title: Control eCLIP from K562 (ENCSR481MVN)

summary:
eCLIP control experiment on K562 against EXOSC10

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


title: eCLIP from K562 (ENCSR767OEY)

status: Public on Jan 14 2025

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

summary:
eCLIP experiment on K562 against FXR2

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


title: total RNA-seq from HCT116 (ENCSR502PAY)

type: Expression profiling by high throughput sequencing

summary:
HCT116-CDK7-treated-new_bulk-A4

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


title: total RNA-seq from HCT116 (ENCSR257FJF)

summary:
HCT116-POLR2A-clone1-treated-new_bulk-B10

For data usage terms and conditions, please refer to http://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 liver (ENCSR740PXN)

type: Genome binding/occupancy profiling by high throughput sequencing

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


title: Control eCLIP from K562 (ENCSR254NWE)

summary:
eCLIP control experiment on K562 against RNF187

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


title: total RNA-seq from neutrophil (ENCSR251XVY)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.neutrophil_spleen_M_59days

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


title: total RNA-seq from heart right ventricle (ENCSR727DPU)

summary:
UW068 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: DNase-seq from adrenal gland (ENCSR756AFB)


title: eCLIP from K562 (ENCSR256NCI)

summary:
eCLIP experiment on K562 against APEX1

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


title: total RNA-seq from B cell (ENCSR243UCH)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.CD19_spleen_M_62days

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


title: eCLIP from K562 (ENCSR248TXP)

summary:
eCLIP experiment on K562 against FXR1

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


title: eCLIP from K562 (ENCSR498DQS)

summary:
eCLIP experiment on K562 against METTL1

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


title: eCLIP from K562 (ENCSR497XZI)

summary:
eCLIP experiment on K562 against MBNL1

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


title: total RNA-seq from heart right ventricle (ENCSR278TQR)

summary:
UW067 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: eCLIP from K562 (ENCSR720BJU)

summary:
eCLIP experiment on K562 against TARDBP

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


title: Control eCLIP from HepG2 (ENCSR240ZFU)

summary:
eCLIP control experiment on HepG2 against DDX20

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


title: Control eCLIP from HepG2 (ENCSR265LJL)

summary:
eCLIP control experiment on HepG2 against TARDBP

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


title: Control eCLIP from K562 (ENCSR237YKY)

summary:
eCLIP control experiment on K562 against GARS

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


title: eCLIP from K562 (ENCSR750YOM)

summary:
eCLIP experiment on K562 against ADAT1

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


title: total RNA-seq from HCT116 (ENCSR714CHF)

summary:
HCT116-SMARCA5-clone1-untreated-new_bulk-E3

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


title: DNase-seq from heart (ENCSR231NBX)


title: PRO-cap from K562 (ENCSR220XSM)

summary:
A run-on assay that precisely maps the transcription start sites genome-wide with high sensitivity and specificity in K562 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: total RNA-seq from B cell (ENCSR703ACF)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.CD19_spleen_F_62days

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


title: Control eCLIP from K562 (ENCSR701KRV)

summary:
eCLIP control experiment on K562 against RPS10

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


title: Control eCLIP from HepG2 (ENCSR224ECB)

summary:
eCLIP control experiment on HepG2 against RPL23A

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


title: total RNA-seq from HCT116 (ENCSR729VMM)

summary:
HCT116-CTCF-untreated-new_bulk-D12

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


title: total RNA-seq from activated T-helper 1 cell (ENCSR475KPG)

summary:
CD4 N (RA+ MACS sort)Th1 (aIL-4 1ug/ml+IL-12 30ng/ml)(day 13)+beads (1:3) day 1

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


title: total RNA-seq from ovary (ENCSR231ICM)

summary:
W71 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: total RNA-seq from heart right ventricle (ENCSR197GCF)

summary:
UW054 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: DNase-seq from B cell (ENCSR224YYX)

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


title: Control eCLIP from K562 (ENCSR720EEM)

summary:
eCLIP control experiment on K562 against TARDBP

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


title: Control eCLIP from K562 (ENCSR181YHI)

summary:
eCLIP control experiment on K562 against METTL1

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


title: eCLIP from K562 (ENCSR179MPN)

summary:
eCLIP experiment on K562 against RYBP

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


title: Control eCLIP from HepG2 (ENCSR188OHK)

summary:
eCLIP control experiment on HepG2 against TNRC6A

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


title: eCLIP from HepG2 (ENCSR187VEQ)

summary:
eCLIP experiment on HepG2 against TARDBP

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


title: eCLIP from K562 (ENCSR168VUE)

summary:
eCLIP experiment on K562 against MORC2

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


title: total RNA-seq from neutrophil (ENCSR167IUG)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.neutrophil_spleen_M_83days

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


title: RIP-seq from K562 (ENCSR192OSC)


title: Control eCLIP from K562 (ENCSR143CTS)

summary:
eCLIP control experiment on K562 against HNRNPK

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


title: icLASER from K562 (ENCSR167VHJ)

summary:
K562 icLASER control experiment

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


title: total RNA-seq from adrenal gland (ENCSR176KEW)

summary:
W73 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: total RNA-seq from HCT116 (ENCSR146GSS)

summary:
HCT116-SMARCA5-clone1-treated-new_bulk-E3

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


title: eCLIP from K562 (ENCSR153STI)

summary:
eCLIP experiment on K562 against RNF187

For data usage terms and conditions, please refer to http://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 kidney (ENCSR218AFD)


title: total RNA-seq from HCT116 (ENCSR113CCF)

summary:
HCT116-MED14-clone1-untreated-new_bulk-4C

For data usage terms and conditions, please refer to http://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 liver (ENCSR146KDZ)


title: total RNA-seq from heart left ventricle (ENCSR131FDP)

summary:
UW040 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 eCLIP from K562 (ENCSR219TIG)

summary:
eCLIP control experiment on K562 against SRSF9

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


title: total RNA-seq from neutrophil (ENCSR698PIS)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.neutrophil_spleen_M_65days

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


title: DNase-seq from T-cell (ENCSR101RCL)

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


title: DNase-seq from liver (ENCSR102OZE)


title: eCLIP from K562 (ENCSR100ARZ)

summary:
eCLIP experiment on K562 against RPS6

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


title: total RNA-seq from HCT116 (ENCSR096UGR)

summary:
HCT116-SUPT16H-clone1-treated-new_bulk-F1

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


title: eCLIP from K562 (ENCSR448GXJ)

summary:
eCLIP experiment on K562 against GARS

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


title: total RNA-seq from HCT116 (ENCSR094RQC)

summary:
HCT116-RAD21-clone1-treated-new_bulk-C1

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


title: total RNA-seq from B cell (ENCSR092BBW)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.CD19_spleen_M_67days

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


title: iCLIP from K562 (ENCSR096IJV)


title: eCLIP from K562 (ENCSR090LNQ)

summary:
eCLIP experiment on K562 against ELAVL1

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


title: Control eCLIP from K562 (ENCSR060MRW)

summary:
eCLIP control experiment on K562 against MBNL1

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


title: DNase-seq from T-cell (ENCSR035JYT)


title: Control eCLIP from K562 (ENCSR058PIY)

summary:
eCLIP control experiment on K562 against DDX47

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


title: long read RNA-seq from layer of hippocampus (ENCSR038FOD)

summary:
ENC4_409, ENC4_410 hippocampus_B6Cast F1_PND10_3x female_4,5,6_ENC4_cDNA493

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


title: total RNA-seq from HCT116 (ENCSR034DEZ)

summary:
HCT116-SUPT16H-clone1-untreated-new_bulk-F1

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


title: total RNA-seq from T-cell (ENCSR034MGF)

summary:
MouseF1 of C57BL/6 (f) x CAST Eij (m)_m.CD3_spleen_F_66days

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


title: eCLIP from K562 (ENCSR004VIR)

summary:
eCLIP experiment on K562 against EEF2

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


title: RIP-seq from K562 (ENCSR026JZX)


title: eCLIP from K562 (ENCSR008MQM)

summary:
eCLIP experiment on K562 against DDX43

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


title: Detailed delineation of the immune response to COVID-19 mRNA vaccination via high-temporal frequency blood transcriptomics [third]

city: Doha

first: Darawan

last: Rinchai

state: Qatar

address: Al Gharrafa St

department: Research

country: Qatar

institute: Sidra Medicine

summary: mRNA vaccines have played a crucial role in combating the COVID-19 pandemic, but the long-term dynamics of immune responses to repeated vaccination remain poorly understood. In this study, we extend our previous work on first and second dose responses by characterizing the immune signatures elicited by a third dose of COVID-19 mRNA vaccines. Using high-resolution temporal profiling of blood transcriptomes, we analyzed samples collected daily for 9 days post-vaccination across all three doses. We observed distinct patterns of gene expression related to interferon responses, inflammation, erythroid cell signatures, and plasmablast activity. While the first dose elicited a modest response primarily characterized by interferon signaling, the second dose induced a robust, polyfunctional response. Surprisingly, the third dose, administered months later, showed a response pattern that shared similarities with both previous doses but also exhibited unique features. The interferon response following the third dose mirrored the timing of the first dose, peaking on day 2, but matched the amplitude of the second dose. Notably, we observed a progressive amplification of the plasmablast response across the three doses, with an earlier peak (day 4) compared to other vaccines, potentially a unique feature of mRNA vaccines. These findings provide crucial insights into how the immune system adapts to repeated mRNA vaccination over extended periods. They demonstrate that the heightened responsiveness induced by initial doses is maintained months later, suggesting effective immune memory. Our results contribute to a more comprehensive understanding of mRNA vaccine-induced immunity, with implications for optimizing booster strategies and developing next-generation vaccines.

overall_design:
After puncturing the skin with a finger stick, 50 µl of blood was collected in a capillary/microfuge tube assembly supplied by KABE Labortechnik (Numbrecht, Germany) containing 100 µl of tempus RNA-stabilizing solution aliquoted from a regular-sized tempus tube (designed for the collection of 3 ml of blood and containing 6 ml of solution; ThermoFisher, Waltham, MA, USA). Blood was collected prior to the vaccine being administered (day 0), on the same day, and daily thereafter over the next 10 days. This protocol was followed for both the priming and booster doses.

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first: Sara

last: Deola

first: Giusy

last: Gentilcore

first: Basirudeen

last: Kabeer

first: Mohammed

last: Toufiq

first: Davide

last: Bedognetti

first: Jean-Charles

last: Grivel

first: Damien

last: Chaussabel


title: Genome-wide rearrangement of protein translation levels for cell and organelle proliferation in a simple unicellular alga

city: Tokyo

first: Yoshitaka

last: Matsuo

address: 4-6-1, Shirokanedai, Minato-Ku

department: IMSUT

country: Japan

institute: The University of Tokyo,

summary: Cell proliferation is a fundamental characteristic of organisms, driven by the holistic functions of multiple proteins encoded in the genome. However, the individual contributions of thousands of genes and the millions of protein molecules they express to cell proliferation are still not fully understood, even in simple eukaryotes. Here, we present proteome maps of cells during proliferation in the unicellular alga Cyanidioschyzon merolae, based on the sequencing of ribosome-protected messenger RNA (mRNA) fragments. Ribosome footprint profiling of genes encoded by nuclear, mitochondrial, and chloroplast DNAs has revealed qualitative and quantitative changes in mRNA transcription and protein translation within each gene during cell division. Comparisons of ribosome footprints from non-dividing and dividing cells allowed the identification of proteins involved in cell proliferation. Given that in vivo experiments on two selected candidate proteins identified a division-phase-specific mitochondrial nucleoid protein and a mitochondrial division protein, these results offer key insights into the comprehensive protein functions that facilitate cell and organelle division.

overall_design: 2 replicates in 2 different states in same strain

first: Yuko

last: Mogi

first: Yuiki

last: Kondo

first: Tetsuya

last: Higashiyama

first: Toshifui

last: Inada

first: Yamato

last: Yoshida


title: Microbial iCLIP2: Enhanced mapping of RNA-protein interaction by promoting protein and RNA stability

city: Würzburg

first: Kathi

last: Zarnack

address: Biocenter, Am Hubland

department: Theodor Boveri Institute

country: Germany

institute: University Würzburg

summary: From synthesis to decay, the entire lifecycle of RNAs is precisely regulated by RNA-binding proteins (RBPs). Understanding the RBP-RNA interaction network, specifically their binding position on the transcriptome, is crucial for uncovering the regulatory potential of these proteins. CLIP-based methods, particularly the iCLIP method, represent a state-of-the-art technique for identifying RBP binding sites at single-nucleotide resolution. However, these methods require adaption for microbiological applications. Here, we have optimized the recent iCLIP2 method using the RBP Rrm4 for use in the fungal model system Ustilago maydis and successfully demonstrated its efficacy in conditions with high RNAse and protease activity.

overall_design: Optimizing iCLIP2 for detecting protein-RNA interactions in microbial conditions using the fungal model system Ustilago maydis

first: Nina

middle: K

last: Stoffel

first: Srimeenakshi

last: Sankaranarayanan

first: Anke

last: Busch

first: Julian

last: König

first: Michael

last: Feldbrügge


title: Signatures of IL1b, IL6 and TNFa in immune cell-types

city: Boston

first: Liang

last: Yang

state: MA

address: 77 Avenue Louis Pasteur

department: Pathology

institute: Harvard Medical School

summary: A complete profiling of inflammatory cytokines (IL1b, IL6 and TNFa) in 14 immune cell-types

overall_design: 5-8 week old C57Bl/6J mice shipped from the Jackson Laboratory, Bar Harbor. Mice were injected intravenously with either a free cytokine (5ug of IL1b, IL6 or TNFa in 120uL of PBS)  or PBS (120uL).  At 2 hours post-injection,  1,000 cells of the 14 immune cell-types from spleen and peritoneal cavity were double-sorted in 5uL of TCL Buffer containing 1% 2-mercaptoethanol and then processed for RNA-seq.

first: Juliana

last: Lee

first: Christophe

last: Benoist


title: Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation [scRNA-seq]

city: Baltimore

first: JP

last: Courneya

state: United States of America

address: 685 W Baltimore St., HSF2 Room 480

institute: University of Maryland, Baltimore

summary: While the function of many leukocytes in transplant biology has been well defined, the role of  eosinophils is controversial and remains poorly explored.  Conflicting data exist regarding eosinophils’ role in alloimmunity based on context and organ type.   Due to their prevalence in the lung, and their defined role in other pulmonary pathology such as asthma, we set out to explore the role of eosinophils in the long-term maintenance of the lung allograft.  We noted that depletion of eosinophils results in the generation of donor-specific antibodies. Eosinophil depletion increased memory B cell, plasma cell, and antibody secreting cell differentiation and resulted in de novo-generation of follicular germinal centers.  Germinal center formation depended on the expansion of CD4+Foxp3-Bcl6+CXCR5+PD1+ T follicular helper cells (Tfh) which increase in number after eosinophil depletion. Mechanistically, we demonstrate that eosinophils prevent Tfh generation by acting as the dominant source of IFN-γ in an established lung allograft, thus facilitating Th1 rather than Tfh polarization of naïve CD4+ T cells.  Our data thus describe a unique and previously unknown role for eosinophils in maintaining allograft tolerance and suggests that indiscriminate administration of eosinophil-lytic corticosteroids for treatment of acute cellular rejection may inadvertently promote humoral alloimmunity.

overall_design: Lung allograft samples harvested and digested to single cells. zmlx175 and zmlx176 were eosinophil deficient group while zmlx180 and zmlx181 were eosinophil sufficent group as control. No replicates for any sample.

first: Luke

last: Tallon

first: Jean-Paul

first: Alexander

last: Krupnick

first: Zhongcheng

last: Mei


title: Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation

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

overall_design: Refer to individual Series


title: Corpus luteum proximity alters molecular signature of the small extracellular vesicles and cumulus cells in the bovine ovarian follicle environment

city: Québec

first: Ricardo

middle: Perecin

last: Nociti

state: Québec

address: 2425, Rue de l'Agriculture

department: Animal Science

country: Canada

institute: Université Laval

summary: Progesterone (P4) is predicted to act as a negative regulatory hormone for oocyte maturation events; however, its local effects during follicular development remain poorly understood in bovine. The complex process of oocyte meiosis progression is dependent on cellular communication among follicular cells. Besides, the breakdown of this communication, mainly between cumulus cells and oocyte, through the retraction of cumulus projections connecting these cells can impact oocyte maturation. In our study, we observed that ipsilateral follicles containing high intrafollicular P4 concentrations enhance the expression of proteins in follicular small extracellular vesicles predicted to be involved in the retraction of membrane projections based on actin filaments, such transzonal projections (TZPs). Additionally, we found that contralateral follicles containing low intrafollicular P4 concentrations are predicted to regulate cellular communication pathways inducing the maintenance of membrane projections in cumulus cells. Our functional analysis confirmed that supplementation of cumulus-oocyte complexes during in vitro maturation with P4 at concentration similar to ipsilateral follicles reduces the number of TZPs. In summary, our study underscores a direct association between P4 concentration and cumulus-oocyte interaction, with potential consequences for the acquisition of oocyte competence.

overall_design: Following the OPU sessions, the FF from both groups (ipsilateral and contralateral follicles) were placed separately in a 100 mm petri dish, and pools of COCs were retrieved using a stereomicroscope. Four pools were collected per experimental group. Each pool contained samples from 3 different animals.

first: Paola

last: Maria da Silva Rosa

middle: P

first: Juliano

last: Coelho da Silveira


title: Small extracellular vesicles are mediators of embryo-endometrium-corpus luteum crosstalk

summary: A single Day-7 in vivo or in vitro-produced bovine embryo differentially modifies the endometrial transcriptome and the miRNA content in the released sEVs, which can also lead to modifications in the miRNA profile of luteal cells.

overall_design: To elucidate the embryo-endometrium-corpus luteum crosstalk, the Endometrium Explants (Ees) were cultured in the presence or absence of a single day-7in vivo(EE-AI) orin vitro(EE-IVF) embryo.

first: Alessandra

last: Bridi

middle: C

last: da Silveira

first: Felipe

last: Perecin


title: A multi-omics census reveals miRNA miR-let-7 as instigator of paternal mitochondrial dysfunction and in epigenetic heredity of intergenerational metabolic decline

city: Odense

first: Jan

middle: Wilhelm

last: Kornfeld

address: Campusbej 50

department: Biochemistry and Molecular Biology

country: Denmark

institute: University of Southern Denmark

type: Non-coding RNA profiling by high throughput sequencing

first: Ali

last: Altintas

first: Chien

last: Huang

first: Rocio

middle: V

last: Malmros


title: Beta-hydroxybutyrate alters bovine preimplantation embryo development through transcriptional and epigenetic mechanisms.

summary: Developing embryos are susceptible to fluctuations in the nutrients and metabolites concentrations within the reproductive tract, which can lead to alterations in their developmental trajectory. Ketotic dairy cows have diminished fertility, and elevated levels of the ketone body beta-hydroxybutyrate (BHB) have been associated with poor embryonic development. We used an in vitro model based on either in vitro fertilization (IVF) or parthenogenesis to investigate the effects of BHB on the preimplantation bovine embryo development, epigenome, and transcriptome. Embryo culture medium was supplemented with BHB at a similar concentration to that present in the blood of cows suffering with severe ketosis, followed by analysis of blastocysts formation rate, diameter, total number of cells, levels of H3K9 beta-hydroxybutyrylation (H3K9bhb), apoptosis, and transcriptional alterations. As a result, we observed that BHB reduced the blastocysts rates, the diameter and the total number of cells in both parthenotes and IVF embryos. Exposure to BHB for either 3 or 7 days greatly increased the H3K9bhb levels in parthenotes at the 8-cells and blastocyst stages, and affected the expression ofHDAC1,TET1,DNMT1,KDM6B,NANOGandMTHFD2genes. Additionally, culture of IVF embryos with BHB for 7 days dramatically increased H3K9bhb and reduced NANOG in blastocysts. RNA-seq analysis of IVF blastocysts revealed that BHB modulated the expression of 118 genes, which were involved with biological processes such as embryonic development, implantation, reproduction, proliferation, and metabolism. These findings provided valuable insights into the mechanisms through which BHB disrupts preimplantation embryonic development and affects the fertility in dairy cows.

overall_design: bovine blastocyst embryos (from slaughterhouse) produced in-vitro and treated with or without BHB

last: Rodrigues Sangalli

last: Perecin Nociti

first: Flávio

last: Vieira Meirelles


title: Dendritic Cell Immunotherapy with Homologous Antigenic Loading as Adjuvant Treatment for Glioblastoma: Phase I Trial Analysis [Spatial Transcriptome]

status: Public on Jan 13 2025

city: Houston

first: Briana

middle: Amicarella

last: Burns

state: TX

address: 1 Baylor Plaza

institute: Baylor College of Medicine

summary: Glioblastoma is a devastating CNS tumor for which median survival remains only 14-18 months. Homologous antigenic loading provides a powerful PAMP signal that initiates cDC1-like skewing of monocyte-derived DC and downstream development of tissue-homing, cytolytic memory effectors. Here we report results of a phase I trial in which DC vaccines prepared through homologous antigenic loading were administered principally to newly-diagnosed MGMT unmethylated GBM patients. AEs were mild, with none >grade 2 attributable to the regimen. Enrolled patients exhibited post-vaccination elevations in central memory and MPEC cells in peripheral blood, evidence of in situ immune responses by spatial transcriptomics, and a vaccine cell gene signature that correlated with outcomes. One-year OS of the 15/16 MGMT unmethylated newly-diagnosed cohort was 87.5%. Among nine patients who did not receive reoperation, GBM-specific OS was 88.9% with median OS yet-to-be-reached after 17.2 months follow-up among this group and late pseudoprogression notable among long-term survivors.

overall_design: Samples used for Visium spatial transcriptomic analysis were FFPE blocks of brain tumor tissue adhered to analysis slides in 5 micron slices. In the analysis, tissue derived from pre-vaccination first operation was compared to post-vaccination second operation.

first: Joseph

middle: F

last: Georges

first: Christina

last: Clay

first: Sabina

last: Amin

first: Ashley

last: Goralczyk

first: Corey

last: Mossop

first: Christopher

middle: J

last: Bilbao

first: Amber

last: Valeri

last: Ifrach

first: Mazen

last: Zaher

first: Lindsey

last: Colman

first: Lynne

last: Kohler

first: Thuy

last: Cao

first: Kennisha

middle: N

last: Okereke

first: Cathy

last: Schilero

first: Rahul

last: Garg

first: Nicholas

last: Troy

first: Eva

middle: H

last: Schumann

first: Mia

last: Vu

middle: A

first: Akshar

last: Trivedi

first: Wei

last: Liu

first: Madhuri

last: Namekar

first: Colby

last: Hofferek

first: Keenan

last: Ernste

first: Damilola

last: Oyewole-Said

first: Nalini

last: Bisht

first: Jonathan

last: Vazquez-Perez

first: Sharon

middle: B

last: Amanya

first: Victoria

last: Rodriguez

first: Daniel

last: Kraushaar

first: Vinod

last: Ravi

first: Deancy

last: Okoebor

first: Ian

last: Bellyar

first: Jay

last: Hartenbach

first: Matthew

middle: M

last: Halpert

first: Laura

last: Aguilar

first: Sigmund

last: Hsu

last: Zhu

first: Roderick


title: total RNA-seq from pancreas (ENCSR075ZTG)

first: ENCODE

last: DCC

summary:
W64 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: The conserved N-terminal SANT1-binding domain (SBD) of EZH2 Regulates PRC2 Activity [es-cells-gof-chip]

city: New York City

first: Agata

middle: Lemiesz

last: Patriotis

state: New York

address: 1230 York ave

institute: Rockefeller University

summary: Polycomb group proteins maintain gene expression patterns established during early development, with Polycomb Repressive Complex 2 (PRC2) methyltransferase a key regulator of cell differentiation, identity and plasticity. Consequently, extensive somatic mutations in PRC2, including gain- or loss- of function (GOF or LOF), are observed in human cancers. The regulation of chromatin structure by PRC2 is critically dependent on its EZH2 (Enhancer of Zeste Homolog 2) subunit, which catalyzes the methylation of histone H3 lysine 27 (H3K27). Recent structural studies of PRC2 revealed extensive conformational changes in the non-catalytic EZH2 N-terminal SANT-Binding Domain (SBD) during PRC2 activation, though the functional significance remains unclear. Here, we investigate how the SBD regulates PRC2 function. The domain is highly conserved in metazoans, dispensable for PRC2 assembly and chromatin localization, yet required for genome-wide histone H3K27 methylation. Further, we show that an intact SBD is necessary for the proliferation of EZH2-addicted lymphomas, and its deletion in the presence of EZH2 GOF mutations inhibits cancer cell growth. These observations provide new insights to the regulation of PRC2 activity in normal development and malignancy.

overall_design:
EZH2, SUZ12, H3K27me3, H3K27me2 ChIP-Rx experiment with S2 chromatin spike-in of A1 (WT) mESCs, EZH2 KO and EZH2 ΔSBD.
MTF2, JARID2 ChIP-seq experiment of A1 (WT) mESCs, EZH2 KO and EZH2 ΔSBD.
Cut and Run experiment of Lymphoma Karpas-422 cells, with shEZH2, and rescue with EZH2-Y641 (GOF) and EZH2-ΔSBD-Y641N (ΔSBD-GOF)
RNA-seq experiment of Lymphoma Karpas-422 cells, with shEZH2, and rescue with EZH2-Y641 (GOF) and EZH2-ΔSBD-Y641N (ΔSBD-GOF), 72 hours after EZH2-KO induction.
H3K27me3 ChIP-Rx experiment with S2 chromatin spike-in of A1 (WT) mESC with the expression of  EZH2-Y641 (GOF) and EZH2-ΔSBD-Y641N (ΔSBD-GOF)

middle: L

first: Douglas

middle: W

last: Barrows

first: C. David

last: Allis


title: Copper oxide nanoparticles treated C57 mice

city: Chengdu

first: xiaojing

last: zhang

address: Sichuan University, No. 24 South Section 1, Yanshan Road, Chengdu, Sichuan Province, China

country: China

institute: Sichuan University

summary: The C57BL/6J mice were randomly divided into three groups: control group (n=3), CuO NPs group (n=3), and CuO NPs + TTM group (n=3). A suspension of 2 mg/mL CuO NPs in 100 μl sterile saline was directly once administered by intratracheal instillation in CuO NPs treatment group. Mice in control group received 100 μl sterile saline. In the CuO NPs + TTM intervention group, 0.02 mg/mL TTM was added to the daily drinking water. All mice were sacrificed on day 7. Total RNA of the mouse lung tissues were extracted using tissue RNA isolation kit. All samples were sent to Majorbio Biotech (Shanghai, China) for transcriptome sequencing.

overall_design: The three groups of  C57BL/6J mice were control group, 2 mg/mL CuO NPs group, and 2 mg/mL CuO NPs + 0.02 mg/mL TTM group. Three samples were randomly selected from each mouse group (n = 3 mice/group). A suspension of 2 mg/mL CuO NPs in 100 μl sterile saline was directly once administered by intratracheal instillation in CuO NPs treatment group.    Mice in control group received 100 μl sterile saline.    In the TTM intervention group, 0.02 mg/mL TTM was added to the daily drinking water.    All mice were sacrificed on day 7 and lung tissue samples were taken.

first: Xiaojing

last: Zhang

first: Donglei

last: Sun


title: Decoding transcriptional identity during Neuron-Astroglia Cell Fate driven by RAR-specific agonists [Spatial transcriptomics]

city: Evry

first: Marco Antonio

last: MENDOZA-PARRA

address: 2 rue Gaston Crémieux

country: France

institute: CNRS UMR8030

summary: How cells respond to different signals leading to defined lineages is an open question to understand physiological differentiation leading to the formation of organs and tissues. Among the various morphogens, retinoic acid signaling, via the RXR/RAR nuclear receptors activation, is a key morphogen of nervous system development and brain homeostasis. Here we analyze gene expression in ~80,000 cells covering 16 days of monolayer mouse stem cell differentiation driven by the pan-RAR agonist all-trans retinoic acid, the RAR-alpha agonist BMS753 or the activation of both RAR-beta and RAR-gamma receptors (BMS641+BMS961). Furthermore, we have elucidated the role of these retinoids for driving nervous tissue formation within 90 days of brain organoid cultures, by analyzing > 8,000 distinct spatial regions over 28 brain organoids. Despite a delayed progression in BMS641+BMS961, RAR-specific agonists led to a variety of neuronal subtypes, astrocytes and oligodendrocyte precursors. Spatially-resolved transcriptomics performed in organoids revealed spatially distinct RAR isotype expression leading to specialization signatures associated to matured tissues, including a variety of neuronal subtypes, retina-like tissue structure signatures and even the presence of microglia.

overall_design: mouse embryonic stem cells were cultured in monoloayer in presence of either the pan-RAR agonist ATRA, the RAR-alpha agonist BMS753, or the combination of the RAR-beta and RAR-gamma agonists (BMS641+BMS961). Monolayer cultures driven into differentiation by the action of these RAR ligands were analyzed by single-cell transcriptomics after 4, 8 and 16 days of treatment. Samples collected after 16 days of differentiation were also used for Cut&tag assays for revealing histone modification signatures associated to promoter regions as a way to reveal active, repressed or bivalent promoter chromatin states. To further reveal the role of retinoids action in nervous tissue development, we have cultured mouse stem cells in 3-dimensional conditions. After 3 months of culture, the obtained brain organoid tissues were anlaysed by spatial transcriptomics.

first: Ariel

last: Galindo-Albarrán

first: Aysis

last: Koshy

first: Maria-Grazia

last: Mendoza-Ferri

first: Marco-Antonio

last: Mendoza-Parra


title: The conserved N-terminal SANT1-binding domain (SBD) of EZH2 Regulates PRC2 Activity [Karpas-rna-seq]


title: The conserved N-terminal SANT1-binding domain (SBD) of EZH2 Regulates PRC2 Activity [karpas-cutrun]


title: Decoding transcriptional identity during Neuron-Astroglia Cell Fate driven by RAR-specific agonists [CUT&Tag]


title: Decoding transcriptional identity during Neuron-Astroglia Cell Fate driven by RAR-specific agonists [scRNA-seq]


title: PRC2 Promotes Canalisation During Endodermal Differentiation [microarray]

city: Edinburgh

first: Rob

middle: S

last: Illingworth

state: Midlothian

address: Centre for Regenerative Medicine

department: Centre for regenerative Medicine

country: United Kingdom

institute: The University of Edinburgh

summary: In this study we employed a mouse embryonic stem cell in vitro system to differentiate ESCs into Anterior Definitive Endoderm (ADE) to model primitive streak formation and early gastrulation. To establish the gene expression changes which occurred during this differentiation we performed whole genome expression analysis on RNA isolated from FACS purified cell populations. We utilised a dual reporter mESC line (B6), bearing fluorescent reporters knocked in to the Gsc (GFP) and Hhex (Redstar) loci. GSC is a marker of the PS/mesendoderm and HHEX marks definitive endoderm lineages and expression of these reporters allowed us to isolate developmentally distinct populations during the differentiation. Using the expression profile of the untreated differentiation as a reference, we investigated the developmental impact of impaired H3K27me3 deposition on ADE differentiation by inhibiting EZH2, the core catalytic component of polycomb repressive complex 2 (PRC2) using the small molecule inhibitor EPZ6438. We found that ADE differentiation recapitulated the in vivo developmental tradjectory and that PRC2 inhibition enhanced endodermal differentiation efficiency, but did so at the cost of lineage fidelity.

overall_design: Gene expression was measured for bulk or FACS sorted ADE populations that were either untreated or treated with DMSO or the small molecule inhibitor EPZ6438 under different regimens. Three independent experiments were performed for each condition.

first: Robert

first: Jurriaan

last: Hölzenspies

first: Dipta

last: Sengupta

first: Wendy

last: Bickmore

first: Joshua

last: Brickman


title: Identification of the differently expressed genes regualted by PD0325901 and Danofloxacin

city: Hefei

first: shoudong

last: ye

address: No 111, Jiu Long Road

department: Cell Biology

institute: Anhui University

summary: Mouse embryonic stem cells (mESCs) treated by 1 μM PD0325901 and 10 μM Danofloxacin (named PDF) can matain undifferentiated state in vitro. To identify the differently expressed genes regulated by them, mESCs treated with PD0325901 (PD) and PDF for 12 h and 24 h were sent to do transcriptome sequencing. These results will extend our outstanding of the regulatory network of ESC pluripotency.

overall_design: ESCs cultured in PD  and PDF conditions were collected by using Trizol. Two repeat groups were set for each treatment group. These samples were sent to MajorBIO (Shanghai, China) company to do deep sequencing by using illumina Hiseq.


title: Chronic stress-induced cholesterol metabolism abnormalities promote ESCC tumorigenesis and predict neoadjuvant therapy response

city: Zhengzhou

first: Ting

last: Wang

address: No. 100 Keke Avenue, Zhengzhou City, Henan Province

institute: Zhengzhou University

summary: Recent studies have demonstrated that chronic stress can enhance the development of multiple human diseases, including cancer. However, the role of chronic stress in esophageal carcinogenesis and its underlying molecular mechanisms remain unclear. This study uncovered that dysregulated cholesterol metabolism significantly promotes esophageal carcinogenesis under chronic stress conditions. Our findings indicate that the persistent elevation of glucocorticoids induced by chronic stress stimulates cho-lesterol uptake, contributing to esophageal carcinogenesis. The activated glucocor-ticoid receptor (GCR) enrichment at the promoter region of High Mobility Group Box Protein 2 (HMGB2) facilitates its transcription. As a transcription co-activator, HMGB2 enhances Sterol Regulatory Element-Binding Transcription Factor 1 (SREBF1) transcription and regulates cholesterol metabolism through LDL particle uptake into cells via Low-Density Lipoprotein Receptor (LDLR). These results em-phasize the significant impact of chronic stress on esophageal carcinogenesis and establish cholesterol metabolism disorder as a crucial link between chronic stress and the development of ESCC. The implications suggest that effectively managing chronic stress may serve as a viable strategy for preventing and treating ESCC.

overall_design: CUT&Tag to verify if GCR enrichment at the promoter region of HMGB2 promotes its transcription and binding with SREBF1 and treating cells with cortisol increases the regulatory effect of HMGB2 on LDLR transcription


title: Esrrg inhibition protects against PM2.5-induced asthma aggravation by reducing Pde3b

city: Hebei

first: Xin

address: 372 Shengli North Street

institute: Hebei Chest Hospital

summary: PM2.5 exposure is closely linked to the exacerbation of asthma. Estrogen related receptor gamma (Esrrg), an orphan nuclear receptor, exerts a crucial role as a transcription factor in various metabolic diseases. Nevertheless, the impacts of Esrrg on PM2.5-triggered asthma aggravation have not been investigated. Herein, ovalbumin (OVA)-induced asthmatic mice were exposed to PM2.5 to establish a mouse model of asthma aggravation by PM2.5. In view of mRNA sequencing, Esrrg was the only member of nuclear receptor superfamily in the up-regulated differentially expressed genes in OVA compared with Naive groups as well as OVA+PM2.5 compared with OVA groups (|log2 (fold change)|>1 and p<0.05). In vivo, adeno-associated virus carrying Esrrg shRNA (AAV-shEsrrg) was applied to silencing Esrrg. In addition, Esrrg activity was suppressed pharmacologically with an inverse agonist GSK5182. Either AAV-shEsrrg or GSK5182 ameliorated airway inflammation in the PM2.5-aggravated asthmatic mice. In vitro, isolated mouse primary tracheobronchial epithelial cells (MTEC) from mice were identified by detecting cytokeratin 7-positive cells. The treatment of adenovirus vector with shEsrrg or GSK5182 mitigated the cell damage induced by PM2.5. Notably, phosphodiesterase 3B (Pde3b) expression was declined by Esrrg inhibition in vivo and in vitro. Dual luciferase reporter and ChIP-PCR assays showed the binding of Esrrg to the Pde3b promoter. Taken together, these results revealed that Esrrg inhibition alleviated airway inflammation in the PM2.5-deteriorated asthmatic mouse model and prevented PM2.5-driven MTEC injury through binding to the Pde3b promoter, which might contribute to further study the therapy of PM2.5-aggravated asthma.

overall_design: mRNA-seq profiling of lung tissues from Naive control mice, OVA-induced asthmatic mice as well as PM2.5-exacerbated asthmatic mice (Naive, OVA and OVA+PM2.5).

first: Zhihua

first: Tao

last: Cai

first: Xingbin

last: Li


title: Sequencing of chondrocytes under dermal fibroblast co-culture

city: Shanghai

first: Lei

last: Shi

state: 请选择

address: 115 Jinzun Road, Pudong New Area, Shanghai

institute: Shanghai Jiaotong university

summary: Knee osteoarthritis (KOA), as a degenerative multifactorial disease, affects the quality of life and mental health of patients, and also brings a huge socioeconomic burden. Treating synovitis have shown promise as anti-inflammatory therapeutics in mitigating OA symptoms and disease progression. Here, by analysing synovial single-cell sequencing (scRNA-seq) data from KOA, we found that synovial fibroblasts (FLS) in OA synovium showed a distinct pro-inflammatory phenotype. We collected synovial tissue from patients with clinical OA as well as from healthy donors, and histological examination was consistent with findings in scRNA-seq. Inspired by recent cross-tissue fibroblast lineage studies, we identified by sequencing that healthy FLS in synovial tissues share transcriptome-level similarities with dermal fibroblasts (DFb). Subsequently, we revealed the local as well as systemic distribution of intra-articular injected DFbs by constructing/extracting two types of rat fibroblasts (luciferase DFbs as well as GFP DFbs). The results demonstrate that DFbs can be locally retained in the synovium for up to three weeks following targeted engrafting on it. And intra-articular injection does not result in DFbs migration to vital organs or the occurrence of histological changes in these organs. A rat model of KOA was constructed by anterior cruciate ligament transection (ACLT) in order to study the therapeutic effect of DFbs on KOA. After injection, the rats showed improvement in painful gait. In addition, histological as well as imaging results showed reduced synovitis and improvement in articular cartilage. Finally we verified the protective effect of DFbs on cytokine-stimulated chondrocytes in a co-culture system.

overall_design: In order to achieve this objective, a co-culture experiment was conducted in which extracted primary chondrocytes were combined with primary DFbs in transwell chambers. IL-1β (10ng/ml) was added 24 h after cell attachment. After 36 h and 72 h of IL-1β addition, the chondrocytes from the lower chamber were obtained for bulk RNA sequencing

first: Kewei

last: Rong

first: Kexin

last: Liu

first: Jie

last: Zhao


title: Sequencing of dermal fibroblasts and synovial fibroblasts cultured in vitro

overall_design: Three main groups of cells were involved in this experiment. Group D refers to dermal fibroblasts cultured in vitro. Group HF refers to synovial fibroblasts of healthy donor origin cultured in vitro. Group OAFILB refers to synovial fibroblasts of OA patient origin cultured in vitro with IL-1β stimulation.


title: Unraveling the ceRNA Network: Insights into PI3K-AKT Pathway in Irradiated Mouse Thymus [mRNA and lncRNA]

city: Zaozhuang

first: Ping

last: Xu

address: Beian road 1

institute: Zaozhuang University

summary: Background: Excessive or inappropriate radiation exposure can cause serious damage to organisms. Radiation-induced thymus injury (RITI) is a serious complication associated with radiation and is mediated by RNAs. Methods: The thymus tissues of mice were analyzed using RNA-sequencing (RNA-seq) and their libraries 24 h after exposure to 6 Gy of X-ray radiation. The target mRNAs were functionally annotated and the target lncRNA-based miRNAs and miRNA-based mRNAs were predicted after irradiation to develop the lncRNA-miRNA-mRNA ceRNA axis. Results: The results revealed that after irradiation, 6214 mRNAs, 160 miRNAs, and 1999 lncRNAs were significantly upregulated while 2676 mRNAs, 165 miRNAs, and 941 lncRNAs were considerably downregulated. Angiogenesis and ameboidal-type cell migration for Biological Process; actin cytoskeleton and extracellular matrix (ECM) for Cellular Component; and actin binding and ECM structural component for Molecular Function represent the most prominent changes in GO analysis function. A total of 333 cellular function were significantly altered by PTEN, while 175 CFs were substantially changed by PDPK1. Pathways involved in cancer, ECM-receptor interaction, focal adhesion, axon guidance, PI3K-AKT signaling, and adrenal signaling in cardiomyocytes were identified via KEGG pathway analysis. For experimental confirmation, the crucial pathway PI3K-AKT was selected to have a role in thymus degeneration after radiation exposure. Conclusion: A lncRNA-miRNA-mRNA ceRNA axis of RITI was successfully developed in a mouse model after irradiation. The PI3K-AKT pathway contributes to preventing radiation-induced cell death in RITI, and the differentially expressed RNA in the initial stage of this injury may result in serious consequences.

overall_design: Thymus  lncRNA,mRNA and miRNA profiles of 5 weeks old control and 1d after radiation group mice were generated by deep sequencing, in triplicate, using Illumina GAIIx.

first: Fei

first: Qing-hua

last: Yu


title: Multi-omic and spatial analysis of mouse kidneys highlights sex-specific differences in gene regulation across the lifespan

city: Saint Louis

first: Li

last: Ding

state: MO

address: 660 S Euclid Ave

institute: Washington University in St Louis

summary: We utilized the Xenium single-cell platform to analyze spatial expression patterns for kidneys from female and male mice at W12 and W92. Four distinct kidney zones were identified: the cortex, the outer stripe of the outer medulla (OSOM), the inner stripe of the outer medulla (ISOM), and the inner medulla (IM) based on their histology and cell type compositions. Female kidneys had a thinner cortex and thicker OSOM, while males had a vastly larger IM, contributing to sex-based size differences.

first: Ruiyang


title: PRC2 Promotes Canalisation During Endodermal Differentiation [4sU-seq]

first: Rob

summary: In this study we employed a mouse embryonic stem cell (ESCs) differentiation system to convert pluripotent ESCs into Anterior Definitive Endoderm (ADE) to model primitive streak formation and early gastrulation. To monitor the progression of the differentiation we utilised a dual reporter mESC line (B6) bearing fluorescent reporters knocked in to the Gsc (marker of the PS/mesendoderm tagged with GFP) and Hhex (marker of definitive endoderm lineages tagged with Redstar) loci. To establish the transcriptional changes which occurred during a phase of differentiation that resembles the epithelial to mesenchymal transition (EMT) at the primitive streak (PS), we performed 4sU-seq analysis on FACS sorted GSC negative and positive populations from day 3 and day 4 of differentiation. Using this approach, in combination with genome-wide gene expression analysis and ChIP-seq data, we: i).  Found that changes in the gene expression where primarily regulated at the levels of transcription; ii). Identified putative enhancer elements with bi-directional transcription signatures proximal to developmentally regulated genes; iii). Determined that transcriptional upregulation of genes did not require the prior loss of H3K27me3 at gene TSSs.

overall_design: 4sU-seq was performed on GSC negative and positive FACS sorted populations form days 3 and 4 of ADE differentiation. Three independent experiments were performed for each condition.

first: Robert

first: Jurriaan

first: Dipta

first: Wendy


title: Novel PET/CT Imaging Biomarkers of CB-839 in Combination With Panitumumab and Irinotecan in Patients With Metastatic and Refractory RAS Wildtype Colorectal Cancer

city: NASHVILLE

first: Marisol

last: Ramirez

state: TENNESSEE

address: 2220 Pierce Avenue, 571 Preston Research Building

department: Center for Quantitative Sciences, Department of Biostatisticss

institute: Vanderbilt University Medical Center

summary: In managing patients with rat sarcoma virus (RAS) wild-type (WT) metastatic colorectal cancer (mCRC), monoclonal antibodies against the epidermal growth factor receptor (EGFR) represent a key therapeutic strategy. However, their limited ongoing effectiveness in this setting underscores the importance of elucidating other factors that affect response, including underlying immunological and metabolic repertoires. An emerging therapeutic target, glutamine metabolism is crucial for cancer cell growth; symbiotically, tumor glutamine demand relative to the microenvironment disadvantages potential anti-tumor immunity. We conducted a phase I/II clinical trial in patients with RAS WT mCRC combining panitumumab, an EGFR inhibitor, and CB-839, a glutaminase inhibitor, hypothesizing that antagonizing glutamine-centric tri-carboxylic acid (TCA) cycle metabolism and mitogen-activated pathway kinase (MAPK)-mediated growth would favor response in well-selected patients. Here, we demonstrate that a novel B cell activation signature, ‘Bscore’ was associated with clinical benefit from combined therapy in patients who previously progressed on anti-EGFR therapy. Patient ‘Bscore’ was positively associated with treatment-induced change in lesion size. Furthermore, patients with lower ‘Bscore’ tended to exhibit greater tumor avidity of glutamine by non-invasive positron emission tomography (PET), suggesting the sensitivity of B cell activation to a glutamine-depleted microenvironment and highlighting future opportunities to enhance immune response in the treatment of mCRC and potentially other glutaminolysis-dependent solid tumors.

overall_design: Tumor core biopsies were collected from participants enrolled on the phase II portion of the study. Tissue was collected at baseline prior to treatment. One tumor sample was analyzed per participant.

first: Seong-Woo

last: Bae

first: Kristen

middle: K

last: Ciombor

first: Quanhu

last: Sheng

first: Gregory

middle: D

last: Ayers

first: Cathy

last: Eng

first: Laura

last: Goff

first: Dana

last: Cardin

first: Jordan

last: Berlin

first: H

last: Manning


title: Short communication: Upregulation of hypoxia/reoxygenation-induced Shc3 by downregulated miR-455-5p, suppresses trophoblasts implantation and is associated with placental inflammation and angiogenesis of preeclampsia

city: Nanjing

first: Hui-zhi

last: Gong

state: JiangSu

address: No. 123, Tianfei Lane, Mo Chou Road

institute: Nanjing Women and Children’s Healthcare Hospital

summary: Preeclampsia is characterized by insufficient implantation of trophoblasts. It is relevant in the failure adaptation of trophoblasts to changes in the intrauterine embryo development environment. Fewer miRNAs have been reported on this. MiR-455-5p expressed lowly in preeclampsia but its role remains unknown. Combining cell and molecular biology methods, we suggested the function and relevant mechanisms of miR-455-5p and its potential target Shc3 in preeclampsia. In vitro, HTR-8/SVneo migrated and invaded more rapidly under H/R than in hypoxic or normoxic conditions when miR-455-5p was overexpressed. And the apoptosis of HTR-8/SVneo is in contrast to the migration and invasion in H/R. Shc3 was identified as a direct downstream target gene of miR-455-5p, where overexpression of this gene reversed the miR-455-5p impact, promoting apoptosis and suppressed invasion and migration of HTR-8/SVneo under H/R. Shc3 was highly expressed in H/R, but its level was low in isolated hypoxic or normoxic environments. Further, Shc3 overexpression is involved in placental inflammation and angiogenesis inhibition. Finally, we got the conclusion that the downregulation of miR-455-5p in preeclampsia contributes to the elevation of Shc3 in trophoblast, thereby deteriorating trophoblast cells implantation. The elevated Shc3 is associated with placental inflammation and angiogenesis inhibition. Shc3 serves as a potential biomarker for preeclampsia diagnosis and treatment.

overall_design: To explore the target genes of miR-455-5p that affect the phenotypes of migration, invasion, and apoptosis of HTR8/Svneo cells under hypoxia/reoxygenation conditions, we overexpressed miR-455-5p mimic and miR-455-5p mimic-NC in HTR8/Svneo under hypoxia/reoxygenation. We detected the transcriptomic gene changes in HTR8/Svneo by RNA-Seq.

first: Jing

last: Guan

first: Ying-zi

last: Pan

first: Hong-juan

first: Ai-wu

last: Shi

first: Ning

last: Gu


title: Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy [RNA-Seq]

city: Lincoln

first: Ivan

last: Vechetti

state: NE

address: 1700 N. 35th Street

institute: University of Nebraska-Lincoln

summary: MicroRNAs (miRNAs) are small, non-coding RNAs that play a critical role in regulating gene expression post-transcriptionally. Skeletal muscle-specific miRNAs, including miR-1, are important for skeletal muscle development and maintenance. In response to mechanical loading, skeletal muscle levels of miR-1 decrease by approximately 50%, suggesting a potential involvement in muscle hypertrophy. In the current investigation, we hypothesized that a reduction of miR-1 levels in response to mechanical loading would be necessary for skeletal muscle growth to occur. By significantly elevating miR-1 levels during the hypertrophic process via lentiviral delivery, we observed a blunted growth response in the plantaris muscle subjected to synergist ablation. A deeper RNA-based integrative analysis (transcriptomics and RNA eCLIP) indicates that miR-1 inhibits the expression of Itm2a and Melusin, two membrane-related proteins. While their exact mechanism in muscle hypertrophy is yet to be identified, our results suggest that miR-1-regulated membrane proteins are important for skeletal muscle hypertrophy.

overall_design:
To explore the role of miR-1 in skeletal muscle, we overexpressed miR-1 (lentivirus injection) in mice (Mimic group) that underwent 10 days of MOV-induced muscle hypertrophy.
We then perform the gene expression analysis using data from RNA-seq

first: Shengyi

last: Fei


title: Transcriptional profiles of before and after activation in CD4 T cells

first: SI

last: SUN

address: 8055 Cambridge Street Apt 16, 16

department: Transplant

institute: Transplant

summary: For RNA preparation, 2 million resting and 48-h activated CD4+ T cells were used for RNA extraction using the miRNeasy Mini Kit (QIAGEN).This project focuses on differences in the transcriptome before and after CD4 T cell activation.

overall_design: Control group:WT-d0-1;WT-d0-2;WT-d0-3      Experimental group:WT-d2-1;WT-d2-2;WT-d2-3

first: XianC

last: Li

first: Xiang

last: Xiao

first: Xiaojun

last: Su

first: Si

last: Sun


title: Expression microarray comparison of medulloblastoma in Math1-Cre/SmoM2 mice with and without Cre-conditional Bcl2l1 deletion

city: Atanta

first: Tim

last: Gershon

state: GA

address: Emory University School of Medicine

department: Pediatrics

institute: Emory University

summary: We compared gene expression in medulloblastomas in mice with conditional Bcl2l1 deletion versus medulloblastomas in mice with WT Bcl2l1. We generated mice with medulloblastomas by crossing Math1-Cre and SmoM2 mouse lines. We generated mice with medulloblastomaswith Cre-conditional Bcl2l1 deletion by breeding Bcl2l1 f/f mice into both Math1-Cre and SmoM2 mouse lines. We harvested tumors at P15 and then isolated RNA for expression array analysis.

overall_design: Bulk trasncriptomic comparions of medulloblastomas that form in mice using 4 replicate animals per condition and 2 conditions- Bcl2l1 Cre conditonal deletion versus Bcl2l1 WT

first: Timothy

first: Katherine

last: Veleta


title: RUNX1 expression is regulated by a super-enhancer and is a therapeutic target in adult T-cell leukemia/lymphoma

city: Nagasaki

first: Koji

last: Ando

state: Nagasaki

address: 1-12-7 Sakamoto

department: hematology

institute: Nagasaki University

summary: Super-enhancers (SEs)—genomic enhancer regions with dense accumulation of mediator complexes—play an important role in regulating tumor-specific gene expression and are potential therapeutic targets for neoplastic diseases. Bromodomain-containing protein 4 (BRD4) is a component of the protein complexes that bind to the SE region. JQ1, one of the known BRD4 inhibitors, exerts antitumor effects by suppressing SE-mediated regulation of gene expression. Adult T-cell leukemia/lymphoma (ATL) is highly resistant to available treatments, and its prognosis is extremely poor. As JQ1 has potential as a therapeutic agent for various malignancies, we investigated the anti-ATL effects of JQ1. JQ1 induced apoptosis and inhibited ATL cell proliferation. JQ1 suppressed the expression of RUNX1 through the disruption of SE-mediated gene regulation, indicating that RUNX1 could be a novel therapeutic target molecule. AI-10-104 and Ro5-3335 are RUNX1 inhibitors developed for hematologic malignancies such as acute myeloid leukemia (AML) and lymphoblastic leukemia (ALs). We demonstrated that these two agents reduced cell proliferation in ATL cell lines and patient samples at effective concentrations in ALs with RUNX1 mutations. Simultaneously, AI-10-104 suppressed MYC proto-oncogene (c-MYC) expression. RUNX1 is a potential therapeutic target for ATL that promotes c-MYC expression. For the first time, we showed that RUNX1 expression is regulated via SEs in ATL, a hematologic malignancy of peripheral mature T cells. This study indicates that RUNX1 may be a novel therapeutic target for ATL.

overall_design: ATL cells ST-1 and KOB were incubated with 500 nM JQ1 or DMSO for 18 hours, and then RNA was harvested.  Genes whose expression levels were altered  in ST-1 and KOB with JQ-1 identified.

first: Yuji

last: Kobayashi


title: Impact of URT1 and HESO1 TUTases on the steady state level of mRNAs in Arabidopsis seeds and flowers

city: Strasbourg

first: Dominique

last: Gagliardi

address: 12, rue du General Zimmer

department: IBMP

institute: CNRS

summary: To evaluate the contribution of both TUTases on the mRNA steady state level, we produced total RNA-seq libraries from flowers and dry seeds of WT plants and of mutant for URT1 and HESO1. We performed a differential gene expression analysis to identify mRNAs that are differentially accumulated in mutant seeds and flowers when compared to WT

overall_design: Total RNA-seq library for flowers and seed for WT plants and for urt1-1, heso1-4 and heso1-4 urt-1 mutants  (4 genotypes, 3 biological replicates each) 12 flower samples (4 genotypes with 3 biological replicates)

first: Hélène

last: Zuber

first: Jeanne

last: Roignant


title: Oxidative phosphorylation inhibition with IACS-010759 treatment in colorectal cancer cells

city: Callaghan

first: Xiaohong

last: Zhao

address: University Drive

country: Australia

institute: University of Newcastle

summary: Although targeting oxidative phosphorylation (OXPHOS) in cancer is currently impeded due to dose-limiting toxicities, there remain opportunities through combination treatments that provide therapeutic benefits at doses attainable in patients. While glycolysis-deficient cancers are generally vulnerable to OXPHOS inhibition in preclinical models, the full extent of phenotypical and mechanistic consequences of inhibiting OXPHOS in cancers capable of glycolysis is not yet well understood. We aimed to clarify the response and underlying mechanisms of glycolysis-competent colorectal cancer (CRC) to OXPHOS inhibition and to identify potential approaches to render such cells more sensitive to OXPHOS inhibitors.

overall_design: To investigate the mechanisms of CRC cells response to OXPHOS inhibition, we treated LIM1215 and Colo205 with OXPHOS inhibitor IACS-010759 (IACS) at 100 nM for 24 hours. Cells treated with DMSO was set as control. Each sample has duplicate repeat.


title: Clinical and Immunological Outcomes after Randomized Trial of Baked Milk Oral Immunotherapy for Milk Allergy

city: La Jolla

first: Jeamin

last: Jung

address: 9420 Athena Cir

department: Bioinformatics Core

institute: La Jolla Institute for Immunology

summary: BACKGROUND. Cow’s milk allergy (CMA) is the most common food allergy in young children.  Treatment with oral immunotherapy (OIT) has shown efficacy but also high rates of adverse reactions.  We sought to determine if baked milk (BM) OIT could reduce adverse reactions while still inducing desensitization, and to identify immunological correlates of successful BMOIT. METHODS. This phase II, randomized trial evaluated the safety and efficacy of BMOIT in children age 3-18 years. After the initial placebo-controlled first year of treatment, placebo-treated participants crossed over to active BMOIT for year two.  Double-blind, placebo-controlled food challenges (DBPCFC) were conducted to BM after year one and to both BM and unheated milk (UM) after year two. IgG/IgE antibodies were measured along with cow’s milk (CM)-specific CD4 memory T cell populations, profiled using flow cytometry and scRNA-Seq. RESULTS. Twenty-one of 30 (70%) reached the primary endpoint of tolerating 4044mg of BM protein at month-24, and 11/30 tolerated ≥2000mg of UM. Dosing symptoms were common, but >98% were mild with no severe reactions. Immunological changes associated with desensitization included increased CM IgG4, CM+ FOXP3+ cells, and Tregs and corresponding decreases in CM IgE, CM+ Th2A cells, and CD154+ cells. T cell and antibody measurements were combined to build a model that predicted UM oral food challenge (OFC) outcomes. CONCLUSION. BMOIT was well tolerated and induced a substantial level of desensitization to baked and unheated milk. This desensitization corresponded to significant redistribution within antigen specific antibody and T cell compartments that provide novel insight into the mechanistic changes that occur with OIT treatment.

overall_design:
Antigen specific CD4 memory T cells from cow milk allergic children across BMOIT analyzed by scRNA-Seq

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Proper consent was not given for upload of raw data, therefore not included.
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first: Jennifer

last: Dantzer

first: Sloan

last: Lewis

first: Kevin

last: Psoter

first: Aaron

last: Sutherland

first: April

last: Frazier

first: Eve

last: Richardson

first: Synaida

last: Maiche

first: Gregory

last: Seumois

first: Robert

last: Wood

first: Bjoern

last: Peters


title: PRC2 Promotes Canalisation During Endodermal Differentiation

first: Rob

last: Illingworth

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

overall_design: Refer to individual Series


title: PRC2 Promotes Canalisation During Endodermal Differentiation [ChIP-Seq]

summary: In this study we employed a mouse embryonic stem cell (ESCs) differentiation system to convert pluripotent ESCs into Anterior Definitive Endoderm (ADE) to model primitive streak formation and early gastrulation. To monitor the progression of the differentiation we utilised a dual reporter mESC line (B6) bearing fluorescent reporters knocked in to the Gsc (marker of the PS/mesendoderm tagged with GFP) and Hhex (marker of definitive endoderm lineages tagged with Redstar) loci. To monitor changes in the chromatin landscape during this differentiation we performed ChIP-seq for H3K27me3 and H3K4me3 (modifications associated with gene repression and activation respectively) in each of nine FACs sorted ADE populations. Using this approach, in combination with genome-wide gene expression analysis, we; i). Found that changes in gene expression/transcription were both predictive of and predicted by dynamic changes in the levels of these histone modifications at gene promoters; ii). Found that changes in H3K27me3 levels at TSS are more dynamic than the levels of H3K4me3; iii). Determined that transcriptional upregulation of genes did not require the prior loss of H3K27me3 at gene TSSs.

overall_design: ChIP-seq was performed on nine ADE populations isolated by FACS sorting based on GSC-GFP and HHEX-RedStar expression levels. Two or three independent experiments were pooled and sequenced for each ChIP and input sample.

first: Jurriaan

last: Hölzenspies

first: Dipta

last: Sengupta

first: Wendy

last: Bickmore

first: Joshua

last: Brickman


title: Stimulation of skeletal stem cells in the growth plate promotes linear bone growth.

city: Gothenburg

first: Andrei

last: Chagin

state: Västra Götaland

address: Guldhedsgatan 10a

department: Institute of Medicine

country: Sweden

institute: University of Gothenburg

summary: Recently, skeletal stem cells were shown to be present in the epiphyseal growth plate (epSSCs), but their function in connection with linear bone growth remains unknown. Here, we explore the possibility that modulating the number of epSSCs can correct differences in leg length. First, we examined regulation of the number and activity of epSSCs by Hedgehog signaling (Hh). Both systemic activation of Hh pathway with Smoothened agonist (SAG) and genetic activation of Hh pathway by Patched (Ptch1) ablation in Pthrp-CreER;Ptch1 fl/fl;tdTomato mice promoted proliferation of epSSCs and clonal enlargement. Transient intra-articular administration of SAG also elevated the number of epSSCs. When SAG-containing beads were implanted into the femoral secondary ossification center (SOC) of one leg of rats, this leg was significantly longer one month later than the contralateral leg implanted with vehicle-containing beads, an effect that was even more pronounced two and 6 months after implantation. We conclude that Hh signaling activates growth plate epSSCs, which effectively leads to increased longitudinal growth of bones. This opens new therapeutic possibilities for the treatment of differences in leg length

overall_design: To activate hedgehog signaling, mice were injected i.p. with SAG (n=4) or DMSO (dimethyl sulfoxide) as a control vehicle (n=4) once a day from postnatal day 30 (P30) till P36. Mice were sacrificed at P38. For each mouse, cells from two femoral growth plates were isolated by FACS-sorting with stem cell markers: genetic PTHRP-mCherry and CD73 antibody staining.

first: Dana

last: Trompet

first: Anastasiia

last: Kurenkova

first: Ostap

last: Dregval


title: TGF-β Signaling Pathway and Cell-Cell Interactions in the Tumor Microenvironment Drive Bladder Cancer Progression after BCG Instillation Treatment: Insights from longitudinal Single-Nucleus RNA-Seq

city: Seocho-gu

first: Kim

last: Tae-Min

address: Banpo-daero

country: South Korea

institute: The Catholic University of Korea

summary: In this study, we aimed to characterize cellular subtypes and cognate genetic markers using single nuclear RNA sequencing on 8 NMIBC samples treated with BCG, including 3 cases exhibited disease progression.

overall_design: 14 samples from 9 patients with BCG. 3 cases show progression after BCG treatment; NP = non-progression, P = Progression sample, CF = Cancer Cell Free

first: Tae-Min

last: Kim

first: Seo-Young

last: Lee

first: Yun-Hee

first: Y-Syn

last: Ha


title: Unraveling the ceRNA Network: Insights into PI3K-AKT Pathway in Irradiated Mouse Thymus [miRNA]

first: Ping

last: Xu

overall_design: Thymus lncRNA,mRNA and miRNA profiles of 5 weeks old control and 1d after radiation group mice were generated by deep sequencing, in triplicate, using Illumina GAIIx.

first: Fei

last: Wang

first: Qing-hua

last: Yu


title: Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy

first: Ivan

last: Vechetti

overall_design:
To explore the role of miR-1 in skeletal muscle, we overexpressed miR-1 (lentivirus injection) in mice (Mimic group) that underwent 10 days of MOV-induced muscle hypertrophy.
We then perform an exploratory eCLIP-seq to find out the mRNA traget of microRNA

first: Shengyi

last: Fei


title: Early mechanisms of aortic failure in a zebrafish model for thoracic aortic dissection and rupture

city: Ghent

first: Michiel

last: Vanhooydonck

address: Corneel Heymanslaan  10

department: Biomolecular medicine

country: Belgium

institute: Ghent University

summary: Thoracic aortic dissection (TAD) is associated with a high mortality rate. Despite the existence of different mouse models for TAD, the underlying disease mechanisms remain elusive. Treatment options are limited and mainly consist of surgical repair at critical diameters as current pharmacological interventions are unable to stop disease progression.  In humans, loss of function (LOF) of SMAD3 and SMAD6 impair vascular homeostasis, increasing the risk for TAD. We developed a zebrafish model for thoracic aortic dissection/rupture by targeting both ohnologs of smad3 and smad6. We discovered an increased diameter of the ventral aorta in smad3a-/-;smad3b-/- double knockout zebrafish larvae,  while smad6a-/-;smad6b-/- double knockout  zebrafish have a reduced diameter associated with early mortality. Surprisingly, the smad3a-/-;smad3b-/-;smad6a-/-;smad6b-/- quadruple knockout (qKO) zebrafish model is viable and survives to adulthood, although exposure to stress leads to sudden death. Histological analysis of the adult ventral aorta showed medial elastolysis and aortic dissections and ruptures at sites exposed to high hemodynamic stress. RNA-sequencing of qKO larvae indicated a profile of reduced negative regulation of proteolysis and upregulation of melanogenesis, a previously unaddressed pathway in this pathology. We confirmed that pharmacological modulation of tyrosinase has an effect on aortic morphology. Our study shows that dysregulation of SMAD3/6-dependent signaling has an important impact on thoracic aortic homeostasis, and that using the qKO zebrafish model, thus far the only known model of aortic dissection and rupture in this species, can identify novel pathophysiological pathways leading to TAD.

overall_design: For RNA extraction, the Rneasy® minikit (Qiagen; Hilden, Germany) was used following manufacturers guidelines. One experiment was performed using TruSeq. RNA sequencing was performed on five pools, each containing five smad3a-/-;smad3b-/-;smad6a-/-;smad6b-/- quadruple knockout (qKO) zebrafish or wt control cousins.  Only samples with RNA integrity number (RIN) values higher than 9 were considered. All other experiments were performed using Quantseq. For quantseq sample 1-10, RNA sequencing was performed on five pools, each containing three smad3a-/-;smad3b-/-;smad6a-/-;smad6b-/- quadruple knockout (qKO)  adult aortas  and five pools of three wt control cousins aortas. For quantseq sample 11-20, RNA sequencing was performed on five pools, each containing three smad3a-/-;smad3b-/- double knockout (DKO) zebrafish or wt control cousins.  For quantseq sample 21-30, RNA sequencing was performed on five pools, each containing three smad6a-/-;smad6b-/- double knockout (DKO) zebrafish or wt control cousins.

first: Maxim

last: Verlee

first: Marta

last: Santana Silva

first: Lore

last: Pottie

first: Annekatrien

last: Boel

first: Matthias

last: Van Impe

first: Hanna

last: De Saffel

first: Lisa

last: Caboor

first: Piyanoot

last: Tapaneeyaphan

first: Adelbert

last: De Clerq

first: Andy

last: Willaert

first: Delfien

last: Syx

first: Patrick

last: Sips

first: Bert

last: Callewaert


title: Centromere inactivation during aging can be rescued in human cells

city: Bethesda

first: Songjoon

last: Baek

state: MD

address: 41 Library Drive

department: CCR

institute: NCI / NIH

summary: Aging involves a range of genetic, epigenetic, and physiological alterations. A key characteristic of aged cells is the loss of global heterochromatin, accompanied by a reduction in canonical histone levels. In this study, we track the fate of centromeres during aging in human cells. Our findings reveal that the centromeric histone H3 variant CENP-A is downregulated in aged cells, in a p53-dependent manner. We observe repression of centromeric noncoding transcription through an epigenetic mechanism via recruitment of a lysine-specific demethylase 1 (LSD1/KDM1A) at the centromeric DNA. This suppression results in defective de novo CENP-A loading at aging centromeres. By dual inhibition of p53 and the lysine-specific demethylase 1 in aged cells, we mitigate the reduction in centromeric proteins and centromeric transcripts, leading to the rejuvenation of these cells. These results offer insights into a novel mechanism for centromeric inactivation during aging and provide valuable information on strategies to reactivate it.

overall_design: BJ fibroblasts was treated with DMSO/Dox 250nM for 24 hours and then allowed to senesce for 10 days. Total RNA extracted from BJ skin fibroblast cells  DMSO and DOX treated. Each sample is given in 2 replicates(Rep). Gene expression analysis to be done untretaed/DMSO vs Dox treated.

first: Sweta

last: Sikder

first: Truman

last: Mcneil

first: Yamini

last: Dalal


title: Chemogenomic screening of acute myeloid leukemia samples

city: Montreal

first: Brian

last: Wilhelm

address: 2950 Chemin Polytechnique

institute: University of Montreal

summary: Acute myeloid leukemia (AML) represents 20% of pediatric leukemia, but accounts for most of disease-related mortality in children, due to chemo-resistance or relapse. Treatment modalities tailored according to specific AML genetic subgroups are critically needed to improve survival and decrease morbidity. To address this need we report here the results of a small molecule screen that was performed using 12,000 compounds using human leukemia models, matched patient diagnostic and relapse samples, and cell lines. As part of this work, expression profiling was performed in order to correlate drug response to gene expression differences between samples.

overall_design: Expression profiling of AML samples from patients, established cell lines, and synthetic models

first: Safia

last: Safa-Tahar-Henni

first: Verena

last: Greß

first: Karla

last: Paez Martinez

first: Élodie

last: Roques

first: Mélanie

last: Bilodeau

first: Kolja

last: Eppert

first: Sonia

last: Cellot

first: Frédéric

last: Barabé


title: Ultrasound-activated piezoelectric nanostickers for neural stem cell therapy of traumatic brain injury therapy

city: Jinan

first: Keyi

last: Li

state: Shandong Province

address: 27 Shanda Nanlu

institute: Shandong University

summary: Piezoelectric stimulation can promote neuronal differentiation of neural stem cells. Here we report a piezoelectric nanostickers that activate voltage-gated calcium channels (VGCC) on the surface of neural stem cells under ultrasound, inducing calcium ion influx.The influx of calcium ions leads to the upregulation of CaMKⅡ expression and phosphorylation, which initiates downstream signal transduction pathways in the process of neurogenesis. Phosphorylated CaMKⅡ (P-CaMKⅡ) enters the nucleus, where it facilities the phosphorylation of CREB. The phosphorylation of CREB enhances the expression of target gene, BDNF, ultimately leading to the completion of neurogenesis.

overall_design: After NSCs received different treatments for 5 days, RNA-seq was performed

first: Wenhan

last: Wang


title: Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

city: NEW YORK

first: Mayukh

last: Biswas

state: NY

address: 1130 Saint Nicholas Ave, Room 401B

department: Irving Cancer Research Center

institute: Columbia University Medical Center

summary: We have carried out high-throughput profiling of histone modifications and transcription factors in mammalian cells. First we generated stable PHF6 knock out lines by CRISPR-Cas9 technology in wild type Jurkat cells. We electroporated the RNP complex in Jurkat cells conatining guide RNAs against either non-targeting (EV) or PHF6 (KO) followed by single clone isolation and expansion. We confirmed absolute loss of total protein by WB and indel formation (mutation efficiency) at the PHF6 genomic locus by Sanger sequencing. By obtaining over six to ten billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of well studied histone modifications and transcription factors. This study provides a framework for eluciadting the role of PHF6 in regulating the chromatin landscape encompassing both activating and repressive histone modifications and chromatin remodelers in the context of leukemia.

overall_design: Examination of 3 different histone modifications and 3 ATP-dependent chromatin remodeling factors in PHF6-KO Jurkat T-ALL cells.

first: Biswas

last: Mayukh

first: Albero

last: Robert

first: Alvarez

last: Silvia

first: Ferrando

last: Adolfo


title: Neural tRNA Expression Patterns in Brain Organoids

city: Santa Cruz

first: Todd

middle: Michael

last: Lowe

state: CA

address: 1156 High Street / MS: SOE-2

department: Biomolecular Engineering

institute: University of California, Santa Cruz

summary: Transfer RNAs (tRNAs) are traditionally known for their role in protein translation, yet recent discoveries highlight their broader functions in gene regulation, particularly through tRNA-derived small RNAs (tDRs). Studies have shown the singular importance of one unique ArgUCU tRNA isodecoder in mouse neural development, yet potential function(s) of tDRs derived from this and all other tRNAs remain largely unexplored in early human brain development. In this study, we employed cerebral cortical organoid models and AlkB-facilitated RNA methylation sequencing (ARM-seq) to profile tDRs across distinct stages of early human cerebral cortex development. Our analysis reveals dynamic expression patterns of diverse tDR groups derived from a wide range of isodecoders, with several distinct groups showing neural-specific expression. Computational analyses of these tDRs shows biased sequence motifs in over-represented tRNAs that are enriched with particular RNA modifications, giving initial clues to traits that change within the pool of tDRs during neural development. This expanded catalog of tDRs provides a framework for future studies on tRNA function in brain development and offers a deeper understanding of the complexity of tDR dynamics in neural differentiation.

overall_design: Included are ARM-seq libraries derived from isolated total small RNA from GM-12878-c305 human induced pluripotent stem cells and brain organoids.  These experiments were performed in duplicate or triplicate (biological) and subjected to NGS.

first: Alex

last: Bagi

first: Sofie

middle: R

last: Salama


title: Arabidopsis CRL interacts with OEP80 to facilitate its complex formation

city: Paris

first: Jing

last: An

address: 630 Rue Noetzlin

institute: Universite Paris Saclay

summary:
Purpose: we conducted a froward genetic screen to isolate suppressors of the chloroplast-deficient crl mutant, and isolated a mutation affecting the OEP80 protein.
Methods: We used EMS mutagenesis to find supressors of the crl mutant. Suppressors were phenotyped at the cellular and molecular (transcriptome) level, and OEP80 complex formation was investigated in the WT and crl mutant background.
Results: a mutation in OEP80 fully restores the phenotype of the crl mutant,  at the whole plant level, as well as at the cellular or transcriptome level

overall_design: 3 biological replicates of RNA-seq from plantlets of WT, crl, and crloep80 suppressor mutants

first: Ryo

last: Yoshimura

first: Yasushi

last: Yoshioka

first: Moussa

last: Benhamed

first: Sanchari

last: Sincar

first: Cécile

last: Raynaud


title: Distinct RNA-RNA spatial interaction sub-networks of tran-scription factors in human hepatoma cells

status: Public on Jan 12 2025

city: Chengdu

first: yuan

last: Yang

institute: Sichuan Agricultural University

summary: We applied the latest RIC-seq technology to study the RNA-RNA interactions in human liver HepG2 cells. Integrating ChIP-seq data with the RIC-seq data, we clas-sified various transcription factors (TFs) into three distinct clusters based on the spatial interaction levels of the uaRNA (RNA transcribed in promoter regions) and eRNA (RNA transcribed in enhancer regions) potentially transcribed by the TF binding sites.

overall_design: Using RIC-seq technology, we performed high-throughput sequencing of HepG2 cells and integrated publicly available HepG2 datasets to systematically an-alyze eRNA-uaRNA interactions. By combining this analysis with ChIP-seq, we classified 115 transcription factors (TFs) into three distinct clusters. Integrating Hi-C data, and clinical data from liver cancer patients, we further explored the ge-nomic characteristics of these TF clusters and examined their correlation with tumor patient prognosis, shedding light on their potential role in tumor initiation and pro-gression.


title: Genomic, tanscriptomic and metabolimic analyses of Amorphophallus albus provides insights into the evolution and resistance to southern blight pathogen

city: 陕西省

first: longfei

last: duan

address: 陕西杨凌示范区西农路22号

institute: 西北农林科技大学

overall_design: Total RNA was extracted using Trizol reagent (thermofisher, 15596018) following the manufacturer's procedure. The total RNA quantity and purity were analysis of Bioanalyzer 2100 and RNA 6000 Nano LabChip Kit (Agilent, CA, USA, 5067-1511) , high-quality RNA samples with RIN number > 7.0 were used to construct sequencing library.

first: baofu

last: qin

first: chuan

last: shen


title: Pyrimidine synthase CAD deamidates and inactivates p53

city: shanghai

first: tan

last: zizheng

address: songhu road

institute: Fudan university

summary: p53, a critical tumor suppressor, regulates the cell cycle in response to DNA damage and metabolic changes. While p53 stability and activity are predominantly governed by post-translational modifications, the role of deamidation in modulating p53 function remains unclear. This study demonstrates that 6-diazo-5-oxo-L-norleucine (DON) inhibits CAD, a glutamine amidotransferase, to block p53 deamidation, thereby activating the p53 signaling pathway and suppressing tumor cell proliferation. Metabolomic analyses confirmed that DON inhibits CAD-mediated pyrimidine biosynthesis, but this metabolic disruption is not the primary driver of p53 activation. CAD deamidates p53 at N235 and N239, impairing its transcriptional activity and promoting tumor growth. DON restores p53 function by inhibiting CAD’s deamidase activity. Clinical data revealed elevated CAD expression in tumors with wild-type TP53, correlating with poor patient survival. Our findings uncover a novel mechanism by which CAD suppresses p53 activity via deamidation and propose that DON treatment may benefit cancer patients with wild-type TP53 and high CAD expression.

overall_design: To investigate the impact of DON on gene expression in HCT116 cells, we treated the cells with DON, using DMSO as a control. RNA sequencing (RNA-seq) was then performed, followed by data analysis to compare the differential expression of genes between the two groups.

first: Qi

last: Yue

first: Tan

last: Zizheng

first: Chen

last: Hanyu

first: Xiao

last: Ziqi

first: Zhang

last: Liang

first: Wu

last: Boxuan

first: Liu

last: Chennan

first: Gao

last: Yunqian

first: Yang

last: Xueyan

last: Lingqian

first: Lu

last: Lei

first: Wang

last: Hongyan


title: Microbial-derived Hyodeoxycholic Acid Ameliorates Painful Diabetic Neuropathy by Modulating Dorsal Root Ganglion TLR4-Mediated Neuroinflammation Signaling Pathway

city: Beijing

first: Jing

last: Yang

address: No. 49, North Garden Street, Haidian District, Beijing

institute: Peking University Third Hospital

summary: To explore the mechanism underlying the PDN, we performed transcriptome analysis via RNA-seq on dorsal root ganglion from control and PDN rats.

overall_design: We performd gene expression profiling analysis using data obtained from RNA-seq of 3 control rats and 3 PDN rats.


title: Nuclear-localized HKDC1 promotes hepatocellular carcinoma through phosphorylating RBBP5 to activate H3K4me3 [RNA-Seq]

city: Hefei

first: Ling

last: Ye

address: 443 Huangshan Road

institute: University of Science and technology of China

summary: Histone methyltransferases KMT2A (also known as mixed lineage leukemia 1, MLL1) can convert H3K4me1 to H3K4me2 with limited activity. However, it fully trimethylates H3K4 when associated with core subunits, including WDR5, RBBP5, ASH2L, and DPY30. We demonstrated that HKDC1 binds and phosphorylates RBBP5, promoting the assembly of MLL1 complex and the activating H3K4me3. Consequently, HKDC1 transcriptionally activates gene expression. We used CUT&Tag to study H3K4me3 levels of the promoter regions regulated by HKDC1 and RBBP5. Here, we also performed RNA-seq assay in PLC cells with HKDC1 or RBBP5 knocked down to study the role of HKDC1 and RBBP5 in regulating gene expression.

overall_design: We performed RNA-seq in PLC cells in wich HKDC1 or RBBP5 was knocked down to address whether HKDC1 and RBBP5 regulates gene expression.

first: Shengqi

last: Shen

first: Huafeng

last: Zhang

first: Ping

last: Gao


title: Spatial characterization of sex differential regulations in kidney across lifespan

city: Saint Louis

first: Li

last: Ding

address: 660 S Euclid Ave

institute: Washington University in St Louis

summary: There is a clear sex bias in the incident rates and progressions of many kidney diseases and kidney cancers. To obtain a comprehensive understanding of the genetic and epigenetic regulation of kidney sexual dimorphism, we integrated single nucleus RNA and ATAC sequencing (snRNA-Seq and snATAC-Seq) and Visium spatial transcriptomics (ST) data to build a spatially resolved cell-type-specific molecular atlas for the mouse kidney throughout the lifespan, from embryo, newborn, youth, adolescence, adult to old age, of both sexes. We demonstrate that proximal tubules (PT) have the most sex-biased differentially expressed genes (DEGs) (164 and 227 for male and female respectively), which appear after 3 weeks of age and are associated with hormonal regulations. Notably, we reveal the potential mechanism of indirect and direct involvement of estrogen and androgen, respectively, in sex-biased gene expression regulations in the kidney. Specifically, regulon analysis shows that a set of female-biased DEGs, including Socs2, might be indirectly regulated by estrogen through prolactin-induced Jak2/Stat5 activation. On the other hand, chromatin accessibility investigation identifies androgen receptor motifs as significantly enriched in males, might be directly involved in regulating male-biased DEGs, such as Slco3a1, Serpinf2, Slc7a13, Slc22a30, Cyp4b1, and Acsm2. Sex-biased DEGs identified from mice, including several not previously highlighted, were validated by immunofluorescence and multiplex imaging data in human kidneys. Moreover, older male mice (92 weeks) display more aging-related gene alterations in loops of Henle and PTs, while older females have more aging-related gene alterations in fibroblasts. Our results provide the community with rich resources and better understanding of spatially resolved gene expression and hormone regulation for sexual dimorphism in the kidney across the lifespan.

overall_design: C57BL/6J mice were originally purchased from the Jackson Laboratory. Mouse kidneys were collected at embryos (E16.5), newborns (P0), 3 weeks (W3), 12 weeks (W12), 52 weeks (W52), and 92 weeks (W92). To get E16.5 kidneys, 4 female mice and 1 male mouse were grouped for mating on day 1 at 5 pm. Then the male was removed from the females on day 2 at 10 am. Day 2 was designated as E0.5 for any pregnant females. For kidneys collected from other ages, mice were purchased from the Jackson Laboratory. Mice at E16.5 and P0 were euthanized by decapitation. Older mice were euthanized by carbon dioxide asphyxiation. For each mouse, one kidney was embedded in optimal cutting temperature compound (OCT) and the other one was fixed in 10% neutral buffered formalin (Epredia, 5725) then embedded in paraffin. For Visium ST, 10 μm mid-sagittal OCT sections were used on the 10x Genomics Visium platform; for snRNA-Seq and snATAC-Seq, pooled snap-frozen tissues were used for E16.5 and P0 mice, and 300 μm of mid-sagittal OCT sections were used for mice from W3 to W92. All animal experiments were approved by the Washington University in Saint Louis Institutional Animal Care and Use Committee (IACUC) office.

first: Ruiyang

last: Liu


title: Analysis of miRNA expression in urine of Hirschsprung's disease (HSCR) patients

city: Mannheim

first: Carolina

last: Delatorre

address: Theodor-Kutzer-Ufer 1-3

institute: University Heidelberg

summary:
Urine miRNA signature as potential non-invasive diagnostic biomarker for Hirschsprung’s Disease (HSCR):
Unfortunately, HSCR diagnosis remains a challenge: current diagnostic methods are too invasive and difficult to conduct and to interpret. We designed this study in urine with the aim of identifying a non-invasive biomarker, which undoubtfully, would be a more convenient method for both babies and parents in the future.

overall_design: We collected urine from 5 HSCR patients and 5 Controls (healthy volunteers), extracted miRNA and analyzed in microarrays

first: Abhijit

last: Sreepada

first: Rasul

last: Khasanov

first: Enas

last: Zoheer Elkrewi

last: de la Torre

first: Judith

last: Felcht

first: Ahmad

last: Al Abdulqader

first: Richard

last: Martel

first: Nicolas

last: Hoyos

first: Michael

last: Boettcher

first: Lucas

last: Wessel

first: Karl-Herbert

last: Schäfer

first: María

last: Ángeles Tapia-Laliena


title: Nuclear-localized HKDC1 promotes hepatocellular carcinoma through phosphorylating RBBP5 to activate H3K4me3

first: Ling

last: Ye

summary: Histone methyltransferases KMT2A (also known as mixed lineage leukemia 1, MLL1) can convert H3K4me1 to H3K4me2 with limited activity. However, it fully trimethylates H3K4 when associated with core subunits, including WDR5, RBBP5, ASH2L, and DPY30. We demonstrated that HKDC1 binds and phosphorylates RBBP5, promoting the assembly of MLL1 complex and the activating H3K4me3. Here, we used CUT&Tag to study H3K4me3 levels of the promoter regions regulated by HKDC1 and RBBP5. We knocked down HKDC1 or RBBP5 in PLC cells and performed CUT&Tag assay.

overall_design: We performed CUT&Tag-sequceing for H3K4me3 in PLC cells in wich HKDC1 or RBBP5 was knocked down to address whether HKDC1 and RBBP5 regulates the H3K4me3 levels of the promoter regions.

first: Shengqi

last: Shen

last: Zhang