last: Bakker

last: Kaufman

first: Andre

middle: L

last: Moreira

first: Mariano

last: Carossino

first: Udeni

middle: B

last: Balasuriya

first: Minji

last: Byun

first: Emily

middle: R

last: Miraldi


title: Disparate interferon signaling and shared aberrant basaloid cells in single-cell profiling of idiopathic pulmonary fibrosis and systemic sclerosis-associated interstitial lung disease

city: Pittsburgh

first: Tracy

last: Tabib

state: PA

address: 200 Lothrop Street

department: Department of Medicine

institute: University of Pittsburgh

summary: Idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD) differ in the predominant demographics and identified genetic risk alleles of affected patients, however both diseases frequently progress to respiratory failure and death. Contrasting advanced SSc-ILD to IPF provides insight to the role dysregulated immunity may play in pulmonary fibrosis. To analyze cell-type specific transcriptome commonalities and differences between IPF and SSc-ILD, we compared single-cell RNA-sequencing (scRNA-seq) of 21 explanted lung tissue specimens from patients with advanced IPF, SSc-ILD, and organ donor controls. Comparison of IPF and SSc-ILD tissue identified divergent patterns of interferon signaling, with interferon-gamma signaling upregulated in the SPP1hi and FABP4hi macrophages, cytotoxic T cells, and natural kill cells of IPF, while type I interferon signaling and production was upregulated in the corresponding SSc-ILD populations. Plasmacytoid dendritic cells were found in diseased lungs only, and exhibited upregulated cellular stress pathways in SSc-ILD compared to IPF. Alveolar type I cells were dramatically decreased in both IPF and SSc-ILD, with a distinct transcriptome signature separating these cells by disease. KRT5-/KRT17+ aberrant basaloid cells exhibiting markers of cellular senescence and epithelial-mesenchymal transition were identified in SSc-ILD for the first time. In summary, our study utilizes the enriched capabilities of scRNA-seq to identify key divergent cell types and pathways between IPF and SSc-ILD, providing new insights into the shared and distinct mechanisms between idiopathic and autoimmune interstitial lung diseases.

overall_design: To reduce batch effects in analyzing multiple samples, all control, IPF, and SSc-ILD samples were combined into 3 objects by disease status using Seurat’s IntegrateData function, followed by integration of these 3 objects. Following clustering and visualization with uniform manifold approximation and projection (UMAP), cell populations were classified using multiple gene markers in the transcriptome. Doublet cells were manually identified  and subsequently removed.  To better define individual cell types, the myeloid, lymphoid, epithelial, and stromal populations were separately reclustered.  Differential gene expression analysis for IPF versus SSc-ILD cells for each cluster was performed using the Wilcoxon rank-sum statistical test.

first: Eleanor

last: Valenzi

last: Papazoglou

first: John

last: Sembrat

first: Humberto

middle: E

last: Trejo Bittar

first: Mauricio

last: Rojas

last: Lafyatis


title: BRCA1 Balances the Action of a Transcription Elongation Factor In Mammary Gland Development and Tumorigenesis (sequencing)

city: San Antonio

first: Rong

last: Li

state: TX

address: 7703 Floyd Curl Drive

department: Molecular Medicine

institute: University of Texas Health Science Center at San Antonio

summary: Work from our mouse models showed that COBRA1, the B subunit of NELF, could facilitate R-loop (DNA:RNA hybrid) accumulation in the BRCA1-deficient mouse mammary epithelium. Since NELF could promoter RNA PolII pausing at promoter proximal regions, we asked whether COBRA1-mediated RNA Pol II pausing could contribute to accumulated R-loops. To answer this question, we performed chromatin immunoprecipitation-sequencing (ChIP-seq) for RNA Pol II, as well as two NELF subunits, NELF-A and NELF-B (COBRA1) in mouse primary mammary epithelium cells. To locate R-loops in the same cell population, we performed DNA:RNA immunoprecipitation-sequencing (DRIP-seq) with or without treatment of RNase H, a nuclease that specifically degrades RNA in the R-loop structure. Our sequencing results showed that RNA Pol II, NELF and R-loops are all enriched at transcription start sites (TSSs). Notably, genes with TSS R-loop accumulation are significantly enriched for COBRA1 binding. Taken together, the genomic data lent additional support to the notion that COBRA1-mediated RNAPII pausing contributes to R-loop dynamics in mammary epithelium.

overall_design: Examination of RNA Pol II, NELF and R-loop distribution in the mouse mammary genome.

first: Xiaowen

last: Zhang

first: Yao

last: Wang

first: Victor

middle: X

last: Jin

first: Yanfen

last: Hu


title: Transcriptomic and Metabolomic Analysis Revealed Roles of Yck2 in Carbon Metabolism and Morphogenesis of Candida albicans

status: Public on Mar 29 2021

city: Seoul

first: Yong-Sun

last: Bahn

address: 50, Yonsei-ro, Seodaemun-gu, Seoul, Republic of Korea

department: Department of Biotechnology

country: South Korea

institute: Yonsei university

summary: Candida albicans is a part of the normal microbiome of human mucosa and is able to thrive in a wide range of host environments. As an opportunistic pathogen, the virulence of C. albicans is tied to its ability to switch between yeast and hyphal morphologies in response to various environmental cues, one of which includes nutrient availability. Thus, metabolic flexibility plays an important role in the virulence of the pathogen. Our previous study has shown that C. albicans Yeast Casein Kinase 2 (CaYck2) regulates the yeast-to-hyphal switch, but its regulatory mechanisms remain unknown. This study further elucidated the role of Yck2 in governing morphology and carbon metabolism by analyzing the transcriptome and metabolome of the C. albicans YCK2 deletion mutant strain (yck2Δ strain) in comparison to the wild type strain. Our study revealed that loss of CaYck2 perturbs carbon metabolism, leading to a transcriptional response that resembles a transcriptional response to glucose starvation with coinciding intracellular accumulation of glucose and depletion of TCA cycle metabolites. This shift in the metabolome is likely mediated by derepression of glucose-repressed genes in the Mig1/2-mediated glucose sensing pathway and by downregulation of glycolytic genes, possibly through the Rgt1-mediated SRR pathway. In addition, genes involved in beta-oxidation, glyoxylate cycle, oxidative stress response, and arginine biosynthesis were upregulated in the yck2Δ strain, which is highly reminiscent of C. albicans engulfment by macrophages. This coincides with an increase in arginine degradation intermediates in the yck2Δ strain, suggesting arginine catabolism as a potential mechanism of CaYck2-mediated filamentation as seen during C. albicans escape from macrophages. Transcriptome analysis also shows differential expression of hyphal transcriptional regulators Nrg1 and Ume6. This suggests dysregulation of hyphal initiation and elongation in the yck2Δ strain which may lead to the constitutive pseudohyphal phenotype of this strain. Metabolome analysis also detected a high abundance of methyl citrate cycle intermediates in the yck2Δ strain, suggesting the importance of CaYck2 in this pathway. Taken together, we discovered that CaYck2 is an integral piece of carbon metabolism and morphogenesis of C. albicans.

overall_design: Candida albicans WT and deletion mutant strains were inoculated into 50 ml of YPD medium liquid medium and cultured overnight at 30°C in a shaking incubator. Cells were subinnoculated in fresh YPD medium until OD600 indicated 0.6. Incubated cells were spun down, frozen in liquid nitrogen and lyophilized overnight. Total RNA was isolated by trizol extraction method using Easy-blue (iNtRON). The prepared total RNAs were purified with RNeasy Mini Kit (QIAGEN). The concentration was measured by Quant-IT RiboGreen (Invitrogen). The quality of the RNA was verified by the TapeStation RNA screentape (Agilent) and the RNA Integrity Number (RIN) greater than 7.0 was used to construct the cDNA library (TruSeq mRNA Sample Prep kit, Illumina) and RNA-seq performed.

first: Karl

last: Liboro

first: Seong-Ryong

last: Yu

first: Juhyeon

last: Lim

first: Yee-Seul

last: So

first: Hyungjin

last: Eoh

first: Hyunsook

last: Park


title: Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scRNA-seq]

status: Public on Mar 26 2021

city: Paris

first: Paul

last: Gueguen

address: 26 rue D'Ulm

department: Inserm U932

country: France

institute: Institut Curie

summary: Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

overall_design: Thawed  PBMC  from  patient  UM1 were  stained  with PE  and  APC  tetramers  loaded with  peptide 37,  then  tetramer  positive  cells  were  positively enriched  using  anti-APC  and  anti-PE  microbeads (Miltenyi Biotech), stained with CD3 A700 and CD8 FITC and finally with DAPI. The positive fraction was sorted in a FACS ARIA (BD). To combine 5 tetramer positive populations from 2 donors (14, 17, 26  and  37  for  UM2  and  18  for  UM3)  the  tetramers  were  prepared  using  5  different  TotalSeq-PE streptavidins  (BioLegend)  and  1  classical  fluorochrome-streptavidin  (APC,  PE-CF594,  PE-Cy5,  PE-Cy7), PE-CF594 was used for UM3 who had only one population sorted. The PBMC were stained with the 4 pairs of tetramers for patient UM2 and 1 pair of tetramers for patient UM3, enriched with anti PE-microbeads (Milteny Biotech), stained with CD3 A700 and CD8 FITC and DAPI and sorted separately. The  cells  were  then  counted,  mixed  and  loaded  onto  a  Chromium  controller  using  Chromium  next GEM  Single  Cell  V(D)J  reagent  kit  with  feature  barcoding  technology  according to manufacturer’s instructions

first: Jeremy

last: Bigot

first: Ana

middle: I

last: Lalanne


title: Cardiac Oxidative Signaling and Physiological Hypertrophy in the Na/K-ATPase a1s/sa2s/s Mouse Model of High Affinity for Cardiotonic Steroids

status: Public on Mar 27 2021

city: Huntington

first: Sandrine

last: Pierre

state: West Virginia

address: 1676 Third Avenue

department: MIIR

institute: Marshall University

summary: The Na/K-ATPase is the specific receptor for cardiotonic steroids (CTS) such as ouabain and digoxin. At pharmacological concentrations used in the treatment of cardiac conditions, CTS inhibit the ion-pumping function of Na/K-ATPase. At much lower concentrations, in the range of those reported for endogenous CTS in the blood, they stimulate hypertrophic growth of cultured cardiac myocytes through initiation of a Na/K-ATPase-mediated and reactive oxygen species (ROS)-dependent signaling. To examine a possible effect of endogenous concentrations of CTS on cardiac structure and function in vivo, we compared mice expressing the naturally resistant Na/K-ATPase α1 and age-matched mice genetically engineered to express a mutated Na/K-ATPase α1 with high affinity for CTS. In this model, total cardiac Na/K-ATPase activity, α1, α2 and β1 protein content remained unchanged, and the cardiac Na/K-ATPase dose-response curve to ouabain shifted to the left as expected. In males aged 3–6 months, increased α1 sensitivity to CTS resulted in a significant increase of cardiac carbonylated protein content, suggesting that ROS production was elevated. A moderate but significant increase of about 15% of the heart-weight-to-tibia-length ratio, accompanied by an increase of myocyte cross-sectional area was detected. Echocardiographic analyses did not reveal any change in cardiac function, and there was no fibrosis or re-expression of the fetal gene program. RNA sequencing analysis indicated that pathways related to energy metabolism were upregulated, while those related to extracellular matrix organization were downregulated. Consistent with a functional role of the latter, an angiotensin-II challenge that triggered fibrosis in the α1r/rα2s/s mouse failed to do so in the α1s/sα2s/s. Taken together, these results are indicative of a link between circulating CTS, Na/K-ATPase α1, ROS, and physiological cardiac hypertrophy in mice under baseline laboratory conditions.

overall_design: Whole heart mRNA from 3-month old Na/K-ATPase a1r/ra2s/s (resistant) and Na/K-ATPase a1s/sa2s/s (sensitive) mice.

first: Marco

middle: T

last: Pessoa

first: Laura

last: Kutz

first: Jiang

last: Tian


title: Functional genomics of SNRPA1/B2

first: Hani

last: Goodarzi

sample_organism:
Homo sapiens
synthetic construct

platform_organism:
Homo sapiens
synthetic construct


title: Epigenomic Tensor Predicts Disease Subtypes and Reveals Constrained Tumor Evolution

city: Urbana

first: Jun

last: Song

state: IL

address: 1110 West Green Street, MC 704

department: Department of Physics

institute: University of Illinois, Urbana-Champaign

summary: Understanding the epigenomic evolution and specificity of disease subtypes from complex patient data remains a major biomedical problem. We here present DeCET (Decomposition and Classification of Epigenomic Tensors), an integrative computational approach for simultaneously analyzing hierarchical heterogeneous data, to identify robust epigenomic differences between tissue types, differentiation states, and disease subtypes. Applying DeCET to our own data from 21 uterine benign tumor (leiomyoma) patients identifies distinct epigenomic features discriminating normal myometrium and leiomyoma subtypes. Leiomyomas possess preponderant alterations in distal enhancers and long-range histone modifications confined to chromatin contact domains that constrain the evolution of pathological epigenomes. Moreover, we demonstrate the power and advantage of DeCET on multiple publicly available epigenomic datasets representing different cancers and cellular states. Epigenomic features extracted by DeCET can thus help improve our understanding of disease states, cellular development, and differentiation, thereby facilitating future therapeutic, diagnostic and prognostic strategies.


title: The Effect of Calcium on Activity, Immunogenicity and Efficacy of a Recombinant N1/N2 Neuraminidase Vaccine

city: Seattle

first: kathie

last: walters

state: WA

address: 401 Terry Ave N

institute: Institute for Systems Biology

summary: Despite the importance of immunity against neuraminidase (NA), NA content and immunogenicity is neglected in current influenza vaccines. To address this, a novel recombinant N1/N2 NA vaccine (NAV) was developed. Stability assays were used to determine optimal temperature and buffer conditions for vaccine storage. The effect of calcium-related enhancement of NA stability and activity on N1 and N2 immunogenicity and efficacy against viral challenge was assessed. Differences in activity between N1 and N2 and calcium-related activity enhancement did not translate into differences in immunogenicity or efficacy. NAV vaccinated mice showed robust antibody titers against N1 and N2, decreased viral titers, and decreased antiviral and inflammatory responses by transcriptomic analysis.

overall_design: The host lung transcriptional response to influeuza virus infection was assessed in mock vaccinated (PBS), NAV PBS and NAV DPBS-vaccinated mice at days 3 and 6 post-viral infection. All samples were compared to mock vaccinated, mock infected (PBS) animals.

first: Kathie-Anne

last: Walters

first: Luca

last: Giurgea

first: Jeffery

last: Taubenberger


title: Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes


title: RNA-seq of Human Epithelioid Hemangioendothelioma and genetically engineered mouse model of EHE

status: Public on Mar 25 2021

city: Cleveland

first: Brian

middle: P

last: Rubin

state: OH

address: 9620 Carnegie Ave NE2-215

department: Cancer Biology

institute: Cleveland Clinic

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Global gastrocnemius skeletal muscle transcript data from fasted male Gcn5skm-/- (HSAcre Tg/0 x Gcn5 L2/L2) and Gcn5skm+/+ mice (HSAcre 0/0 x Gcn5 L2/L2) on a chow diet

city: Ottawa

first: Goutham

last: Vasam

state: ON

address: 451 Smyth Rd

department: Faculty of Health Sciences

country: Canada

institute: University of Ottawa

summary:
Transcript data from gastrocnemius muscle from fasted-state male muscle-specific General Control of Amino Acid Synthesis Protein 5 knockout mice (Gcn5 skm-/- ) and wild-type mice (Gcn5skm+/+).
We used microarrays to detail the effects of muscle-specific loss of GCN5 on the global program of gene expression in gastrocnemius muscle.

overall_design: Chow diet fed 6-months-old male mice were fasted for 5 hours, anesthetized under isoflurane, then gastrocnemius skeletal muscles were snap-frozen in liquid nitrogen for RNA extraction and RNEasy cleanup. Samples included 4 animals for each geneotype which were prepared and run on Affymetrix arrays.

first: Johan

last: Auwerx

first: Keir

last: Menzies

first: Hongbo

last: Zhang

first: G

last: Williams


title: The AXL-PYK2-PKCα axis as a nexus of stemness circuits in TNBC

city: Rehovot

first: Sima

last: Lev

address: 234 Herzl St.

department: Molecular Cell Biology

country: Israel

institute: Weizmann Institute of Science

summary: Cancer stem cells (CSCs) are implicated in tumor initiation, metastasis and drug resistance, and are considered as attractive targets for cancer therapy. We identified a clinically relevant signaling nexus mediated by PYK2 and its impact on stemness in triple negative breast cancer (TNBC). PYK2 depletion in multiple mesenchymal TNBC cell lines markedly reduced the expression of PKCα and AXL proteins and reduced the number of mammosphere-forming cells and cells harboring CSCs characteristic markers. PYK2 and PKCα cooperate at a convergence point of multiple stemness-inducing pathways to regulate AXL levels and concomitantly the levels/activation of key transcription factors implicated in stemness including STAT3, TAZ, FRA1 and SMAD3 as well as the pluripotent transcription factors Nanog and Oct4, and in-turn affect their target genes. Targeting the AXL-PYK2-PKCα circuit could be a promising strategy to eliminate CSCs in TNBC and possibly overcome drug resistance.

overall_design: PYK2 (PTK2B) was knocked-down in the triple negative breast cancer cell line MDA-MB-231 using shRNA. The empty lentiviral vector (PLKO) was used as control. Experiment was done in duplicates.

first: Lohit

last: Khera

first: Yaron

last: Vinik


title: RNA-Seq of Human Epithelioid Hemangioendothelioma

summary: Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. We aimed to investigate the transcriptional pathways activated in EHE. Total RNA was isolated from EHE tumors from surgical resection or autopsy specimens (n=6) followed by RNA-Seq. The results of this study identified a unique transcriptional profile for EHE and helped to validate a novel murine model of EHE.

overall_design: RNA Sequencing of Epithelioid Hemangioendothelioma Tumors in Human

first: Caleb

last: Seavey


title: Long Non-coding RNA LINC02474  Affects Metastasis and Apoptosis  of Colorectal Cancer by Inhibiting  the Expression of GZMB

city: Jinan

first: Du

last: Tiantian

state: Shandong

address: The Second Hospital of Shandong University, 247 Beiyuan Road, Jinan 250033, Shandong, China

summary: Background: Colorectal cancer (CRC) is one of the most frequently diagnosed  malignancies. Metastasis is the main event that impedes the therapeutic effect on CRC,  and its underlying mechanisms remain largely unclear. LINC02474 is a novel long  noncoding RNA (lncRNA) associated with metastasis of CRC, while little is known  about how LINC02474 regulates these malignant characteristics.  Methods: Expressions of LINC02474 and granzyme B (GZMB) were assessed by  quantitative real-time polymerase chain reaction (qRT-PCR) or Western blotting  analysis. Cell metastasis was detected by transwell assay and metastatic nude mouse  model, and apoptosis was determined by Western blotting analysis and ﬂow cytometry.  Besides, the interaction between LINC02474 and GZMB was detected by dual-luciferase  reporter assays.  Results: The expression of LINC02474 was signiﬁcantly up-regulated in CRC tissues.  Moreover, depletion of LINC02474 damaged the metastatic abilities of CRC cells in vivo  and in vitro while boosting apoptosis. Besides, up-regulation of LINC02474 could  promote migration and invasion, while apoptosis was inhibited in CRC cells. Besides,  down-regulation of LINC02474 promoted the expression of GZMB, and interference of  GZMB could increase the metastatic abilities of CRC cells while reducing apoptosis.  Furthermore, LINC02474 was related to the transcriptional repression of GZMB in CRC  cells determined by the dual-luciferase reporter assay.  Conclusions: The ﬁndings revealed that a novel lncRNA, LINC02474, as an oncogene,  could promote metastasis, but limit apoptosis partly by impeding GZMB expression in  CRC. Besides, LINC02474 had the potential to be used as a biomarker in the prognosis of  CRC.

overall_design: there are 6 samples totally which have been grouped into 2 groups including three duplicates for each group. For group named "DLD-1-356", LINC02474 is knocked down stably, and for group named "DLD-1-NC", it is the control group.

first: Tiantian

last: Du

first: Chuanxin

last: Wang

first: Lutao


title: RNA-Seq of genetically engineered mouse model of Epithelioid Hemangioendothelioma tumors

summary: Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. Using an adaptation of the FLEx system, we generated a genetically engineered mouse model of EHE whereby the endogenous Wwtr1 Locus is replaced with an Wwtr1-Camta1 locus. RNA was isolated from the resultant tumors and from control liver tissue and RNA sequencing was performed. Cross species analysis between human and mice tumors demonstrated murine EHE maintains the defining transcriptional features of human EHE.


title: An Atlas of the Binding Specificities of Transcription Factors in Pseudomonas aeruginosa Directs Prediction of Novel Regulators in Virulence

city: Hong Kong

first: Jian

last: Yan

state: Hong Kong Special Administrative Region

address: 83 Tat Chee Avenue, Kowloon

department: Department of Biomedical Sciences

institute: City University of Hong Kong

summary: We performed a high-throughput systematic evolution of ligands by exponential enrichment (HT-SELEX) approach on all 371 annotated TFs in P. aeruginosa. This study provides a valuable resource for TF binding specificities in P. aeruginosa and demonstrates a novel and an integrative analysis for seeking the virulence-associated TFs and its target genes.

overall_design: In order to globally profile the DNA binding specificities of all TFs in P. aeruginosa, we purified the proteins for all 371 annotated TFs in the genome and applied a high-throughput systematic evolution of ligands by exponential enrichment (HT-SELEX) approach.

first: Xin

last: Deng

first: TingTing

first: Wenju

last: Sun

first: Ligang

last: Fan

first: Canfeng

last: Hua


title: Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scADT-seq]

first: Paul

last: Gueguen

first: Jeremy

last: Bigot

first: Ana

last: Lalanne


title: mRNA expression quantitative Analysis of MOLM-13 and THP-1 treated with JOA compared with control

city: Weifang

first: Liuya

last: Wei

address: 7166 number, Baotong West Street

institute: Weifang Medical University

summary: The goals of this study are toevaluate the mRNA expressions of genes in MOLM-13 and THP-1 cell lines treated with JOA

overall_design: There are 12 samples. There are 6 samples  for MOLM-13 cell line ( control and JOA-treated). There are 6 samples  for THP-1 cell line ( control and JOA-treated),

first: Mei

last: Qu


title: Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair

city: Shanghai

first: Wei

last: Wu

state: Shanghai

address: 320 yueyang road

department: Center for Excellence in Molecular Cell Science

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

sample_organism:
Homo sapiens
Mus musculus
Rattus norvegicus


title: scRNA-Seq of genetically engineered mouse model of Epithelioid Hemangioendothelioma tumors

first: Brian

last: Rubin

summary: Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. Using an adaptation of the FLEx system, we generated a genetically engineered mouse model of EHE whereby the endogenous Wwtr1 Locus is replaced with an Wwtr1-Camta1 locus. Tumors generated from this mouse model were dissociated and a 10X genomics library preparation was performed. The barcoded library was then deep sequenced.

overall_design: scRNA Sequencing of Epithelioid Hemangioendothelioma Tumors in Mouse

first: Brain

first: Caleb


title: RNA-seq of uncultured CD112high and CD112low and cultured long-term (LT) and short-term (ST) human hematopoietic stem cells (HSC) overexpressing INKA-1

city: Toronto

first: Alexander

middle: James

last: Murison

state: Ontario

address: 101 College Street, TMDT room 11-706

institute: University Health Network

summary:
RNA-seq of uncultured CD112high and CD112low long-term(LT) human hematopoietic stem cells (HSC) and cultured and lentiviral transduced (CTRL, INKA1-OE) LT- and short-term HSC from umbilical cord blood
We performed RNA-sequencing to elucidate the biological pathways (1) altered by INKA1 overexpression in LT-HSC and ST-HSC that may contribute to the induced transient restraint in generating proliferative hematopoietic output in vivo and in vitro; and (2) that underlie the differential in vitro priming and regeneration phenotypes of CD112high and CD112low LT-HSC. Therefore, we prospectively isolated indicated subpopulations from 3 independent human umbilical cord blood pools and subjected them either to RNA-sequencing directly or following culture, lentiviral transduction and purification of the transduced cell fractions. We show that distinct subsets of human LT-HSC respond differently to regeneration-mediated stress and that INKA1 governs these distinct stemness states where CD112low  LT-HSC are marked by an alternative state of quiescence with high INKA1 preserving self-renewal and regenerative capacity upon successive rounds of regeneration-mediated stress.

overall_design:
Gene expression profiling of RNA from 2-3 pools of human cord blood sorted by flow cytometry into indicated suppopulations either directly (CD112high/low LT-HSC) or after lentiviral transduction of prospectively isolated LT- and ST-HSC and sorting for transduced cells (BFP+) 6 days post-transduction

>>>Submitter states that raw data will be submitted to EGA due to data access requirements.<<<

first: Kerstin

last: Kaufmann

first: Michelle

last: Chan-Seng-Yue

first: John

last: Dick


title: Down-regulation of MTSS1 is associated with a poor prognosis in acute myeloid leukemia and differentially affects responses to different drugs

city: Vienna

first: Rotraud

last: Wieser

address: Waehringer Guertel 18-20

department: Department of Medicine I

country: Austria

institute: Medical University of Vienna

summary: Acute myeloid leukemia (AML) is an aggressive malignancy of hematopoietic cells. Despite recent approvals of targeted drugs, chemotherapy with cytosine arabinoside (araC) and an anthracycline like daunorubicin remains an important pillar of treatment. In a previous work, we have shown that MTSS1 is down-regulated at relapse compared to diagnosis of AML and its down-regulation was previously implicated in aggressiveness of solid tumors.  Our results showed that MTSS1 expression was regulated by methylation and reduced by araC and daunorubicin. Experimental down-regulation rendered human AML cell lines more resistant to araC, daunorubicin, and eight additional drugs. In contrast, venetoclax, a BCL2 inhibitor, was more effective towards cells with low MTSS1 expression. A CRISPR/Cas9-mediated knock-out of the MTSS1 gene was used to generate insight into the molecular changes induced by the down-regulation of MTSS1. The knock-out led to the deregulation of > 900 genes which included numerous target genes of transcription factors with a confirmed role in hematopoiesis and AML. A gene ontology analysis of the differentially expressed genes revealed that genes linked to transcription, cell cycle, and immune response were strongly affect.  In summary, down-regulation of MTSS1 is associated with primary and secondary chemotherapy resistance in AML. In experimental models, it confers refractoriness to several cytotoxic drugs, yet sensitizes cells to venetoclax, pointing towards ways to overcome therapy resistance in MTSS1low AML.

overall_design: Gene expression profiles of TF-1 MTSS1 knock-out pools and TF-1 control pools, in triplicate for the knock-out and duplicate for the control, using Illumina HiSeq 2500. MTSS1 was knocked-out in TF-1 cells by CRISPR/Cas9 and pools of 4 clones each were preapred.

first: A

middle: M

last: Grandits

first: H

last: Hackl

first: G

last: Heller

first: R


title: A distinct subset of blood stem cells resists regenerative stress to preserve stemness

overall_design: Refer to individual Series


title: Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scTCR-seq]

first: Paul

first: Jeremy


title: Acquisition of Innate Odor Preference Depends on Spontaneous and Experiential Activities During Critical Period

city: Kansas City

first: Congrong

middle: Ron

last: Yu

state: Missouri

institute: Stowers Insitute for Medical Research

summary: Animals possess inborn ability to recognize certain odors to avoid predators, seek food and find mates. Innate odor preference has been thought to be genetically hardwired. Here we report that acquisition of innate odor recognition requires spontaneous neural activity and is influenced by sensory experience during early postnatal development. Genetic silencing of mouse olfactory sensory neurons during the critical period has little impact on odor sensitivity, discrimination and recognition later in life. However, it abolishes innate odor preference and alters the patterns of activation in brain centers. Moreover, exposure to an aversive odor during the critical period abolishes aversion in adulthood in an odor specific manner. The loss of innate aversion is associated with broadened projection of OSNs. Thus, a delicate balance of neural activity is required during critical period in establishing innate odor preference and ectopic projection is a convergent mechanism to alter innate odor valence

overall_design:
Olfactory Epithelial mRNA profiles of 5-day old wild type (WT) and Kir+/- mice
Olfactory Epithelial mRNA profiles of 5-day old control (Ctrl) and PEA-treated mice

first: Qiang

last: Qiu

first: Yunming

first: Limei

last: Ma

first: Wenjing

last: Xu

first: Max

middle: H

last: Hills Jr.

first: Vivekanandan

last: Ramalingam


title: Gene expression profiling in cervical cancer tissue

city: Hyderabad

first: Smita

last: Pawar

state: Telangana

address: College of Science, Osmania University

department: Genetics

country: India

institute: Osmania University

summary: Comparision of transcriptome profiling in tumour and non tumour samples by using Clariom_D_Human array , provide a vital information of dysregulated genes in tumour samples, hence identify the biomarkers and theraputic targets in disease progression

overall_design: 10 samples (7cervical cancer squamous cell carsinoma tissue and 3 controls)


title: IFN-γ and TNF-α drive a CXCL10+ CCL2+ macrophage phenotype expanded in severe COVID-19 lungs and inflammatory diseases with tissue inflammation

status: Public on Mar 24 2021

city: Boston

first: Soumya

last: Raychaudhuri

state: MA

address: 77 Avenue Louis Pasteur

institute: Brigham and Women's Hospital, Harvard Medical School

summary: We explored how the human macrophages response to different inflammatory factors, focusing particularly on the effects of antiviral interferons (IFN-β and IFN-γ), pro-inflammatory cytokines such as TNF-α, and other mediators like IL-4. Co-cultured fibroblasts were a component in some conditions to generate factors produced by resident stroma. We used a single-cell antibody-based hashing strategy to multiplex samples from different stimulatory conditions in one sequencing run. This macrophage transcriptomic data reveals distinct macrophage activation states and polarizations shaped by different tissue-related inflammatory conditions at single-cell resolution. We further performed an unbiased integration between tissue-level macrophages and this stimulated human blood-derived macrophages, which pinpoint an IFN-γ and TNF-α synergistically driven inflammatory macrophage phenotype expanded in severe COVID-19 lungs and other inflamed disease tissues.

overall_design:
We isolated CD14+ monocytes from each of the 4 healthy blood samples using human CD14 microbeads (Miltenyi Biotec) and differentiated these cells into blood-derived macrophages.  Human CD14+ MCSF-differentiated macrophages were cultured with or without synovial fibroblasts in trans-well chambers. In total, we created 9 wells per donor. We added either IFN-β (200 pg/mL), IL-4 (20 ng/ mL), TNF-α (20 ng/mL), and/ or IFN-γ (5 ng/mL) to each trans-well and underlying plate per donor. All plates were incubated at 37° C for 19 hours. We applied a modified version of the staining protocol from CITE-seq, using only Totalseq-A Hashing antibodies from Biolegend. We followed the Chromium Single Cell 3' v3 kit (10x Genomics) processing instructions and super-loaded 30,000 cells per lane. We used one lane per donor, with 9 conditions multiplexed per donor sample. Pairs of libraries were pooled and sequenced per lane on an Illumina NovaSeq S2 with paired-end 150 base-pair reads. We quantified mRNA and antibody unique molecular identifiers (UMI) counts, respectively. Cellranger v3.1.0 was used to process the raw BCL files. Then, raw BCL files were demultiplexed using cellranger mkfastq to generate FASTQ files. FASTQ files were aligned to the GRCh38 human reference genome. Gene/antibody reads were quantified simultaneously using cellranger count.
---------------------------------------------------
Authors state the following:
These are human blood samples that required control for access. We will put the raw sequencing data to dbGap.

first: Fan

last: Zhang

first: Laua

last: Donlin


title: Single T-cell landscape identifies tissue regeneration program in murine and human regulatory T cells

city: Regensburg

first: LIT

last: NGS-Core

address: Franz-Josef-Strauß-Allee 11

department: NGS-Core

country: Germany

institute: Leibniz Institute for Immunotherapy

summary: Several studies over the past decade identified a subpopulation of murine regulatory T cells (Tregs) which have the intrinsic capacity to promote tissue homeostasis and, upon damage, enhance tissue regeneration and re-organization. In humans, this population of tissue regeneration-promoting Treg cells has not been identified and characterized yet. Using single-cell chromatin accessibility as well as single-cell RNA and TCR expression profiles of murine and human tissue-derived CD4 T cells, we identified the murine Treg repair signature and performed a liftover on human single T cell data. We identified a FOXP3+CCR8+HLA-DR+ population in peripheral blood, which has characteristics of human tissue Treg cells and promotes tissue regeneration and wound healing in-vitro. This population was dependent on the transcriptional regulator BATF, a factor that also drives the development of tissue regeneration-promoting Treg cells in the murine system. Human CCR8+HLA-DR+ Treg cells could be used as a novel T-cell product to promote tissue repair in regenerative medicine.

overall_design: Isolation of CD4+ T cells and CD25+ T cells from murine tissues and spleen

first: Delacher

last: Michael

first: Simon

last: Malte

first: Strieder

last: Nicholas

first: Feuerer

last: Markus


title: Transcriptomic heterogeneity of Coeliac Disease biopsies from the duodenum

city: Halle

first: Edith

last: Willscher

state: Deutschland

address: Ernst-Grube-Straße 40

department: Internal Medicine IV

institute: Martin Luther University of Halle-Wittenberg

summary:
Here, we present a high-resolution analysis of the transcriptomes extracted from duodenal probes of 25 children and adolescents with active CD and 21 children without CD but with diverse intestinal afflictions as controls. We found that the transcriptomes of CD patients divide into three subgroups, a mixed group resembling part of control cases and a CD-low and CD-high groups referring to lower and higher levels of CD severity
Despite generally increased inflammation, considerable variation in inflammation-level between subgroups was observed, which was further de-chiffred into immune cell types using immune cell de-convolution

overall_design: one biopsy (15–20 mg) was taken from descending duodenum of each patient. Fresh tissue samples were snap frozen and stored in liquid nitrogen until preparation. Frozen biopsies were disrupted and homogenized by TissueLyzer from Quiagen (Hilden, Germany). Total RNA was isolated using AllPrep® DNA/RNA Micro kit (QIAGEN, Hilden, Germany) and stored at -70°C.

first: Johannes

last: Wolf

first: Henry

last: Loeffler-Wirth

first: Maria

last: Schmidt

first: Gunter

last: Flemming

first: Marlen

last: Zurek

first: Holm

last: Uhlig

first: Norman

last: Händel

first: Hans

last: Binder


title: Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse brain tissue.

city: Zurich

first: Ge

last: Tan

address: Winterthurerstrasse 190

department: Functional Genomics Center Zurich

country: Switzerland

institute: University of Zurich

summary: Analysis of brain from C57BL/6 mice expressing V338Y mutant mitochondrial ribosomal protein.

overall_design: mRNA profiles of wild-type and V338Y mutant mouse brain tissue samples at two time points (3 months and 19 months) generated by deep sequencing.

first: Dimitri

last: Scherbakov

first: Erik

last: Böttger


title: Enhancers are Activated by p300/CBP Activity-Dependent PIC Assembly, RNAPII Recruitment and Pause Release

city: Copenhagen N

first: Chunarum

last: Choudhary

state: --- Select a state ---

address: Blegdamsvej 3B

department: Novo Nordisk Foundation Center for Protein Research

country: Denmark

institute: University of Copenhagen


title: Enhancers are Activated by p300/CBP Activity-Dependent PIC Assembly, RNAPII Recruitment and Pause Release [ATAC-Seq]

summary: The metazoan-specific acetyltransferase p300/CBP is involved in activating signalinduced, enhancer-mediated transcription of cell-type-specific genes. However, the global kinetics and mechanisms of p300/CBP activity-dependent transcription activation remain poorly understood. We performed genome-wide, time-resolved analyses to show that enhancers and super-enhancers are dynamically activated through p300/CBP-catalyzed acetylation, deactivated by the opposing deacetylase activity, and kinetic acetylation directly contributes to maintaining cell identity at very rapid timescales. The acetyltransferase activity is dispensable for the recruitment of p300/CBP and transcription factors, but essential for promoting the recruitment of TFIID and RNAPII at virtually all enhancers and enhancer-regulated genes. This identifies pre-initiation complex assembly as a dynamically controlled step in the transcription cycle and reveals p300/CBP-catalyzed acetylation as the signal that specifically promotes transcription initiation at enhancer-regulated genes. We propose that p300/CBP activity uses a ‘recruit-and-release’ mechanism to simultaneously promote RNAPII recruitment and pause release, and thereby, enables kinetic activation of enhancer-mediated transcription.

overall_design: Chromatin accessibility changes before and after A-485 treatment in mouse ES cell using ATAC-Seq.

first: Takeo

last: Narita

first: William

last: Hamilton


title: Enhancers are Activated by p300/CBP Activity-Dependent PIC Assembly, RNAPII Recruitment and Pause Release [EU-Seq]

overall_design: EU-seq of mESC treated with JQ1 or A-485 and/or TSA.


title: miRNA profile of serum samples from metabolically healthy and unhealthy obese subjects

status: Public on Mar 23 2021

city: Valencia

first: Susana

last: Rovira-Llopis

address: Av Gaspar Aguilar 90

department: University Hospital Doctor Peset

country: Spain

institute: FISABIO

summary:
Obese individuals without metabolic comorbidities are categorized as metabolically healthy obese (MHO). MicroRNAs (miRNAs) may be implicated in MHO.
This cross-sectional study explores the link between circulating miRNAs and the main components of metabolic syndrome (MetS) in the context of obesity. We also examine oxidative stress biomarkers in MHO vs. metabolically unhealthy obesity (MUO).

overall_design: Unique samples from 20 middle-aged obese individuals were included: 10 MHO (metabolically healthy obese) and 10 MUO (metabolically  unhealthy obese).

first: Ruben

last: Diaz-Rua

first: Carmen

last: Grau-del Valle

first: Francesca

last: Iannantuoni

first: Zaida

last: Abad-Jimenez

first: Neus

last: Bosch-Sierra

first: Joaquin

last: Panadero-Romero

first: Victor

last: Victor

first: Milagros

last: Rocha

first: Carlos

last: Morillas

first: Celia

last: Bañuls


title: RNA sequencing of pancreatic islet-derived beta cells, macrophages, and endothelial cells modulated by vascular endothelial growth factor-A signaling

city: Nashville

first: Shristi

last: Shrestha

address: 2213 Garland Ave

institute: Vanderbilt University

summary: Pancreatic islet endocrine cell and endothelial cell (EC) interactions mediated by vascular endothelial growth factor-A (VEGF-A) signaling are important for islet endocrine cell differentiation and the formation of highly vascularized islets. To dissect how VEGF-A signaling modulates intra-islet vasculature and innervation, islet microenvironment, and beta cell mass, we transiently increased VEGF-A production by beta cells. VEGF-A induction dramatically increased the number of intra-islet ECs but led to beta cell loss. After withdrawal of the VEGF-A stimulus, beta cell mass, function, and islet structure normalized as a result of a robust, but transient, burst in proliferation of pre-existing beta cells. Bone marrow-derived macrophages recruited to the site of beta cell injury were crucial for the beta cell proliferation, which was independent of pancreatic location and circulating factors such as glucose. Identification of the signals responsible for the proliferation of adult, terminally differentiated beta cells will improve strategies aimed at beta cell regeneration and expansion.

overall_design: Examination of RNA profiles from islet-derived beta cells (12 samples), endothelial cells (10 samples), and macrophages (10 samples) from MIP-GFP; RIP-rtTA; TetO-VEGF-A mice with no doxycycline (Dox) treatment (12 samples), after 1 week of Dox (8 samples), and after 1 week of Dox withdrawal (12 samples); cells were isolated by fluorescence-activated cell sorting using GFP for beta cells (MIP-GFP) and antibodies against CD31 abd CD11b for endothelial cells and macrophages, respectively. Related to GSE72546.

first: Alvin

last: Powers

first: Marcela

last: Brissova


title: Stress Resets Transgenerational Small RNA Inheritance

city: Tel-Aviv

first: Leah

last: Houri-Ze'evi

address: Haim Levanon

department: Neurobiology

institute: Tel-Aviv University

type: Non-coding RNA profiling by high throughput sequencing

summary: Transgenerational inheritance is challenging basic concepts of heredity and achieving control over such responses is of great interest. In C. elegans nematodes, small RNAs are transmitted across generations to establish a transgenerational memory trace of ancestral environments. Inheritance of small RNAs is regulated by dedicated machinery and can be tuned by outside cues. Carryover of aberrant heritable small RNA responses was shown to be maladaptive and to induce sterility in certain cases. Here we show that various types of stress (starvation, high temperatures, and hyperosmotic conditions) but not non-stressful changes in cultivation, lead to resetting of small RNA inheritance. We found that stress leads to a genome-wide reduction in heritable small RNA levels and that mutants defective in different stress pathways exhibit irregular RNAi inheritance dynamics. Moreover, we discovered that resetting of heritable RNAi is orchestrated by MAPK pathway factors, the transcription factor SKN-1, and the MET-2 methyltransferase. Termination of small RNA inheritance, and the fact that this process depends on stress, could protect from run-on of environment-irrelevant heritable gene regulation.

overall_design: RNA was extracted from "day one" adult nematodes (strain SX1263) which bears a Pmex-5::GFP transgene, driving GFP expression in the germline. The samples include 3 biological replicates of worms in three stress conditions (heat shock, hyperosmotic conditions, starvation) and a control group, across two generations (F1 and F2), yielding a total of 24 samples.

first: Guy

last: Teichman

first: Hila

last: Gingold

first: Oded

last: Rechavi


title: Factors affecting the rapid changes of protein under short-term heat stress

city: Yangling

first: Wu

middle: bing

last: jin

state: Shaanxi

address: Litai street

institute: Northwest A&F University

summary: The protein content determines the cell state. The variation in protein abundance is crucial when organisms are in the early stages of heat stress, but the reasons affecting their changes are still unknown. We quantified 47,535 mRNAs and 3,742 proteins in filling grain of wheat under two thermal environments. The impact of mRNA abundance and sequence features implicated in protein translation and degradation on protein expression were evaluated by regression analysis. Transcription, codon usage and amino acid frequency mainly affect protein expression, and their combined contribution explains 58.2% and 66.4% of protein abundance variation in two types of heat stresses. Of which, transcription contributes more to the protein expression under severe heat stress (31%) than to mild stress (6%). Codon usage plays a stable and powerful role in protein expression under heat stress, even surpassing transcription. What’s more, the usage of AAG is a key factor regulating rapid protein expression under heat stress. This study revealed the main factors affecting the changes of protein abundance in the early stage of heat stress, and explained the mystery that plants can express protein rapidly under heat stress.

overall_design: The reflection of wheat grains at the filling stage under two heat stresses

first: Bingjin

last: Wu

first: Jianwen

last: Qiao


title: Transcriptional profiling of brain tissues from a Q130 Long Evans Knock-in rat model of Huntington’s disease at 2-, 6-, 10-, 12-, 19- and 24-months of age

status: Public on Mar 22 2021

city: Princeton

first: Jeff

last: Aaronson

state: New Jersey

address: 155 Village Boulevard, Suite 200

department: Discovery & Systems Biology

institute: CHDI


title: IGF2BP1, a conserved regulator of RNA turnover in cancer [polyA RNA]

first: Markus

last: Glaß

address: Kurt-Mothes-Str. 3a

department: Institute of Molecular Medicine

institute: Martin Luther University Halle-Wittenberg

summary: The IGF2 mRNA binding protein 1 (IGF2BP1) promotes tumor progression in a multitude of solid tumors and its expression is associated with adverse prognosis. The main role proposed for IGF2BP1 in cancer cells is the stabilization of mRNAs encoding pro-oncogenic factors. Several binding studies, however, revealed a plethora of putative IGF2BP1-RNA targets. Thus, at present the main, conserved target RNAs and pathways controlled by IGF2BP1 in cancer remain elusive. In this study, we present a set of genes showing a conserved pattern of deregulation in dependence of IGF2BP1 expression in cancer-derived cell lines. By incorporating publicly available data sets, we further compiled a set of RNAs probably stabilized by IGF2BP1 in cancer and characterized them. Functional enrichment analyses revealed conserved pathways influenced by IGF2BP1 in cancer.

overall_design: PolyA RNA-Seq of different solid tumor-derived cells transfected with either control siRNAs (siC) or siRNAs directed against IGF2BP1. Three replicates per condition.

first: Danny

last: Misiak

first: Nadine

last: Bley

first: Simon

last: Müller

first: Sven

last: Hagemann

first: Stefan

last: Hüttelmaier


title: IGF2BP1, a conserved regulator of RNA turnover in cancer


title: IGF2BP1, a conserved regulator of RNA turnover in cancer [total RNA]

overall_design: Total RNA-Seq of different solid tumor-derived cells transfected with either control siRNAs (siC) or siRNAs directed against IGF2BP1. Three replicates per condition.


title: Enhancers are Activated by p300/CBP Activity-Dependent PIC Assembly, RNAPII Recruitment and Pause Release [ChIP-Seq]

first: Chunarum

last: Choudhary

overall_design: Pol2, p300, BRD4, and H3K27ac, H3K27me3, H3K4me1, Oct4, Nanog, TAF1 and TBP ChIP-seq before and after A-485 or JQ1 treatment in mES cell grown in 2i.

first: Takeo

last: Narita

first: Shinsuke

last: Ito

first: Yoshiki

last: Higashijima


title: Single-cell transcriptomics reveals microglia heterogeneity across the nigrostriatal pathway

city: Esch-sur-Alzette

first: Dimitrios

last: Kyriakis

address: 6, avenue du Swing

country: Luxembourg

institute: LUXEMBOURG CENTRE FOR SYSTEMS BIOMEDICINE (LCSB)

summary: Identification of specific microglia phenotypes within the nigrostriatal pathway, which may be relevant in PD

overall_design: Single cell mRNA of wild type (WT) mice, midbrain and striatum, were generated by Dropseq.

first: Oihane

last: Uriarte

first: Tony

last: Heurtaux

first: Kamil

last: Grzyb

first: Rashi

last: Halder

first: Manuel

last: Buttini

first: Alexander

last: Skupin

first: Michel

last: Mittelbronn

first: Alessandro

last: Michelucci


title: DNA G-quadruplexes are transcription factor binding hot spots in human chromatin

city: Cambridge

first: Sergio

last: Martínez Cuesta

address: 1 Francis Crick Avenue

department: Data Sciences and Quantitative Biology, Discovery Sciences

country: United Kingdom

institute: AstraZeneca

summary: Gene expression is governed by transcription factors (TFs) that commonly recognize short DNA sequence motifs. However, TF recruitment to genomic target sites in chromatin is complex and many parameters that ultimately dictate binding-site specificity are still unknown. Here, we systematically explore the interaction of TFs with synthetic and endogenous G-quadruplexes (G4s) DNA secondary structures. Our findings reveal that certain TFs are directly recruited to promoters by endogenous G4s with binding affinities comparable to canonical B-DNA binding and that endogenous G4-TF interactions can be disrupted with synthetic small molecule ligands. G4s in promoters are bound by a large number of TFs and associated with high transcriptional activity. This discovery of structure-specific recognition expands our understanding of how TFs regulate gene transcription.

overall_design: G4 ChIP-seq experiment to detect the presence of DNA G-Quadruplexes. Three technical replicates and one input per cell type.

first: Jochen

last: Spiegel

last: Martinez Cuesta

first: Santosh

last: Adhikari

first: Robert

last: Hänsel-Hertsch

first: David

last: Tannahill

first: Shankar

last: Balasubramanian


title: RNA expression in KATOIII cells harboring biallelic deletions of the +22.6-kb site, epithelial-specific enchancer of ABO gene

city: masbashi

first: Rie

last: Sano

state: gunma

address: 3-39-22 showa-machi

department: Legal Medicine

country: Japan

institute: Gunma University

summary: Wild-type KATOIII cells and their derived mutant clones B3 and B4 harboring biallelic deletions of the +22.6-kb site, located 22.6 kb downstream from the ABO translation start site

overall_design: CRISPR/Cas9 system with a pair of genome-editing plasmids 5′Enhancer and 3′Enhancer was used to create genomic deletions of the +22.6-kb site in KATOIII  cells. The sequencing revealed genomic deletion of the sequences  +22,579/+22,740 and +22,579/+22,742 in clone B3, and the sequences +22,580/+22,740 and +22,580/+22,742 in clone B4 from ABO translation start site.

first: Yosihiko

last: Kominato


title: IGF2BP1, a conserved regulator of RNA turnover in cancer [miRNA-seq]

first: Markus

last: Glaß

overall_design: small RNA-Seq of different solid tumor-derived cells.

first: Glaß

last: Markus

first: Misiak

last: Danny

first: Bley

last: Nadine

first: Müller

last: Simon

first: Hagemann

last: Sven

first: Hüttelmaier

last: Stefan


title: Deconvoluting global cytokine signaling networks in natural killer cells [ATAC-seq]

status: Public on Mar 21 2021

city: Ithaca

first: Colleen

last: Lau

state: New York

address: 930 Campus Road

department: Microbiology & Immunology

institute: Cornell University

summary: Cytokine signaling via signal transducer and activator of transcription (STAT) proteins is crucial for optimal antiviral responses of natural killer (NK) cells. However, the pleiotropic effects of both cytokine and STAT signaling preclude the ability to precisely attribute molecular changes to either source. In this study, we employ a multi-“omics” approach to deconstruct and rebuild the complex interaction of three major STAT signaling pathways in NK cells. We uncover a global STAT4-STAT5 cooperative axis that is distinct and sometimes antagonistic to the STAT1 axis. We generate a network of STAT targets that highlights an integrated negative feedback loop, and demonstrate distinct STAT modes of epigenetic regulation. Finally, we identify shared signatures between mouse in vitro profiles and profiles from viral infection and humans, highlighting clinically translatable targets. Overall, we begin to unravel the intricate crosstalk between cytokine signaling pathways, and offer a valuable resource for improving cellular immunotherapy.

overall_design: ATAC-seq was performed on ex-vivo NK cells stimulated with various cytokine combinations.

first: Joseph

last: Sun


title: DNA methylation profiling of malignant pleural mesothelioma

status: Public on Mar 20 2021

city: Torino

first: Luca

last: Bertero

state: TO

address: Via Santena 7

department: Pathology Unit, Dept. Medical Sciences

country: Italy

institute: University of Turin

summary: Diagnosis of malignant pleural mesothelioma (MPM) is a challenging task because of its overlap with other neoplasms or even reactive conditions. Recently, DNA methylation analysis proved to be an effective tool for tumor diagnosis. We thus set out to test this approach for MPM diagnosis. A discovery (n=33) and an independent validation cohort (n=46) of MPM samples were subjected to array-based DNA methylation analyses and their DNA methylation patterns were compared to a representative set of both malignant and benign diagnostic mimics. By both unsupervised hierarchical clustering and t-distributed stochastic neighbor embedding analysis, MPM samples of the discovery cohort exhibited a distinct DNA methylation profile, different from that of other neoplastic and reactive mimics.

overall_design: Bisulphite converted DNA from 79 samples was hybridized to Illumina Infinium Human MethylationEPIC Methylation BeadChip array

first: Luisella

last: Righi

first: Giammarco

last: Collemi

first: Christian

last: Koelsche

first: Yanghao

last: Hou

first: Damian

last: Stichel

first: Daniel

last: Schrimpf

first: Uta

last: Flucke

first: Iver

last: Petersen

last: Vokuhl

first: Stefan

last: Fröhling

first: Paolo

last: Bironzo

first: Giorgio

middle: V

last: Scagliotti

first: Paola

last: Cassoni

first: Mauro

last: Papotti

first: Andreas

last: von Deimling


title: Deconvoluting global cytokine signaling networks in natural killer cells

first: Colleen

last: Lau

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

overall_design: Refer to individual Series


title: Involvement of ROS1 in gene expression of imazethapyr-treated Arabidopsis thaliana

status: Public on Mar 18 2021

city: Porto Alegre

first: Catarine

last: Markus

address: Av. Bento Gonçalves, 7712

department: Department of Crop Science

country: Brazil

institute: Federal University of Rio Grande do Sul

summary:
Purpose: To determine candidate genes involved in the increased susceptibility of ros1 plants to imazethapyr.
Results: Our study reveled that that imazethapyr up-regulated genes related to chemical stimulus, secondary metabolism, stress condition, flavonoid biosynthesis and epigenetic processes. We identified 31 candidate genes as putative involved in herbicide detoxification, some of this genes are under epigenetic regulation of ROS1.

overall_design: Genome-wide transcriptome analysis of genes expressed at 48 hours after imazethapyr treatment contrasting with control condition, in wild type (WT) and REPRESSOR OF SILENCING 1 (ros1) plants

first: Ales

last: Pecinka

first: Aldo

last: MerottoJr


title: Retinoic acid inhibits tumor-associated mesenchymal stromal cell transformation in melanoma

status: Public on Mar 19 2021

city: Guang zhou

first: qi

last: Lou

state: Guang dong

address: china guangzhou

institute: sun yen san university

summary: Bone marrow mesenchymal stem/stromal cells (BMSCs) can be transformed into tumor-associated MSCs (TA-MSCs) within the tumor microenvironment to facilitate tumor progression. However, the underline mechanism and potential therapeutic strategy remain unclear. Here, we explored that interleukin 17 (IL-17) cooperating with IFNγ transforms BMSCs into TA-MSCs, which promotes tumor progression by recruiting macrophages/monocytes and myeloid-derived suppressor cells (MDSCs) in murine melanoma. IL-17 and IFNγ transformed TA-MSCs have high expression levels of myelocyte-recruiting chemokines (CCL2, CCL5, CCL7, and CCL20) mediated by activated NF-κB signaling pathway. Furthermore, retinoic acid inhibits NF-κB signaling, decreases chemokine expression, and suppresses the tumor-promoting function of transformed TA-MSCs by prohibiting the recruitment of macrophages/monocytes and MDSCs in the tumor microenvironment. Overall, our findings demonstrate that IL-17 collaborating with IFNγ to induce TA-MSC transformation, which can be targeted by RA for melanoma treatment.

overall_design: RNAs were extracted from two biological replicates of cultured from wild-type BMSC incubated with control and 1μM ATRA , digested with DNAse I (AM2222, Ambion) and purified with Rneasy MinElute Spin Columns (Qiagen). TruePrepTM DNA library Prep Kit V2 (Vazyme, TD503) was used to prepare RNA seq library following the manufacturer’s protocol. DNA library sequenced by Illumina HiSeq 2500 platform.

first: Qi

first: Minyi

last: Zhao

first: Quanhui

last: Xu


title: Deconvoluting global cytokine signaling networks in natural killer cells [RNA-seq]

country: USA

overall_design: RNA-seq was performed on ex-vivo NK cells stimulated with various cytokine combinations.

first: Joseph

last: Sun


title: Enhanced insulin signalling ameliorates C9orf72 hexanucleotide repeat expansion toxicity in Drosophila

city: Köln

first: Linda

last: Partridge

address: Joseph-Stelzmann-Straße 9B

department: Biological Mechanisms of Ageing

institute: Max Planck Institute for Biology of Ageing

summary: G4C2 repeat expansions within the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The repeats undergo repeat-associated non-ATG translation to generate toxic dipeptide repeat proteins. Here, we show that insulin/Igf signalling is reduced in fly models of C9orf72 repeat expansion using RNA-sequencing of adult brain. We further demonstrate that activation of insulin/Igf signalling can mitigate multiple neurodegenerative phenotypes in flies expressing either expanded G4C2 repeats or the toxic dipeptide repeat protein poly-GR. Levels of poly-GR are reduced when components of the insulin/Igf signalling pathway are genetically activated in the diseased flies, suggesting a mechanism of rescue. Modulating insulin signalling in mammalian cells also lowers poly-GR levels. Remarkably, systemic injection of insulin improves the survival of flies expressing G4C2 repeats. Overall, our data suggest that modulation of insulin/Igf signalling could be an effective therapeutic approach against C9orf72 ALS/FTD.

overall_design: mRNA profiles from heads of old female control (elavGS/+) and polyGR100 flies

first: Magda

last: Atilano

first: Sebastian

last: Grönke

first: Teresa

last: Niccoli

first: Liam

last: Kempthorne

first: Oliver

last: Hahn

first: Javier

last: Morón-Oset

last: Hendrich

first: Miranda

last: Dyson

first: Mirjam

last: Adams

first: Alexander

last: Hull

first: Marie-Therese

last: Salcher-Konrad

first: Amy

last: Monaghan

last: Bictash

first: Idoia

last: Glaria

first: Adrian

last: Isaacs


title: Substrate discrimination and quality control require each catalytic activity of TRAMP and the nuclear RNA exosome

city: New York

first: Christopher

middle: D

last: Lima

state: NY

address: 1275 York Ave RRL301A

department: Structural Biology

institute: Sloan Kettering Institute

summary:
Abstract: Quality control requires discrimination between functional and aberrant species to selectively target substrates for destruction. Nuclear RNA quality control in Saccharomyces cerevisiae includes the TRAMP complex that marks RNA for decay via polyadenylation and helicase-dependent 3′ to 5′ degradation by the RNA exosome. Using reconstitution biochemistry we show that polyadenylation and helicase activities of TRAMP cooperate with processive and distributive exoribonuclease activities of the nuclear RNA exosome to selectively target and degrade an unmodified tRNA while leaving native tRNA intact. Inactivation of the distributive exoribonuclease activity of Rrp6 results in loss of substrate discrimination, leading to degradation of all RNAs. These data suggest that the activities of the Mtr4 helicase and Rrp6 exoribonuclease endow the TRAMP-RNA exosome complex with the ability to protect stable RNA while degrading defective RNA species.
Rrp6 and its 3′-5′ exonuclease activity have previously been shown to contribute to quality control and processing of various types of nuclear RNAs. Our sequencing analysis further confirms that Rrp6 contributes to this process.

overall_design: Comparison of global RNA analysis of yeast strains containing either wild-type (WT) or exoribonuclease inactive Rrp6 (Rrp6 exo-) or lacking Rrp6 completely (rrp6Δ). Two biological replicates of each sample are included.

first: Mom

last: Das

first: Dimitrios

last: Zattas


title: Resident memory T cells form during persistent antigen exposure leading to allograft rejection

city: Pittsburgh

first: Khodor

last: Abou-Daya

state: PA

address: 200 Lothrop Street

department: Surgery

institute: Starzl Transplantation Institute

summary: Tissue resident memory T cells (TRM) contained at sites of previous infection provide local protection against re-infection. Whether they form and function in organ transplants where cognate antigen persists is unclear. This is a key question in transplantation as T cells are detected long-term in allografts, but it is not known whether they are exhausted or are functional memory T cells. Using a mouse model of kidney transplantation, we showed  that antigen-specific and polyclonal effector T cells differentiated in the graft into TRM and subqeuntly caused allograft rejection. TRM identity was established by surface phenotype, transcriptional profile, and inability to recirculate in parabiosis and re-transplantation experiments. Graft TRM proliferated locally, produced IFNγ upon re-stimulation, and their in vivo depletion attenuated rejection. Importantly, the vast majority of antigen-specific and polyclonal TRM lacked phenotypic and transcriptional exhaustion markers. Single cell analysis of graft T cells early and late after transplantation identified a transcriptional program associated with transition to the tissue resident state that could serve as a platform for the discovery of therapeutic targets. Thus, recipient effector T cells differentiate into functional graft TRM that maintain rejection locally. Targeting these TRM could improve renal transplant outcomes.

overall_design: Single Cell RNA sequencing of graft infiltrating OT-I and polyclonal T cells early and late after transplantation of OVA expressing allogeneic kidneys in mice

first: Martin

last: Oberbarnscheidt

first: Fadi

middle: G

last: Lakkis


title: Transcriptome analysis of assembled embryos using mouse induced pluripotent stem cells (iPSC) and trophectoderm stem cells (TSCC)

city: Beijing

first: Jie

state: Beijing

address: Tsinghua University

department: Basic Medical Sciences, School of Medicine

country: China

institute: Tsinghua University

summary: Purpose: gene expression profiling of single iPSC clone, TSC clone, ITS-iPSC clone, ITS-TSC clone.

overall_design: Perform RNA-seq of single iPSC clone, TSC clone, ITS-iPSC, ITS-TSC clone

first: Jianying

last: Guo

first: Pezhe

last: Wang


title: RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).

status: Public on Mar 17 2021

city: Nanjing

first: Zhenji

last: Gan

address: 12 Xuefu Road

department: Model Animal Research Center of Nanjing University

institute: Nanjing University

summary:
This experiment was conducted to identify FNIP1-dependent mRNA transcripts alteration in skeletal muscle.
Mouse FNIP1 was specifically overexpressed in skeletal muscle in FNIP1-transgenic (FNIP1-Tg) mice. FNIP1-Tg mice were crossed with FNIP1-knockout (FNIP1-KO) mice to generate FNIP1-TgKO mice expressing FNIP1 only in skeletal muscle but not in other tissues.
The muscle glycolytic-to-oxidative transformation is determined, largely in part, at the level of gene expression. To gain insight into the FNIP1-dependent regulation of skeletal muscle energy metabolism, transcriptome analysis was performed by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both FNIP1-KO and FNIP1-TGKO mice. We were particularly interested in the subset of genes that were regulated only in the FNIP1-KO mice but not in FNIP1-TGKO mice. Gene ontology (GO) analysis revealed that the primary FNIP1-regulated genes were mitochondrial metabolic genes. A broad array of genes involved in mitochondria was regulated FNIP1-KO muscle in a FNIP1-dependent manner. Together, the transcriptional profiling results indicate that a significant subset of FNIP1 target genes, were those involved in mitochondrial function.

overall_design: Gastrocnemius muscle mRNA profiles of 8-week-old WT, FNIP1-KO and FNIP1-TGKO mice were generated by deep sequencing, in duplicate, using Illumina HiSeq 4000.

first: Liwei

last: Xiao