title: Single-cell transcriptional profiling of lung immune cells after naphthalene club cell injury in adult C57 Bl/6 mice with temporal resolution

city: Boston

first: Irene

middle: Gar-Ling

last: Wong

address: 1 Blackfan St.

institute: Boston Children's Hospital

summary: The aim of this study was to study tissue-wide responses to club cell airway injury.

overall_design: Examination of the transcriptional changes in lung immune cells at various timepoints after naphthalene-mediated airway injury.

first: Carla

middle: F

last: Kim


title: Single cell RNA-seq analysis reveals the crucial role of Collagen triplex helix repeat containing-1 (Cthrc1) cardiac fibroblasts for ventricular remodeling after myocardial infarction

status: Public on Dec 15 2025

city: Pamplona

first: Núria

last: Planell

address: Pio XII, 55

country: Spain

institute: CIMA - UNAV

type: Expression profiling by high throughput sequencing

summary: Cardiac fibroblasts have a central role during the ventricular remodeling process associated to different types of cardiac injury. Recent studies have shown that fibroblasts do not respond homogeneously to heart damage, suggesting that the adult myocardium may contain specialized fibroblast subgroups with specific functions. Due to the limited set of bona fide fibroblast markers, a proper characterization of fibroblast population dynamics in response to cardiac damage is still missing. Using single cell RNA-seq we have identified and characterized a fibroblast subpopulation that emerges in response to myocardial infarction (MI) in a murine model. These activated fibroblasts exhibit a clear pro-fibrotic signature, and localize to the wounded myocardium. Combining epigenomic profiling with functional assays, we unveil important candidate regulators mediating their response to cardiac damage.

overall_design: Time-course of study of cardiac fibroblasts after myocardial infarction. Samples include 3 and 5 days after myocardial infarction.

first: Silvia

middle: C

last: Hernandez

first: Juan

middle: P

last: Romero

first: Marina

last: Ainciburu

first: Nuria

first: Amaia

last: Vilas-Zornoza

first: Patxi

last: San Martin-Uriz

first: Elena

last: Iglesias

first: Gloria

last: Abizanda

first: Diego

last: Alignani

first: David

last: Gomez-Cabrero

first: Adrian

last: Ruiz-Villalba

first: Felipe

last: Prosper


title: Role of CTGF-LRP1 in Impaired Healing of Cesarean Section Incisions

city: Shanghai

first: Chuqing

last: He

address: No. 910, Hengshan Rd

department: Department of Obstetrics and Gynecology

country: China

institute: School of Medicine, Shanghai Jiaotong University

summary: Niche is a long-term complication following a cesarean section, which may increase the risk during subsequent pregnancies, and its pathogenesis remains incompletely understood. In this study, we utilized single-cell RNA sequencing to analyze 43,384 individual cells obtained from adjacent myometrium tissue of the niche (Adjacent), well-healed cesarean scar tissue (Control), and niche tissue (Niche). Our analysis revealed that fibroblasts (FB) could be classified into three subgroups. FB3 in the Niche exhibited a reduced capacity for extracellular matrix synthesis. Cell communication analysis has identified that the secretion of CTGF by Endo3 and the expression of LRP1 by FB3 are involved in the receptor-ligand interaction of uterine fibroblasts during wound healing. Our research findings were supported by tissue staining and in vitro experiments, indicating that silencing LRP1 may prevent CTGF from promoting the synthesis of extracellular matrix by primary uterine fibroblasts. Furthermore, animal models have indicated that CTGF can promote the healing of uterine scars. These results provide insights into the cellular environment and mechanistic background underlying the formation of the uterine niche and poor wound healing following a cesarean section, laying the groundwork for future investigations into therapeutic approaches for the uterine niche.

overall_design: In this study, we utilized single-cell RNA sequencing to analyze 43,384 individual cells obtained from adjacent myometrium tissue of niche (Adjacent), well-healed cesarean scar tissue (Control), and niche tissue (Niche).

first: Xiaoya

last: Zhao

first: Qian

last: Zhu

first: Jian

last: Zhang


title: Open chromatin, HIF binding and mRNA expression analysis in primary tubule and ccRCC cells [RNA-seq]

city: Aachen

first: René

last: Krüger

address: Pauwelsstraße 20

department: Institute for Stem Cell Biology

country: Germany

institute: RWTH Aachen University Medical School

summary: Inactivation of the von Hippel-Lindau tumor suppressor leads to stabilization of HIF transcription factors and subsequent oncogenic HIF-2 signaling in ccRCC. However, little is known about the transcriptional mechanisms leading to dysregulation of HIF-2α mRNA in renal cancer. Epigenetic analysis of the EPAS1 locus (coding for HIF-2α) using ATAC-seq, ChIP-seq and RNA-seq revealed an oncogenic enhancer that maintains a HIF-dependent feed-forward circuit of HIF-2α regulation in renal tumor cells.

overall_design:
This study consists of ATAC-seq, ChIP-seq, CUT&Tag-seq and RNA-seq samples from primary tubular and primary ccRCC cells as well as genetically modified 786-0 and RCC4 cells.

***************************************************************
Access to unprocessed raw data of primary cells is restricted to protect the privacy and intent of research participants consistent with the informed consent agreements provided by individual research participants.
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first: Johannes

last: Schödel

first: Stephanie

last: Naas


title: Open chromatin, HIF binding and mRNA expression analysis in primary tubule and ccRCC cells [CUT&Tag]

type: Genome binding/occupancy profiling by high throughput sequencing

overall_design: This study consists of ATAC-seq, ChIP-seq, CUT&Tag-seq and RNA-seq samples from primary tubular and primary ccRCC cells as well as genetically modified 786-0 and RCC4 cells.


title: Open chromatin, HIF binding and mRNA expression analysis in primary tubule and ccRCC cells [ChIP-seq]


title: Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [ATAC-Seq]

city: TORONTO

first: Xin

last: Xu

state: Ontario

address: 101 COLLEGE ST EAST TOWER 11-601D

country: Canada

institute: Princess Margaret Cancer Center

summary: To investigate the molecular role of CHD9 in prostate cancer, we knockdown CHD9 gene by two different shRNAs in 22Rv1 cells.

overall_design: Differential gene expression analysis of RNA-seq data for KD control cells and KD CHD9 cells

first: Yujuan

last: Wang

first: Helen

first: Housheng

middle: H


title: Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [ChIP-Seq]


title: RNAseq of proximal small intestine scrapings of mice fed a galactose, glucose, or lactose-containing diet during postweaning

city: Wageningen

first: Evert

middle: M.

last: van Schothorst

address: De Elst 1

country: Netherlands

institute: Wageningen University

summary: Gene expression profiles from mouse intestinal scrapings fed with either a glucose (n=13), galactose (n=13), or lactose-containing diet (n=13) were prepared. The mice were fed the isocaloric intervention diets during the postweaning period (postnatal days PN21-PN42) and sacrificed at PN42 in the fed state. Differential gene expression analysis reveals a clear effect of galactose consumption on metabolic pathways, especially fatty acid metabolism.

overall_design: Nutritional intervention study for 3 weeks ad libitum feeding isocaloric diets differing only in type of part of the dietary carbohydrate composition: 32en% glucose, 16en% galactose + 16en% glucose, or 32en% lactose, on a background of 32en% starch and 3en% fructose. All diets had the same 20en% proteins and 20en% fats.

first: Ferran

middle: S

last: Fos-Codoner

middle: M

first: Jaap

last: Keijer


title: MCF-7 ESR1 drug response

city: South San Francisco

first: Marc

last: Hafner

state: CA

address: Building 45-1, 1 DNA Way

department: Oncology Bioinformatics

country: USA

institute: Genentech

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

overall_design: Refer to individual Series


title: MCF-7 ESR1 drug response scRNA

summary: To investigate the effect of single and combination treatments in breast cancer, we performed transcriptome profiling using scRNAseq

overall_design: MCF7 parental and MCF7 with ESR1 mutation cells were treated with single and combination treatments at multiple time points, hashed with lipid modified oligos and profiled with scRNAseq

first: Diana

last: Wu

first: Jenille

last: Tan

first: Russell

last: Xie


title: Gene expression signatures for mouse organ aging

city: Kyoto

first: Masahiro

last: Kameda

state: Kyoto

address: Sakyoku Shougoin Kawaramati 54

department: Geriatric Unit

country: Japan

institute: Kyoto University Hospital

summary: We asseced gene expression profiles in 4 organs including lung, liver, kidney and white adipose tissue between 10 week (n=3) old and 90 week old mice (n=3).

overall_design: Each organs of C57BL/6J mice male mice were collected. Total RNA of each organ was extracted and microarray data analysis was performed.

first: Hiroshi

last: Kondoh

first: Takumi

last: Mikawa


title: Immune polarization of type 1 and type 2 human eosinophils

city: Scottsdale

first: Elizabeth

middle: A.

last: Jacobsen

state: AZ

address: 13400 E. Shea Blvd.

institute: Mayo Clinic

summary: Eosinophils have specific immune phenotypes in type 2 and type 1 environments both in vitro and in translational models of disease in vivo. RNA sequencing was completed on human blood eosinophils cultured with cytokines that represent a Th2 (IL-33, IL-4, GM-CSF) or Th1 (TNFα/IFNγ)-associated environment cytokines.

overall_design: Eosinophils were isolated from the blood of  otherwise healthy human donors (no allergy, atopy, pregnancy, 0r autoimmunity) and cultured for 18 hrs in different conditions prior to RNA isolation for RNA sequencing. Eosinophils were cultured at 2 million cells per ml in standard RPMI-1640+10% FBS + 1X streptomycin-penacllin-glutamine and split into three conditions: E0: [IL-5 (1ng/mL)], E1: [IL-5 (1ng/mL)+ TNF-alpha (15ng/mL) + IFN-gamma (15ng/,L);  E2: [ Il-5 (1ng/mL) +IL-4 (10ng/mL )+ GM-CSF (10ng/mL) + IL-33 (50ng/mL) for 18 hrs and then isolated for RNA and RNA sequencing.


title: Immune polarization of type 1 and type 2 mouse eosinophils

summary: Eosinophils have specific immune phenotypes in type 2 and type 1 environments both in vitro and in translational models of disease in vivo. RNA sequencing was completed on mouse blood eosinophils cultured with cytokines that represent a Th2 (IL-33, IL-4, GM-CSF) or Th1 (TNFα/IFNγ)-associated environment cytokines.

overall_design: Eosinophils were isolated from the blood of IL-5 Tg mice (NJ.1638) and cultured for 18 hrs in different conditions prior to RNA isolation for RNA sequencing. Eosinophils were cultured at 5 million cells per ml in standard RPMI-1640+10% FBS + 1X streptomycin-penacllin-glutamine.  One experiment included duplicates of control eosinophils (CN) has no cytokines added conducted at the same time as eosinophils (E1) were cultured with 15ng/mL IFN-gamma and TNF-alpha. A second experiment included duplicates of IL-5 eosinophils (E0) were cultured with IL-5 10 ng/mL and eosinophils  (E2) were cultured with 10ng/ml of IL-5, GM-CSF, IL-4 and 30ng/mL IL-33.

middle: A


title: Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [RNA-Seq_shKD]

last: Zhu

last: He


title: Open chromatin, HIF binding and mRNA expression analysis in primary tubule and ccRCC cells [ATAC-seq]

first: René

last: Krüger

first: Johannes

last: Schödel


title: Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [CRISPR screen_22Rv1]

first: Xin

last: Xu

summary: In this study, we used a targeted CRISPR/CasRx-METTL3 screen to identify m6A peaks that are critical for prostate and lung cancers.

overall_design: The CRISPR screen employed in our pooled sgRNA library consisted of ~12,045 sgRNAs targeting m6A peaks in prostate cancer and lung cancer patients, with 5 sgRNAs per gene on average. The sgRNAs were designed using the "cas13design". Stable dCasRx-METTL3-expressing 22Rv1 cell line was generated. dCasRx-METTL3-expressing 22Rv1 cell line was infected with the library at an MOI of ~ 0.3 and coverage of 400x. 24h post-infection, cells were selected with blasticidin for 5 days and part of cells were sujected to DNA extraction as day 0. Other cells were cultured in dish for ~16 days (day 16), maintaining 400x coverage prior to our screening assay. Genomic DNA was extracted from replicate samples and sgRNA inserts were amplified by PCR. The input amount of genomic DNA was calculated to achieve 400x coverage of the library and resulting libraries were sequenced on an Illumina HiSeq500.


title: Single-cell multi-omics identify novel regulators required for the increase of osteoclastogenesis during aging

first: Junjie

last: Gao

address: 600 Yishan Road

institute: Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine

summary: The single-cell multi-omics data analysis revealed that aging substantially promotes the differentiation of osteoclasts.

overall_design: WT and Terc knock-out mice were included in this study

first: Changqing

last: Zhang


title: MCF-7 ESR1 drug response bulk RNA

summary: To investigate the effect of single and combination treatments in breast cancer, we performed transcriptome profiling using bulk RNAseq

overall_design: MCF7 parental and MCF7 with ESR1 mutation cells were treated with single and combination treatments at multiple time points and collected for profiling with bulk RNAseq


title: Comparison by microarray analysis between control and Nutlin 3b treatment in human senescent cells

city: Kyoto City

address: 54 Kawaharacho, Shogoin, Sakyo-ku

department: Graduate School of Medicine

institute: Kyoto University

summary: We found that an aberrant interaction between glycolytic PGAM1 and Chk1 kinase is augmented in senescent cells. Chemical abrogation of PGAM1-Chk1 binding by Nutlin 3b blocks its interaction, followed by elimination of senescent cells, senolysis. To examine the molecular mechanism of senolysis by inhibition of PGAM1-Chk1 binding, transcriptomic analysis was performed.

overall_design: Profiles for gene expression in Ras-induced senescent IMR90 cells was measured at 48 hours with or without Nutlin 3b treatment. Three biological independent samples were prepared in each groups.


title: Time-course analysis of gene expression of HT29 human colon cancer cells incubated with Methotrexate

city: Barcelona

first: Carlos

middle: J

last: Ciudad

state: Barcelona

address: Av. Juan XXIII-27

department: Biochemistry and Molecular Biology

institute: University of Barcelona

summary:
We had previously analyzed the gene expression changes observed in HT29 colon cancer cells resistant to Methotrexate (MTX). Now, we explored the expression changes produced by short term incubation with MTX
HT29 cells were incubated with 70 nM Methotrexate for 0, 8, 24 and 48 h, RNA extracted and Affymetrix Exon microarrays performed to determine gene expression

overall_design: The HT29 human colon cancer cell line sensitive to methotrexate was used in the study. 12 samples are provided, which correspond to triplicates of 4 experimental conditions. The conditions were cells incubated with 70 nM MTX for 0,8,24 and 48 h. The platform used was:  Affymetrix.ExonExprChip.HuGene-1_0-st-v1 (na31_hg19_2010-09-03)

first: Veronica

last: Noe

first: Nuria

last: Mencia


title: Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer

overall_design: Refer to individual Serieshttps://submit.ncbi.nlm.nih.gov/geo/submission/update/?acc=GSE242447

first: Yujuan

last: Wang

first: Helen

first: Housheng


title: Transcriptional profiling of liver biopsies of precancerous viral hepatitis patients

city: Antwerpen

first: Nicolaas

last: Van Renne

address: Universiteitsplein 1

country: Belgium

institute: Laboratory of Experimental Medicine and Pediatrics (LEMP)


title: Regulation of adipogenesis via caveolin-1 in adipose derived mesenchymal stem cells

city: Parkville

first: Matthew

last: Ritchie

state: Victoria

address: 1G Royal Parade

country: Australia

institute: The Walter and Eliza Hall Institute of Medical Research

summary: Using human adipose derived mesenchymal stem cells (ASCs) as a model system, we identified caveolae forming structural protein, caveolin-1 (CAV1) as a key component that limits adipogenic differentiation of ASCs. Using whole transcriptomic analysis by RNA sequencing, we show that lentiviral over expression of human CAV1 gene in ASCs significantly inhibits adipogenesis as evident by inhibition of adipogenic gene network, and conversely, RNAi driven knockdown of endogenous CAV1 significantly promoted adipogenesis.

overall_design: Cells were seeded in 12-well plate (11,000 cells/cm2) in duplicate in growth medium for 24 hr followed by transduction with CAV-1, GFP and shRNA expressing lentiviruses individually in the presence of 4 μg/mL polybrene. Un-transduced ASCs were used as a control. Four days of post-transduction RNA was isolated and, was subjected for RNA-sequencing.

first: Nadeeka

last: Bandara

middle: E

first: Wayne

last: Morrison

first: Ramin

last: Shayan

first: Tara

last: Karnezis

first: Mei

middle: R

last: Du


title: LEFKOTHEA modulates gene expression at the transcriptional and post-transcriptional levels during early light response

status: Public on Dec 14 2025

city: Athens

first: Anastasios

last: Alatzas

address: IERA ODOS 75

country: Greece

institute: Agricultural University of Athens

summary: Light is the source of energy for photosynthetic organisms such as plants. Due to the great significance of light in the regulation of development, plants possess a sophisticated signaling network that controls light response including a massive gene expression reprogramming as well as post-transcriptional mechanisms such as alternative splicing. LEFKOTHEA is a nucleus-encoded splicing factor found in both the nucleus and chloroplast and its nuclear compartmentalization ensures the early embryonic development in Arabidopsis. LEFKOTHEA gene mutations (lefko1, an EMS mutant allele exhibiting aberrant nuclear partitioning and an albino cotyledon phenotype, and lefko2, a severe allele that results in embryo developmental arrest) have defects in splicing of nuclear and chloroplast genes. Time-series transcriptomic analysis upon light encounter revealed an aberrant response to light in lefko1, characterized by down-regulation of genes involved in photosynthetic apparatus and signal transduction pathways. Further, LEFKOTHEA significantly affects the number and the mode of alternative splicing events during light response. A majority of such events occur on spliceosomal components, light-related transcription factors and genes involved in signal transduction. Altogether, the results indicate that LEFKOTHEA is an active component of early light response signaling, regulating gene expression both transcriptionally and post-transcriptionally.

overall_design: RNAseq profiling of dark-grown Arabidopsis wild-type and lefko1 mutant seedlings upon light encounter in a time-series experiment

first: Despina

last: Samakovli

first: Loukia

last: Roka

first: Konstantinos

last: Panagiotopoulos

first: Gerasimos

last: Daras

first: Dimitra

last: Milioni

first: Stamatis

last: Rigas

first: Kosmas

last: Haralampidis

first: Polydefkis

last: Hatzopoulos


title: RNA-seq data of liver tissues from Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model

city: Beijing

first: Weixuan

last: Wang

address: No. 38 Xueyuan Road, Haidian District

institute: Peking University

summary: RNA-seq was performed on liver tissues from Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model. The study aims to characterize gene expression changes associated with hepatic inflammatory responses in the absence of BICD2.

overall_design: Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model. Liver tissues were harvested 2 weeks after the last immunization. Total RNA was extracted and subjected to high-throughput sequencing.

first: Wenyu

last: Tian

first: Dan

last: Lv


title: Enterocloster citroniae and related gut microbiome species modulate Vibrio cholerae biofilm formation through the production of bioactive small molecules

city: Lawrence

first: Luis Caetano

last: Antunes

state: KS

address: 1200 Sunnyside Avenue

institute: University of Kansas

summary: Cholera is a deadly diarrheal disease that affects millions of people globally. Although V. cholerae, the causative agent of the disease, has been extensively studied in isolation, it was relatively recently that scientists started investigating its interactions with the gut microbiota. Our group and others previously showed that microbiota-derived metabolites significantly influence V. cholerae behavior. By investigating how an organic extract of human feces affects V. cholerae gene expression, we recently showed that gut metabolites strongly suppress swimming motility, a virulence factor important for host colonization. Interestingly, extracts of pure cultures of a single gut commensal, Enterocloster citroniae, recapitulated this inhibitory effect. Here, we present a comprehensive examination of the effect of small molecules produced by E. citroniae and related species on V. cholerae behavior. We show that E. citroniae small molecules inhibit motility by various V. cholerae strains. We also show that several phylogenetically related species produce this activity, although the magnitude of the effect varies between strains. Using biofilm formation assays in static and shear flow conditions, we show that V. cholerae strongly induces biofilm formation in response to E. citroniae metabolites. Transcriptome and reporter analyses show that several genes involved in the synthesis of an extracellular polysaccharide are induced by growth in the presence of E. citroniae metabolites. Lastly, we show that V. cholerae interactions with host epithelial cells are also modulated by compounds produced by this commensal. These findings advance our understanding of microbiome-pathogen interactions and how commensal bacteria influence V. cholerae virulence through the production of small molecules. In the future, this knowledge may be used to design novel microbiome-based therapeutic approaches to combat cholera and other infections.

overall_design: RNA-seq profiles of Vibrio cholerae C6706 grown in the absence or presence of an organic extract of Enterocloster citroniae WAL17108 cultures.

first: Antunes

middle: L

last: Caetano


title: Inflammation-induced lncRNA SNHG1 Orchestrates Spermatogonium Development in Non-obstructive Azoospermia via IL-17A Signaling Pathway

city: Guangzhou

first: Rui

last: Hua

state: GuangDong

address: 838 Guangzhou North Avenue

institute: Nanfang Hospital, Southern Medical University

summary: Non-obstructive azoospermia (NOA) is a critical subtype of male infertility associated with inflammation. However, the molecular mechanisms underlying this phenomenon remain poorly understood. This study investigated the role of the inflammation-activated long non-coding RNA SNHG1 in NOA pathogenesis. Using lipopolysaccharide (LPS)-induced orchitis mouse models and spermatogonium cell lines (GC-1 spg and TCAM-2), we observed that both SNHG1 and the transcription factor SP1 were significantly upregulated, correlating with spermatogonium proliferation and loss of stemness. Mechanistically, SP1 directly binds to and transcriptionally activates the SNHG1 promoter, whereas SNHG1 knockdown rescued LPS-induced spermatogonium dysfunction without affecting SP1 expression. RNA-seq revealed that SNHG1 overexpression activated the IL-17A signaling pathway. Notably, IL-17A receptor blockade (Brodalumab) reversed the SNHG1-mediated proliferation arrest and stemness. Our findings demonstrated that the SP1-SNHG1-IL-17A axis drives inflammatory spermatogenic failure, suggesting that IL-17A inhibition is a potential therapeutic strategy for NOA.

overall_design: RNA-seq profiling of Vector-control and SNHG1-overexpressing GC-1 spg cells at 24 hours post-transfection.

first: Yongtong

last: Zhu

first: Maocai

last: Li

first: Xiaomin

last: Zhan

first: Li

last: Liu

first: Cairong

last: Chen

first: Yao

last: Zhou

first: Pei

last: He


title: Fat mass and obesity-associated (FTO)/SOCS6-m⁶A axis epigenetic modification links obesity to atopic dermatitis by regulating keratinocyte function

city: Changsha

first: Zeng

last: Jinrong

address: No.138 Tongzipo Rd, Yuelu District, Changsha, Hunan, China, 410013

institute: the Third Xiangya Hospital, Central South University

summary: Atopic dermatitis is one of the severe skin diseases. Keratinocytes, as the epidermal barrier cells, are an important component for maintaining the skin barrier function. In this dataset, we have included the m⁶A methylation RNA data obtained from normal human keratinocytes (N group) and keratinocytes from patients with atopic dermatitis (AD group).

overall_design: We generated the following comparisons using Fold-change (FC) ≥ 1.5 or ≤ 0.5, and p < 0.05 were used to identify the differentially m6A methylated RNAs.The total RNAs were immunoprecipitated with anti-N6-methyadenosine (m6A) antibody. The modified RNAs were eluted from the immunoprecipitated magnetic beads as the “IP”. The unmodified RNAs were recovered from the supernatant as “Sup”.  Two channel arrays were used for these samples but the data were analyzed as single-channel so that each sample  represents either IP or supernatent and the sample table includes the normalized signal values.

first: Fugang

last: Xiao

first: Jinrong

last: Zeng


title: scRNA-seq data of hepatic immune cells isolated from Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model

summary: To determine the changes in liver immune cells upon hepatic Bicd2 deficiency, we performed scRNA-seq to analyze the hepatic immune microenvironment in  Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model.

overall_design: Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model. To obtain hepatic immune cells, liver tissues were minced and grinded in pre-cold FACS buffer (PBS containing 1% FBS), followed by filtration through a 70 μm cell strainer. Lymphocytes were isolated through 40/70% Percoll (Cytiva, Cat# 17089109) by gradient centrifuging 800 × g for 20 min. Cells located at the inter-layer were collected. After removing red blood cells resuspended with ACK lysis buffer, living cells were sorted and pooled using the 10× Genomics platform and sequenced on an Illumina NextSeq sequencer.


title: study on the role and mechanism of SOCS6 in keratinocytes

summary: Atopic dermatitis is a severe skin disorder. Keratinocytes, as the epidermal barrier cells, are an important component in maintaining the skin barrier function. The role of SOCS6 in keratinocytes is still unclear. In this dataset, we extracted keratinocytes from the foreskin tissue of healthy individuals and conducted mRNA sequencing data for SOCS6 knockdown (KD) and overexpression (OE).

overall_design: Knockdown and overexpression of SOCS6 were respectively compared with the control group to explore the effect of SOCS6 on keratinocytes.


title: Cancer cells transfer invasive properties through microRNAs contained in collagen-tracks

city: Orsay

first: Kevin

last: MOREAU

address: Rue Henri Becquerel – CS 90030

country: France

institute: CNRS

summary: Invasion is a prerequisite for metastasis formation. During tumor development, type I collagen overexpression increases tumor microenvironment stiffness, facilitating cancer cell dissemination. During breast cancer cell migration in 2D and 3D matrices, we observed membrane debris left behind, attached to the collagen fibrils, along the migration path. We named these structures collagen-tracks. Their formation is stimulated by the interaction between the extracellular matrix (ECM) and matrix receptors, such as the discoidin-domain receptor 1 (DDR1). They present a specific nucleic acid and protein contents. When deposited by highly invasive breast cancer cells, internalized collagen-tracks reprogram non-invasive cells into highly pro-metastatic ones by inducing a partial epithelial–mesenchymal transition (EMT) associated with an increase in ECM degradation and cell invasiveness. This cell reprogramming is dependent on specific miRNAs identified in the collagen-tracks. Collagen-tracks thus represent a new form of cell-cell communication important for driving tumor invasion that could be targeted to prevent metastasis.

overall_design: RNA-seq profiling of MCF7 (WT) on collagen and MCF7 with collagen-tracks on collagen after 72H

first: Frederic

last: Saltel

first: Lucile

last: Rouyer

first: Léa

last: Normand

first: Elodie

last: Richard

first: Nathalie

last: Allain

first: Julie

last: Giraud

first: Sylvaine

last: Di-Tommaso

first: Anne-Aurélie

last: Raymond

first: Cyril

last: Dourthe

first: Jean-William

last: Dupuy

first: Kévin

last: Moreau

first: Richard

last: Iggo

last: Dugot-Senant

first: Gaetan

last: MacGrogan

first: Anthony

last: Bouter

first: Sisareuth

last: Tan

first: Alexandre

last: Favereaux

first: Violaine

first: Reini F.

last: Luco

first: Manon

last: Ros


title: Function and mechanism of PAPOLA-mediated poly(A) lengthening in leukemia (mouse)

first: Siyao

last: Guo

address: No.58 Zhongshan Er Road

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

summary: The polyadenylation of mRNA is pivotal for mRNA stability and efficient mRNA translation. The length of poly(A) tail is dynamically changed under various physiological conditions; however, the functions and mechanisms of aberrant poly(A) length control in cancers remain poorly understood. Here we uncovered the aberrant lengthening of poly(A) tail and particularly upregulated expression of poly(A) polymerase alpha (PAPOLA) in acute myeloid leukemia (AML), and the elevated PAPOLA expression significantly correlated with unfavorable AML outcomes. We further demonstrated the critical oncogenic functions of PAPOLA-mediated poly(A) lengthening in promoting AML leukemogenesis and leukemia stem cell self-renewal using human primary AML samples, AML cells and various mouse leukemogenesis models. Mechanistically, we identified GSTM2 as a key downstream target of PAPOLA that regulated metabolic reprogramming through the HNE-DLD axis to promote AML initiation and progression. Moreover, PAPOLA inhibitor cordycepin effectively blocked metabolic reprogramming and AML leukemogenesis in vivo. Overall, our study uncovers the novel functional link between aberrant poly(A) lengthening and cellular metabolic reprogramming in AML, and provides a molecular basis for development of an effective therapeutic strategy for AML patients.

overall_design: To investigate the function of PAPOLA in the regulation of AML, we established the Papola knockout AML mice.

first: Shuibin

last: Lin


title: NGLY1-dependent conversion of N-glycosylated N to D is essential for transcription of proteasome genes

city: Tokyo

first: Yukiko

last: Yoshida

address: 2-1-6, Kamikitazawa, Setagaya-ku

department: Department of Basic Medical Sciences

institute: Tokyo Motrolopotan Institute of Medical Science

summary: To investigate the sequence editing-specific effects on Nrf1 functions, we utilized glycan-less Nrf1 mutants, 9NA and 9ND, in which all nine of the putative N-glycosylation sites (N-X-S/T; asparagine (N) serine (S), threonine (T), and X is any amino acid except proline) were replaced with alanine (A) and aspartic acid (D), respectively. To comprehensively understand the effects of Nrf1 sequence editing on the transcriptome, microarray analysis was performed on NGLY1-KO HeLa cells stably expressing 9NA and 9ND.

overall_design: Three independent total RNA samples from 20 nM Btz (for 15 h) treated NGLY1-KO HeLa cells without/ with stably expressing 9NA-Nrf1-HA or 9ND-Nrf1-HA were purified.

first: Yasumasa

last: Nishito


title: Glycaemic variability identified as a critical determinant of myocyte dysfunction and risk for myocardial injury in preclinical models of diabetes

city: Brisbane

first: Yuanzhao

last: Cao

state: QLD

address: 306 Carmody Road

department: Institute for Molecular Bioscience

institute: The University Of Queensland

summary: This study evaluates mechanisms of glycaemic stress underpinning cardiovascular risk in diabetes. Using in vitro and in vivo models, we demonstrate that glycaemic variability rather than hyperglycaemia alone is a dominant risk factor for heart muscle dysfunction and myocardial injury sensitivity in diabetes. These findings provide new preclinical models for mechanistic and drug discovery studies and inform strategies for managing cardiovascular outcomes in patients with diabetes.

overall_design: hiPSC-CMs cultured in backbone media conditions or underwent constant and variable glycaemic stress disease modelling, and cells were harvested for RNA preparation and genome-wide RNA sequencing.

first: Woo Jun

last: Shim

first: Nathan

last: Palpant


title: Expression analysis of circD-deleted and WT control liver CSCs

first: He

last: Luyun

address: 15 DaTun Road, Chaoyang District

institute: IBP

summary:
Investigation of differentially expressed genes in circD-deleted liver CSCs
The analysis in this study is according to the description in Wang, Y., et al. 2015. The long noncoding RNA lncTCF7 promotes self-renewal of human liver cancer stem cells through activation of Wnt signaling. Cell Stem Cell 16:413-425.

overall_design: Gene expression profiling using  circD-deleted and WT control liver CSC cells. Total RNA from each sample was quantified using the NanoDrop ND-1000.

first: Luyun

last: He

first: Zusen

last: Fan


title: Acute Neuroinflammation Induces Prolonged Transcriptional Reprogramming in Microglia

city: Seoul

first: Hyungseok

last: Seo

address: Gwannak-ro 1

department: Pharmacy

country: South Korea

institute: Seoul National University

summary: Acute neuroinflammation rapidly activates brain immune responses, but its lasting effects on microglia are unclear. Using systemic LPS administration and LCMV-Armstrong infection, we found that blood–brain barrier disruption and cytokine shifts resolved within 30 days, yet microglial recovery was incomplete—marked by persistent numerical loss and an IFN-γ–low phenotype in the LPS model and reduced relative abundance in the LCMV model. Single-cell RNA sequencing revealed sustained transcriptional alterations, including disease-associated microglia (DAM) features and a distinct recovery-biased population. These acute signatures overlapped with profiles from Alzheimer’s model mice and were enriched in human microglia from multiple sclerosis, Alzheimer’s disease, and other neuroinflammatory conditions. Although our observation period was shorter than the chronic course of these diseases, the persistence of disease-like microglial states suggests that transient inflammation can prime the brain for long-term vulnerability. Targeting this primed state may offer new strategies to prevent or mitigate neurodegenerative pathology.

overall_design: Immune cells (CD45+) isolated from the whole brain of C57BL/6J mice at 3 days or 30 days post injection of LPS (2mg/kg), and 7 days or 30 days post injection of LCMV (2x105 PFU) were sorted on flow cytometry and used for single cell RNA sequencing. For the LPS-treated group, the PBS group served as the control, whereas for the LCMV-treated group, the RPMI group was used as the control.

first: Sehoon

last: Moon

first: Cheol Gyun

last: Kim


title: Function and mechanism of PAPOLA-mediated poly(A) lengthening in leukemia [FLAM-Seq]

overall_design: FLAM-Seq was used to study the changes of poly(A) length in different genes in the PAPOLA knockout and control cells.


title: Function and mechanism of PAPOLA-mediated poly(A) lengthening in leukemia

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

overall_design: Refer to individual Series


title: Targeting eIF4A-dependent translation in soft tissue sarcoma

city: New York

first: Prathibha

last: Mohan

state: NY

address: 1275 York Avenue

department: Cancer Biology and Genetics

institute: Memorial Sloan Kettering Cancer Center

summary: Well-differentiated and dedifferentiated liposarcoma (WD/DDLS), myxofibrosarcoma (MFS), and undifferentiated pleomorphic sarcoma (UPS) are the most common types of genetically complex sarcoma. There is an urgent need to develop effective targeted therapy for the over 50% of patients who eventually die of disease. Despite their genetic complexity, all four sarcoma types rely on the oncogenic translation of Hippo pathway proteins, which requires the RNA helicase eIF4A (DDX2). Pharmacological inhibition of eIF4A using CR-1-31B effectively suppressed tumor growth and induced apoptosis in DDLS, MFS, and UPS patient-derived cell lines and mouse xenografts. Transcriptome-scale ribosome footprinting identified eIF4A-dependent mRNAs in DDLS, MFS, and UPS cell lines. These include Hippo pathway effectors such as YAP1, WWTR1 (TAZ), and TEAD1. Combined knockdown of YAP and TAZ induced apoptosis in DDLS, MFS, and UPS cell lines, implicating them as critical targets. Hence, DDLS, MFS, and UPS rely on the eIF4A-dependent and CR-1-31B-sensitive translation of Hippo pathway oncogenes such as YAP, TAZ, and TEAD. eIF4A thus represents a new, promising therapeutic target for these incurable forms of soft tissue sarcoma.

overall_design: We performed ribosome footprinting and RNA sequencing on six samples of DDLS8817 cells including three untreated samples (DMSO) and three samples that were collected 2 hrs after treatment with (-)CR31B (10nM). DMSO treated samples are indicated as CT and (-)CR31B treated samples are indicate as (-)CR31B.

first: Young-Mi

first: Evan

last: Seffar

first: Nikita

last: Persaud

first: Tomoyo

last: Okada

first: Anirudh

last: Kulkarni

first: Jianan

first: Nathalie

last: Lailler

first: Shaleigh

last: Smith

first: Nicholas

middle: D

last: Socci

first: Hans-Guido

last: Wendel

first: Samuel

last: Singer


title: Spatial transcriptomics reveals functional compartmentalization of the lung tissue of OP patient

city: Nanjing

first: Ying

last: Tang

address: Dingjiaqiao 87

institute: southeast university

summary: To characterize the spatial characteristics of the lung tissue of OP patient, we collected lung samples for Visium CytAssist from one patient with OP

overall_design: The Visium spatial gene expression analysis was conducted using the Visium CytAssist Spatial Gene Expression for FFPE kits (10x Genomics, PN-1000520). The tissue slices underwent crosslinking treatment followed by probe hybridization and probe connection on the crosslinked sections. After connecting the probes, RNA from the tissue section was enzymatically digested using RNase with tissue removal enzyme (10x Genomics, PN-3000387) to release the probes from the cells. These released probes, which were captured by the capture sequences on the Visium CytAssist Spatial Gene Expression slide using the Visium CytAssist instrument, were then extended and eluted. Subsequently, the eluted probes were transferred to new tubes for further use.single-cell RNA-seq libraries were pooled and sequenced on a NovaSeq 6000 instrument.

first: Cuilin

last: Chu

first: Siyuan

last: Bu

first: Qin

last: Sun

first: Airan

last: Liu

first: Lingyan

last: Huang

first: Hongmei

last: Wang


title: Function and mechanism of PAPOLA-mediated poly(A) lengthening in leukemia [RNA-Seq]

first: Siyao

last: Guo

overall_design: RNA-Seq was used to study the differentially expressed genes in the PAPOLA knockdown and control cells.

first: Shuibin

last: Lin


title: Targeting the cGAS–STING Pathway Mitigates Huntington Disease Pathogenesis in a Knock-In Mouse Model

status: Public on Dec 13 2025

city: Jupiter

first: Srini

last: Subramaniam

state: FL

address: 5353 parkside drive,, MC19, 213,

department: Neuroscience

institute: Florida Atlantic University

summary: Cyclic GMP–AMP synthase (cGAS) and its downstream effector, stimulator of interferon genes (STING), form a central cytosolic DNA–sensing pathway that drives innate immune activation and pro-inflammatory cytokine production. We previously reported that cGAS is upregulated in Huntington disease (HD) cellular models, where it modulates autophagy and inflammatory signaling. However, its in vivo contribution to HD pathogenesis has remained unresolved. Here, we genetically ablated cGAS in zQ175 knock-in HD mice, a model that closely recapitulates hallmark features of human HD, and conducted longitudinal behavioral analyses from 2 to 14 months of age. cGAS deletion significantly ameliorated HD-associated motor impairments, as evidenced by improved rotarod performance, enhanced coordination on beam walk, and better outcomes across a comprehensive behavioral battery. It also mitigated the progressive body-weight loss characteristic of zQ175 mice. Analysis of brain sections further revealed that cGAS deletion reduced the enlargement of lateral ventricles and attenuated both astrogliosis and microgliosis in the striatum. While cGAS loss produced minimal effects in wild-type littermates, transcriptomic profiling of HD brains showed downregulation of genes associated with development and cell–cell communication (Mid1-ps1, Slc45a3, Ilvbl, Col5a3) and upregulation of transcripts linked to ion transport and synaptic activity (Pgam2, Nos1, Cort, RasGef1a). Targeted lipidomics uncovered elevated levels of bioactive immunoregulatory lipids—particularly 12-HETE (ω-6) and 12-HEPE (ω-3)—in HD mice lacking cGAS. Finally, to assess therapeutic potential of cGAS-STING pathway, we pharmacologically inhibited STING using H-151 in zQ175 mice, which led to improved age-dependent motor performance. Collectively, these findings identify cGAS as a critical contributor to HD pathogenesis and support cGAS–STING pathway inhibition as a promising therapeutic avenue for Huntington disease.

overall_design: In this study, cGAS knockout mice, zQ175 neo-deleted heterozygous knock-in mice, C57BL/6J control mice, and double-mutant Q175DN-cGAS-KO mice were utilized to investigate the impact of cGAS deletion on Huntington’s disease (HD) pathogenesis. These mouse cohorts were monitored longitudinally across multiple disease-relevant time points and subjected to a battery of behavioral assessments to track motor, control, and neuropsychiatric phenotypes. To elucidate the underlying molecular mechanisms, animals were subsequently analyzed using complementary biochemical approaches including whole-transcriptome profiling, lipidomics, quantitative RT-PCR, and immunohistochemistry. Together, this integrative experimental design enabled evaluation of whether loss of cGAS modifies behavioral progression in HD and revealed transcriptional, lipid metabolic, and cellular alterations associated with cGAS-dependent modulation of HD pathology.

first: Sunayana

last: Dagar

first: Anuradha

last: Kesharwani

first: Isabella

last: Zuniga

first: Marianne Charlene

last: Monet

first: Ganesh

last: Halade

first: Gunjan

last: Upadhyay

first: Uri Nimrod Ramírez

last: Jarquín

first: Violeta Gisselle

last: Lopez-Huerta

first: Emaad

last: Mirza

first: Ning

last: Quan

first: Srinivasa


title: Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state IV

city: Urbana

first: Elizabeth

middle: Anne

last: Thayer

state: IL

address: 407 S Goodwin Ave

department: Microbiology

institute: University of Illinois at Urbana-Champaign

summary: Type I and III interferons (IFNs) are among the first lines of defense against viral infections, yet they are generally only produced by a tiny fraction of infected cells. Here, we show that variability in tonic cell signaling significantly influences cells’ ability to produce IFN upon stimulation with the synthetic double-stranded RNA, polyinosinic:polycytidylic acid (pIC). Using single-cell approaches, we found that members of the activator protein (AP)-1 transcription factor were implicated in IFNL1 expression predisposition. This guided us to investigate the role of the mitogen-activated protein kinase (MAPK) pathway, specifically the c-Jun N-terminal kinase (JNK), in IFNL1 production. We found that inhibition of JNK signaling severely altered the nature of the innate antiviral response upon pIC stimulation, independently of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Together, our study emphasizes the influence of intrinsic stochasticity in cell state on heterogeneity in IFN expression.

overall_design: Bulk ATAC-seq of clonal populations dervied from a parental (WT) A549 population. These are unstimulated samples to assess their basal chromatin accessibility profiles.

first: Gabriela

last: Shipman

first: Joel

last: Rivera-Cardona

first: Tarun

last: Mahajan

first: QiWen

last: Teo

first: Sebastian

last: Paez

first: Joseph

last: Lederer

first: Jie

last: Chen

first: Nicholas

last: Wu

first: Sergei

last: Maslov

first: Christopher

middle: B

last: Brooke


title: Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state II

overall_design: Bulk RNA-seq of A549 cells treated with ruxolitinib, JNK-IN-8, both inhibitors, or DMSO. Cells were pretreated with the inhibitors for 4 hours before either being treated with pIC or only lipofectamine.  The cells were then incubated for 16 hours then the RNA was extracted for sequencing.


title: Function and mechanism of PAPOLA-mediated poly(A) lengthening in leukemia [RIP-Seq]

first: Siyao

last: Guo

overall_design: RNA immunoprecipitation sequencing (RIP-seq) was used to detect RNA interactions with PAPOLA protein in AML cells.

first: Shuibin

last: Lin


title: AMPK agonism optimizes the in vivo activation and anti-leukemia efficacy of chimeric antigen receptor T cells

city: Pittsburgh

first: Amanda

middle: Catherine

last: Poholek

state: Pennsylvania

address: 4401 Penn Ave., Rangos Research Center 8129

department: Pediatrics

institute: University of Pittsburgh

summary: BACKGROUND: Chimeric antigen receptor (CAR) T cells have achieved remarkable clinical success. However, up to 50% of CAR T cell-treated leukemia patients relapse and long-term survivor data indicate that CART cell persistence is key to enforcing relapse-free survival. Unfortunately, ex vivo expansion protocols often drive metabolic and functional exhaustion, reducing in vivo efficacy. Preclinical models have demonstrated that redirecting metabolism can improve in vivo T cell function. Here, we hypothesized that exposure to an agonist targeting AMP-activated protein kinase (AMPK) would create CARTs capable of increased in vivo function and enhanced leukemia clearance. METHODS: CART cells were generated from healthy human donor T cells via lentiviral transduction, followed by exposure to either Compound 991 or DMSO for 96 hours, followed by a 48-hour washout. During and after agonist treatment, T cells were harvested for metabolic and functional assessments. To test in vivo efficacy, immunodeficient mice were injected with luciferase+ NALM6 leukemia cells, and one week later with 991- or DMSO-expanded CARTs. Leukemia burden and anti-leukemia efficacy was assessed via radiance imaging and overall survival. RESULTS: Compound 991 treatment activated AMPK without limiting cellular expansion, and increased both mitochondrial density and handling of reactive oxygen species (ROS). Mechanistically, 991 treatment mimicked nutrient starvation, with increased autophagic flux and generation of mitochondrially-protective metabolites in treated cells. Importantly, receipt of 991-exposed CARTs significantly improved in vivo leukemia clearance and prolonged recipient survival, likely as a result of elevated activation and increased CD4+ T cell yields at early times post-injection. DISCUSSION: Ex vivo expansion is necessary to generate sufficient cell numbers, but sustained activation and differentiation often negatively impact in vivo persistence and function. Here, we demonstrate that promoting AMPK activity during in vitro CART expansion metabolically reprograms cells without limiting T cell yield, increases early activation marker expression following in vivo transfer, and ultimately enhances anti-leukemia efficacy. Importantly, Compound 991 treatment achieves these results without further modifying the expansion media, changing the CART construct, or genetically altering the cells. Altogether, these data highlight AMPK agonism as a potent and readily translatable approach to improve the metabolic profile and in vivo efficacy of adoptively transferred T cells.

overall_design: 3 random human donor T cells were expanded in either Compound 991 or DMSO only control. CD4+ and CD8+ T cells were separately isolated for analysis.

first: Erica

last: Braverman

first: Craig

last: Byersdorfer

first: Poholek

last: Amanda

first: Yang

last: Aaron


title: Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state III

first: Elizabeth

last: Thayer

overall_design: scRNAseq data of A549 cells either untreated or treated with 5 ng/mL pIC for 4, 8, 12, or 16 hours before being collected and processed for fixed scRNA sequencing.

first: Gabriela

last: Shipman


title: Transcriptomic Profiling of Splenic Red Pulp Macrophages in Response to Dietary Iron Deficiency

city: Warsaw

first: Katarzyna

last: Mleczko-Sanecka

address: 4 Ksiecia Trojdena

country: Poland

institute: International Institute of Molecular and Cell Biology in Warsaw

summary: This study investigates how dietary iron deficiency affects the transcriptional profile of spleen-derived red pulp macrophages (RPMs) in mice. Female C57BL/6J mice were divided into two groups: Iron-deficient (ID) group: fed a low-iron diet (<5 ppm Fe) from 4 to 9 weeks of age. Iron-balanced (IB) group: maintained on a standard iron-sufficient diet (200 ppm Fe) over the same period. At 9 weeks of age, mice were sacrificed, and spleens were harvested. RPMs were FACS-sorted using F4/80 and TREML4 markers, approx. 100 000 RPMs were sorted/sample. Sorting was performed to TRIzol, and RNA was isolated using Direct-zol columns. For all samples RIN was at least 7. Sequencing was conducted on the Illumina NextSeq 500 platform at the EMBL Genomics Core Facility (Heidelberg, Germany) using 75 bp single-end reads. The dataset consists of 8 samples: 4 from iron-deficient mice (S1_DEF to S4_DEF) 4 from control mice (S5_BAL to S8_BAL) This RNA-seq dataset enables comparison of gene expression changes in red pulp macrophages under conditions of iron deficiency, contributing to our understanding of iron homeostasis and macrophage adaptation.

overall_design: Transcriptomic profile of 8 samples: 4 from iron-deficient mice (S1_DEF to S4_DEF) 4 from control mice (S5_BAL to S8_BAL)

first: Pratik Kumar

last: Mandal

first: Patryk

last: Slusarczyk

first: Komal

last: Chouhan

first: Raghunandan

last: Mahadeva

last: Zurawska

first: Marta

last: Niklewicz

first: Matylda

last: Macias

first: Aleksandra

last: Szybińska

first: Aneta

last: Jończy

first: Zhaoyuan

last: Liu

first: Florent

last: Ginhoux

first: Małgorzata

last: Lenartowicz

first: Wojciech

last: Pokrzywa

first: Elizabeta

last: Nemeth


title: EGR proteins mediate interferon-independent anti-HSV-1 responses through viral and host targets

city: Hangzhou

first: Shuaishuai

last: Wang

address: 866 Yuhangtang Road

institute: Zhejiang University

summary: Herpes simplex virus type I (HSV-1) establishes a latent infection that evades the host's defense system, and the latent virus can be reactivated by some stimulation. At present,a key problem in the latent studies of HSV-1 has not been clarified, that is, HSV-1 mainly selectively latent in neurons. Therefore, we have found the host transcription factor EGR in Neuro-2a cells by RNA-seq. EGR1 regulates HSV-1 replication and latency by binding to the viral genome or recruiting co-factors. Our data intend to find the role and mechanism of EGR family repressing HSV-1 replication and promoting HSV-1 latency. This study will provide a theoretical basis for the development of drugs to treat of HSV-1 infection.

overall_design: Neuro-2a cells( knockout EGR1) were cultured in 100-mm plates for 24 h and then infected with KOS virus strain for 5 h  before being harvested for chip-seq. Library preparation and sequencing were performed by Novogene.

first: Dongli

last: Pan

first: Yuhang

last: Xiang


title: FOLFIRINOX Plus Nivolumab Promotes Irregular Intra-Tumoral Lymphoid Aggregates in Borderline Resectable Pancreatic Adenocarcinoma: A Phase 1 Trial

city: Los Angeles

first: Jason

middle: Michael

last: Link

address: 650 Charles E Young Dr S

department: Surgery

institute: University of California, Los Angeles

summary: Combination therapies of chemotherapy and immune checkpoint inhibitors (ICIs) have failed to improve survival in pancreatic ductal adenocarcinoma (PDAC), except in rare MSI-H cases, despite their success in other solid tumors.  Most prior studies have been conducted in advanced disease. Here, we present clinical, pathologic, and translational results from a phase 1b/2 investigator-initiated study evaluating neoadjuvant modified FOLFIRINOX (mFOLFIRINOX, mFFX) plus nivolumab in patients with borderline-resectable (BR) PDAC. Among 28 patients enrolled, 22 (79%) proceeded to surgery. Treatment was well tolerated with no significant delays or surgical complications, meeting the primary endpoint. Among patients who underwent surgical resection, median disease-free survival was 19.7 months, median progression-free survival was 26 months (95% CI: 14.7-34.3) and median overall survival was 38 months (95% CI: 27.9-not reached). The regimen demonstrated an acceptable safety profile, with all Grade 3-4 treatment-related adverse events due to chemotherapy and no Grade 3 immune related adverse events observed. Treatment effects were assessed using paired pre- and post-treatment samples and by comparing post-treatment tumors from the nivolumab cohort to historical BR mFFX-only controls. In paired analyses, intra-tumoral CD8 T cells and plasma cells increased together; in between-group comparisons, plasma cells were significantly higher in the nivolumab cohort, with a modest CD8 T cell increase. Immunohistochemistry revealed that plasma cell abundance correlated with dense intra-tumoral lymphoid aggregates (LA) lacking germinal center-like morphology, a pattern consistent with extrafollicular B cell differentiation. Single-cell spatial transcriptomics identified irregular lymphoid aggregates with high plasma cell to B cell ratios (PBRs) that were enriched for terminally exhausted CD8 T cells and de-enriched for progenitor exhausted CD8 T cells and central memory CD4 T cells. Together, these findings implicate intra-tumoral LA disorganization and skewed T cell subsets as complementary features associated with limited efficacy of PD-1-based chemoimmunotherapy in PDAC. (Clinicaltrials.gov identifier: NCT03970252).

overall_design:
RNA-seq was performed on RNA extracted from 6 pre-treatment biopsies from patient primary pancreatic adenocarcinoma (PDAC) tumors, 21 post-treatment (FOLFIRINOX+nivolumab) primary PDAC tumors, and 9 post-treatment (FOLFIRINOX) primary PDAC tumors

*** Raw data missing for the following Samples --GSM9360958 GSM9360959 GSM9360960 GSM9360961 GSM9360962 GSM9360963 GSM9360964 GSM9360965 GSM9360966 GSM9360967 GSM9360968 GSM9360969 GSM9360970 GSM9360971 GSM9360972 GSM9360973 GSM9360974 GSM9360975 GSM9360976 GSM9360977 GSM9360990 ***

first: Zev

last: Wainberg

first: Timothy

last: Donahue


overall_design:
Neuro-2a cells( knockout EGR1) were transfected with pEGR1 or pcDNA plasmid for 24 h and then infected with KOS virus strain for 10 h (MOI = 0.5) before being harvested for RNA extraction using a LS1040 Eastep Super total RNA extraction kit (Promega). Library preparation and sequencing were performed by BGI.

pcDNA is mock group, that transfected pcDNA plasmid;EGR1human is experiment group, that transfected EGR1 plasmid. And they all infected HSV-1 10h.
pc is mock group, that transfected pcDNA plasmid; e1human is experiment group, that transfected EGR1 plasmid. And they all infected HSV-1 3h.


title: Liver Transcriptomics Reveals UB-NPs Regulate Lipid Metabolism and Inflammation Genes

city: 北京

first: 尚年

last: 刘

state: 北京

address: 马连洼街道马连洼北路151号

institute: 中国医学科学院药用植物研究所

summary: This study utilized RNA-Seq to investigate hepatic gene expression changes in obese mice following intervention with UB-NPs, based on prior evidence indicating the liver as a primary site of UB metabolism. High-quality sequencing data (Q30 > 95.93%, alignment efficiency 90.69–97.47% to GRCm39) revealed 3,387 differentially expressed genes (DEGs) between UB-NPs and high-fat diet (HFD) groups, including 687 overlapping DEGs with the HFD vs. normal diet comparison. Among these, 570 DEGs showed expression reversal patterns, indicating potential key targets of UB-NPs. Functional enrichment analyses (GO, Reactome, KEGG) demonstrated that UB-NPs significantly modulate genes involved in lipid and fatty acid metabolism, mitochondrial beta-oxidation, TCA cycle, inflammatory pathways (e.g., NF-kappa B), and PPAR signaling. UB-NPs upregulated fatty acid oxidation genes (e.g., Ppara, Ehhadh, Cyp4a14) and downregulated pro-inflammatory genes (e.g., Tnf, Traf1). These results suggest UB-NPs ameliorate obesity-related metabolic dysregulation by enhancing lipid catabolism and suppressing inflammation.

overall_design: The study included both prevention and treatment investigations. 1. Prevention Study. After one week of acclimation, mice were randomly divided into six groups (n=10/group) and treated daily via oral gavage for 10 weeks: NC (Normal Control): Standard diet + equal volume of vehicle (water); MC (Model Control): High-fat diet (HFD) + equal volume of vehicle; UB (UB Prevention): HFD + 60 mg/kg/day UB-NPs. 2. Treatment Study. After acclimation, mice were divided into a normal-fat diet (NFD, n=10) group and a high-fat diet (HFD, n=70) group for 10 weeks. Successful obesity induction was confirmed by a significant 22.47% higher body weight in HFD mice compared to NFD controls (p < 0.05). The obese mice were then randomized into groups (n=10/group) and treated for 8 weeks: NFD: Standard diet + equal volume of water; HFD: Continued HFD + equal volume of water; Uro: Continued HFD + 60 mg/kg/day UB-NPs.

first: Chang

first: Shangnian

first: Chao

last: He

first: Tingting

last: Han

first: Yajuan

last: Zhao

first: Yanjuan

last: Li

first: Yijun

last: Lin

first: Zimeng

last: Niu

first: Dengqun

last: Liao

first: Caixia

last: Chen

first: Xianen


title: Transcriptomics in T2-high severe asthmatics treated with biologics: Comparison between anti-IgE, anti-IL-5 and anti-IL-5R-targeted treatments.

city: Liège

first: Sara

last: Gerday

address: Av. Hippocrate 1/11

institute: GIGA Research Institute

summary: Background : Biologic therapies have transformed severe asthma management, particularly for T2-high asthma. We aimed to investigate blood proteomics and transcriptomics after biologic treatment. Methods : A prospective study was conducted on 35 patients with severe T2-high asthma treated with mepolizumab (n=9), benralizumab (n=14), or omalizumab (n=12). Evaluations occurred at baseline and after 16 weeks (omalizumab) or 24 weeks (mepolizumab, benralizumab) of treatment. Blood samples were collected. Gene expression was analyzed via Illumina TruSeq RNA Prep, with RNA sequencing on the Illumina NovaSeq-6000 platform. Results : RNA-seq analysis revealed 86 down-regulated genes common to both mepolizumab and benralizumab, primarily associated with eosinophils, basophils, and the purinergic receptor signaling pathway. Additionally, there was evidence of gene regulation involved in antiviral immunity. However, specific gene modulation was observed for benralizumab (114 genes) and mepolizumab (68 genes). Changes following omalizumab treatment were minimal, with only three significantly down-regulated genes. Conclusion : While omalizumab showed minimal quantifiable effects on gene expression, mepolizumab and benralizumab—despite exhibiting distinct profiles—both induced down-regulation of genes related to eosinophil and basophil biology and purinergic signaling pathways, alongside up-regulation of genes involved in innate antiviral immunity.

overall_design: RNA-seq profiling to assess the modifications of blood inflammatory signals and inflammatory cell profile in samples collected at baseline and after 16-24 weeks of treatment in severe asthmatic patients.

first: Florence

last: Schleich

first: Mare

last: Sabbe

first: Catherine

last: Moermans

first: Françoise

last: Guissard

first: Carole

last: Sanchez

first: Severine

last: Kenens

first: Virginie

last: Paulus

first: Monique

last: Henket

first: Fabrice

last: Bureau

first: Christophe

last: Desmet

first: Renaud

last: Louis


title: This study compares the differential gene expression patterns of oncogenes and tumor suppressor genes fold changes derived from prostate cancer cell lines of both racial etnicities,a health disparities study.

city: Elizabeth City

first: Hirendranath

last: Banerjee

state: North Carolina

address: 1704 Weeksville Rd,

department: Department of Natural, Pharmacy and Health sciences

institute: Elizabeth City State University

summary: Cell culture, RNA isolation, RNA sequencing using  next gen

overall_design: Kuldeep, Rawat

first: Hirendra

first: Saunadia

last: Deloatch

first: Jamie

last: Noble

first: Narendra

first: Karrington

last: Perry

first: Erik

last: Armstrong

first: Zahidur

last: Abedin

first: Soumya

first: Ahmed

last: El-Hashash

first: Anasua


title: KMT2C deficiency promotes meningioma progression through H3K27ac-mediated HIPPO Pathway Inactivation

first: Liuchao

last: Zhang

state: Jiangsu

address: 300 Guangzhou Road, Nanjing

institute: Nanjing medical universuty

summary: KMT2C is a frequently mutated gene in meningiomas, however, its functional role in meningioma pathogenesis remains poorly understood. Here we demonstrate that KMT2C expression is reduced in high-grade meningiomas and that its deficiency promotes tumor progression by inactivating the Hippo pathway. Mechanistically, KMT2C loss diminishes H3K27ac levels at transcription start sites (TSS) and disrupts chromatin accessibility, leading to transcriptional downregulation of NF2 and subsequent dysregulation of Hippo signaling. We further reveal that KMT2C deficiency impairs the acetyltransferase activity of CBP/EP300, thereby reducing H3K27ac deposition, while the chromatin binding of CBP/EP300 remains unaffected following KMT2C knockout. Treatment with the histone deacetylase inhibitor TSA restores H3K27ac levels and reactivates NF2 expression in KMT2C-deficient meningiomas. Notably, KMT2C loss sensitizes meningioma cells to ferroptosis, and the ferroptosis inducer erastin significantly suppresses tumor growth both in vitro and in vivo. These findings establish a foundation for developing targeted therapies for meningioma patients with KMT2C deficiency.

overall_design: By knockdown the expression of KMT2C in meningioma cells, the role and mechanism of KMT2C in meningioma were explored.

first: Jing

last: Ji


title: Extremes on the benign-malignant tumour spectrum: Distinct transcriptomic landscapes between two common canine perianal neoplasms based on the hallmarks of cancer [RNA-Seq]

city: Berlin

first: Alexander

middle: F. H.

last: Haake

address: Robert-von-Ostertag-Straße 15

department: Department of Veterinary Medicine

institute: Freie Universität Berlin

summary: The hallmarks of cancer describe stepwise changes in cellular functions and molecular pathways of tumour cells that undergo malignant progression. Although 14 hallmarks have been proposed, their manifestation at the molecular level across different tumour types remains incompletely understood. Here, we hypothesised that hallmark-associated transcriptomic signatures reflect the contrasting biological behaviours of a pair of a benign and a malignant tumour. To this end, we compared the two most common canine perianal tumours, the highly malignant apocrine gland anal sac adenocarcinoma (AGASAC) and the benign hepatoid gland adenoma (HGA). Spontaneous primary tumours were analysed using RNA-Seq (AGASAC n = 11, HGA n = 10) and a direct mRNA hybridisation panel (AGASAC n = 28, HGA n = 12). Large transcriptomic differences were observed in both the number of differentially expressed genes and enriched pathways. Surprisingly, transcriptomic differences based on the hallmarks of cancer were less pronounced that anticipated, particularly for “activating invasion and metastasis” and “inducing or accessing vasculature”. Only the HGAs showed a significant enrichment for “deregulating cellular energetics”. However, our data point towards a contrasting immune landscape between the compared tumours and a subgrouping of AGASACs associated with the inflammatory landscape. Overall, the transcriptomes of these two benign-malignant tumour extremes on the tumour spectrum contrasted each other in select aspects of the hallmarks. Still, their malignant or benign behaviours could not generally be mirrored on the mRNA level.

overall_design:
FFPE tissue samples of AGASACs (n = 15; 11 primary tumours, 4 nodal metastases) and HGAs (n = 10) from pet dogs were retrospectively obtained from the archive (spanning the years 2006 to 2021) and total RNA was extracted. The RNA was sequenced with QuantSeq 3'. DESeq2 was used for differential gene expression (DGE) analysis in the comparison AGASAC primary tumours (PT) versus HGA and AGASAC primary PT versus AGASAC nodal metastases (NM). - Attention: This GEO submission only includes the 3' RNA-Seq data pertaining to 6 technical replicates, the other 24 samples are re-used samples already accessible via GEO (GSE261790). The nCounter® data used in the publication were submitted separately to GEO (GSE301538).

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The table below lists GEO accessions reused/reanalyzed for this study.
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middle: F

first: Alina

middle: K

last: Loriani Fard

first: Vladimir

last: Jovanovic

first: Michael

last: Hummel

first: Sandro

last: Andreotti

first: Achim

last: Gruber


title: Electro-assisted cell printing directs in vitro gastrulation and epiblast-like morphogenesis from human pluripotent stem cells II

first: yixue

last: Luo

state: 北京市

address: Biomanufacturing and Rapid Forming Technology Key Laboratory of Beijing, Department of Mechanical Engineering, Tsinghua University, Beijing 100084, China

institute: 清华大学

summary: This study develop a versatile techonology to largely generate biomimetic epiblast-like tissues based on human induced pluripotent stem cells (hiPSCs) and well-defined biomatrix. Single hiPSCs are wrapped in laminin-alginate (L-A) hydrogel with optimized concentration and stably fabricated a large number of uniform hiPSCs-contained microspheres via electro-assisted bioprinting technology. It was observed that hiPSCs self-organized into disc-like cell clusters in L-A microspheres. Transition of microenvironment to L-A microspheres triggers the fate specification of disc-shaped tissues towards gastrulation with the identity resemble posterior epiblast population of human embryos around gastrulating stage, which is supported by transcriptome analysis.

overall_design: To investigate the time-dependent change of the cell fate of hiPSC clusters within bioprinted microspherese. We set samples rep1/rep2 of cell clusters on day6 in the persistent presence of blebbistatin. And samples rep1/2 of  denoting the sample named Day6_dif_1 and presenting the differentiation of cell clusters on day6 for 4 days.

first: Yixue


title: Single‑cell RNA sequencing unveils fibroblast heterogeneity in proliferative vitreoretinopathy membranes

city: Shanghai

first: Xin

last: Huang

address: No.83, Fenyang Rd.

institute: Fudan University

summary: Proliferative vitreoretinopathy (PVR) is a vision-threatening fibrotic disorder characterized by pathological membrane formation, yet its cellular and molecular mechanisms remain incompletely understood. Here, we employed single-cell RNA sequencing (scRNA-seq) to profile 18,213 cells from 5 human PVR membranes (PVRMs), uncovering cellular heterogeneity and novel pathogenic pathways.

overall_design: BD Rhapsody system was used to capture the transcriptomic information of the single cells. Single-cell capture was achieved by random distribution of a single-cell suspension across >200,000 microwells through a limited dilution approach.

first: Fengjuan

last: Gao

first: Yuqiao

last: Ju

first: Lili

first: Ting

first: Qing

last: Chang

first: Shunxiang

first: Yuan

last: Zong

first: Gezhi

last: Xu


title: NELF coordinates Pol II transcription termination and DNA replication

first: Yasukazu

last: Daigaku

address: 3-8-31 Ariake Koto-ku

department: Cancer institute

institute: Japanese Foundation for Cancer Research

summary: Regulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is altered in cancer to favour cell growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally changes transcription elongation velocity and perturbs Pol II transcription termination. This results in Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. We anticipate that NELF will be a potential therapeutic target to restrict colorectal cancers.

overall_design: BrdU-IP sequencing in NELFC-AID and control DLD1 cells.This experiment was designed to examine the effect of NELFC depletion via the auxin-inducible degron system on the progression of DNA replication after release from nocodazole-induced G2 arrest.

first: Daigaku

last: Yasukazu

first: Mami

last: Takahashi

first: Tamiko

last: Minamisawa


title: Daratumumab in systemic lupus erythematosus: a phase 2 trial

first: Frederik

middle: Richard

last: Heinrich

state: Berlin

address: Chariteplatz 1

department: Bioinformatics

summary: Antibody-secreting cells (ASCs) play a central role in the pathophysiology of systemic lupus erythematosus (SLE). This single-arm, open-label, phase 2 clinical trial aimed to evaluate the safety and efficacy of the ASC-depleting anti-CD38 monoclonal antibody daratumumab in patients with refractory SLE. The primary endpoint was a significant reduction in serum anti-double-stranded DNA (anti-dsDNA) antibody levels. Ten female patients with active disease and inadequate responses to at least two disease-modifying drugs received eight weekly subcutaneous injections of 1800 mg daratumumab. By week 12, anti-dsDNA antibody levels were significantly reduced (p=0.002), accompanied by rapid and sustained clinical improvements across all patients and organ domains. Adverse events were mild to moderate. Daratumumab treatment depleted circulating ASCs, reduced type I interferon activity, and profoundly modulated T-cell responses. These findings highlight the pivotal role of ASCs in SLE pathogenesis and support daratumumab as a promising therapeutic option for refractory SLE. ClinicalTrials.gov identifier: NCT04810754.

overall_design: This experiment was designed for an in-depth analysis of human T cells, memory B cells from SLE patients receiving the anti-CD38 monoclonal antibody Daratumumab. We sorted memory T cells (CD3+, not double-positive for CCR7/CD45RA) and memory B cells (CD19+CD27+) from the patients at baseline, week 09 and week 36. When multiple samples for analyzed on the same day, hashtag antibodies were used. Single cell transcriptomes and BCR/TCR sequencing of the sorted cells was performed using the 10X Genomics platform with the Single Cell 5’ Library & Gel Bead Kit v2 (dual index) and Illumina NextSeq2000 or NextSeq500.

first: Ostendorf

last: Lennard

first: Zernicke

last: Jan

first: Klotsche

last: Jens

first: Kempkens

last: Robin

first: Beenken

last: Anne

first: Pawel

last: Durek

first: Biesen

last: Robert

first: Mir-Farzin

last: Mashreghi

first: Cheng

last: Qingyu

first: Khodadadi

last: Laleh

first: Krönke

last: Gerhard

first: Guerra

last: Gabriela Maria

first: Burmester

last: Gerd-Rüdiger

first: Hiepe

last: Falk

first: Alexander

last: Tobias


title: Human Uterine Serous Carcinoma cells and tumors response to CTX-439

city: Kyoto

first: Shunsuke

last: Kawahara

address: 54 Kawahara-cho, Shogoin

department: Obstetrics and Gynecology

institute: Kyoto University Hospital

summary: This study aimed to investigate gene-expression alterations induced by the CDK12 inhibitor CTX-439 in uterine serous carcinoma (USC). USC cell lines (ARK1, ARK2) and patient-derived xenograft (PDX) models (USC1, USC2) were subcutaneously implanted into mice, and treated orally with either CTX-439 (CDK12 inhibitor) or vehicle control. RNA was collected from harvested tumors 6 hours after the final treatment. Differential gene expression analysis revealed significant downregulation of homologous recombination (HR)-related and DNA repair genes in CTX-439-treated groups, highlighting a potential therapeutic mechanism of action for CTX-439 in USC.

overall_design: This dataset includes RNA sequencing (RNA-seq) samples from tumors harvested from mice bearing two human uterine serous carcinoma (USC) cell lines (ARK1 and ARK2) and two USC patient-derived xenograft (PDX) models (USC1 and USC2). Each tumor model was implanted subcutaneously in mice, and animals were divided into two treatment groups: the experimental group received oral administration of CTX-439, a CDK12 inhibitor, and the control group received vehicle treatment only. Tumors were collected 6 hours post-final dose, RNA was extracted, and sequencing libraries were generated. Gene expression profiles were compared between CTX-439-treated tumors and vehicle controls (n=4 per group) to identify genes and pathways affected by CDK12 inhibition.

last: kawahara

first: Ryusuke

last: Murakami

first: Kohei

last: Hamada


title: PPSR1 protein functions as an important hub regulator to enhance plant growth performance under N, P and K deficient stress conditions

city: Saskatoon

first: Jieyu

last: Chen

state: SK

address: Collaborative Science Research Building, 112 Science Place

department: Department of Biology

institute: University of Saskatchewan

summary: Phosphorus (P) is an essential macronutrient for various biological processes in plant growth. Modern agricultural science has advanced the knowledge of regulatory mechanisms underlying phosphorus starvation responses (PSRs), aiming to develop phosphate-efficient crops with sustainable production under reduced Pi fertilizer application. However, information regarding coordinated shoot and root adaptation in response to combined nutrient stresses is limited. This study investigated the role of Phloem Phosphate Stress Repressed 1 (PPSR1) in modulating PSRs and other nutrient adaptation. The Arabidopsis functional homologue of Cucumis sativus PPSR1 (CsPPSR1), designated AtPPSR1, was identified. AtPPSR1 encodes a glycine-rich domain-containing protein, and its ectopic expression confers enhanced growth performance to plants. Transcriptomic analyses revealed AtPPSR1 as a regulatory mediator of PSRs, photosynthesis and root development. We revealed that AtPPSR1 interacted with PHOSPHATE STARVATION RESPONSE 1 (PHR1) to regulate PHR1-target genes for adaptive root development, in response to Pi-starvation stress. Additionally, AtPPSR1 was discovered as graft-transmissible, and the shoot-borne AtPPSR1 played a role in restoring the root phenotype of the ppsr1 mutant. Physiological analyses revealed that enhanced AtPPSR1 expression enabled resilience to nitrogen (N) and potassium (K)-starvation, as well as to Pi-deficiency. Furthermore, we identified homologues of CsPPSR1 and AtPPSR1 in Brassica napus (canola), which displayed similar expression patterns in response to Pi-starvation stress. Overexpression of PPSR1, identified from Arabidopsis, cucumber and canola, improved growth performance and seed yield in canola under N-, Pi- or K-deficient conditions. These findings provide novel insights into PPSR1-mediated molecular coordination to improve growth performance under mineral nutrient-stresses conditions.

overall_design: Transcriptomics analyses on leaves and roots of Col-0 (WT), ppsr1(KO), and a representative AtPPSR1 overexpression line (OE), which were grown hydroponically for four weeks, and given a Pi-sufficient (200 µM Pi, C200) or Pi-deficient (0 µM Pi, C0) treatment for twenty-four hours.

first: Chuanhezi

last: Quan

first: Yang

last: Zhao

first: Zhangjun

last: Fei

first: Leon

last: Kochian

first: William

last: Lucas

first: Byung-Kook

last: Ham


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells [ChIP-Seq]

city: Leicester

first: Michael

last: Tellier

state: Select State

address: Lancaster Road

department: Department of Molecular and Cell Biology

country: United Kingdom

institute: University of Leicester

summary: Regulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognised role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer.

overall_design: Drosophila melanogaster spike-in ChIP-seq of Input, CSTF64, and INTS3 in DLD-1 NELF-C-cells treated with DMSO or IAA for 4 hours. Two biological replicates.

first: Nakayama

last: Chihiro

first: Daigaku

last: Yasukazu

first: Aoi

last: Yuki

first: Fang

last: Qi

first: Kimura

last: Hiroshi

first: Shilatifard

last: Ali

first: Tellier

last: Michael

first: Nojima

last: Takayuki


title: Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state I

first: Elizabeth

last: Thayer

summary: Type I and III interferons (IFNs) are among the first lines of defense against viral infections, yet they are generally only produced by a tiny fraction of infected cells. Here, we show that variability in tonic cell signaling significantly influences cells’ ability to produce IFN upon stimulation with the synthetic double-stranded RNA, polyinosinic:polycytidylic acid (pIC). Using single-cell approaches, we found that members of the activator protein (AP)-1 transcription factor were implicated in IFNL1 expression predisposition. This guided us to investigate the role of the mitogen-activated protein kinase (MAPK) pathway, specifically the c-Jun N-terminal kinase (JNK), in IFNL1 production. We found that inhibition of JNK signaling severely altered the nature of the innate antiviral response upon pIC stimulation, independently of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Together, our study emphasizes the influence of intrinsic stochasticity in cell state on heterogeneity in IFN expression.

overall_design: Bulk RNA-seq of clonal populations dervied from a parental (WT) A549 population. These are unstimulated samples to assess their basal transcriptional profiles.

first: Gabriela

last: Shipman

first: Joel

last: Rivera-Cardona

first: Tarun

last: Mahajan

first: QiWen

last: Teo

first: Sebastian

last: Paez

first: Joseph

last: Lederer

first: Jie

first: Nicholas

middle: C

last: Wu

first: Sergei

last: Maslov

first: Christopher

last: Brooke


title: DNA methylation and lncRNA expression control asynchronous DNA replication at imprinted gene domains

city: Paris

first: Jean-Charles

last: Cadoret

address: 15 rue hélène Brion

institute: CNRS/ Université de Paris

type: Genome variation profiling by genome tiling array

summary: Eukaryotic genomes are structured in zones that replicate predominantly early or late.  Besides these genome-wide patterns of replication timing (RT), some genes display asynchronous replication between the two alleles in certain stem cells, brought about by stochastic processes and genetic polymorphisms.  To what extent epigenetic modifications control asynchronous replication remains unclear.  As a paradigm to address this question we explored imprinted chromosomal domains, at which parental DNA methylation imprints mediate parental allele-specific gene expression.  Our genome-wide and locus-specific RT assays in mono-parental and hybrid mouse embryonic stem cells (mESCs) reveal a pronounced replication asynchrony between the parental chromosomes at the Dlk1-Dio3 and Snrpn domains.  This asynchrony is strictly parent-of-origin dependent.  By generating a range of mutant mESC lines, we find that the replication asynchrony at Dlk1-Dio3 is mediated by parental allele-specific methylation at DMRs (Differentially Methylated Regions).  Moreover, lncRNA polycistron expression controls early replication across parts of the domain on the maternal chromosome.  As a result, at these imprinted domains, RT domains become unlinked from 3D chromatin architecture as assayed by Hi-C.  Our combined data highlight how parental DNA methylation imprints and lncRNA expression can locally be used to override intrinsic RT domain organization.

overall_design: nascent-DNA from early S-phase versus nascent-DNA from late S-phase

first: Yui

last: Imaizumi

first: Robert

last: Feil


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells [POINT-seq]

first: Michael

last: Tellier

overall_design: POINT-seq in biological replicates in DL-1 NELFC-AID, NELFE-AID, or SPT4-AID cells treated with DMSO, Pladienolide B (PlaB, SF3B1 inhibitor), or auxin (IAA) for the indicated time. The SIRV spiked POINT-seq are indicated with "SIRV" in the name of each sample.

first: Nakayama

last: Chihiro

first: Daigaku

last: Yasukazu

first: Aoi

last: Yuki

first: Fang

last: Qi

first: Kimura

last: Hiroshi

first: Shilatifard


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells [TT-seq]

overall_design: Transient transcriptome sequencing (TT-seq) combined with inhibition of promoter-proximal release of RNA Pol II to infer the rate of elongation in NELF-C-depleted or control human DLD-1 cells.

last: Ali

first: Tellier

last: Michael

first: Nojima

last: Takayuki


title: Dll4 coordinates endothelial migration and smooth muscle cell recruitment to assemble the umbilical cord and placental vasculature

city: Philadelphia

first: Mark

last: Kahn

state: PA

address: 3400 Civic Center Blvd

department: Cardiovascular Institute

institute: University of Pennsylvania

summary: Proper development of the umbilical cord and placental vasculature is essential for embryonic growth and development. While the allantois is known give rise to endothelial cells within the placenta, whether the allantois gives rise to endothelial cells (ECs) in the umbilical cord is highly debated. Furthermore, a lack of genetic tools to study placental vascular development independent of the embryo proper has hindered robust investigation into the primary cause of vascular defects from early studies utilizing global knockouts. In this study, we sought to delineate the contribution of the allantois to the umbilical vessels and utilize a novel mouse genetic tool previously developed by our lab to revisit the role of Notch signaling during formation of the placental vasculature. We show that the allantois has mosaic contribution to the umbilical endothelium with higher contributions closer to the placenta. Loss of Notch signaling through deletion of Dll4 in the allantois causes abnormal vascular development in the umbilical cord and placenta with secondary defects on the heart. Lastly, we identify Unc5b as a novel effector of Dll4 signaling that simultaneously restricts EC migration while promoting chemokine signaling for vascular smooth muscle cell recruitment to arteries. These findings identify a novel genetic tool for investigating placental vascular development and give new insights into the ontogeny and mechanisms of placental and umbilical vascular development.

overall_design: Human umbilical artery endothelial cells were treated with siRNAs targeting DLL4, UNC5B, both DLL4 and UNC5B or scrambled control. Total RNA was extracted and sequenced.

first: Derek

last: Sung

first: Jesse

last: Pace


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells [RNA-seq]

overall_design: Whole cell polyA+ RNA-seq in biological replicates in DLD-1 NELFC-AID cells treated with DMSO or auxin (IAA) for 4 hours. Nuclear polyA+ RNA-seq in biological replicates in DLD-1 NELFC-AID cells treated with DMSO or auxin (IAA) for 4, 12, or 24 hours.

first: Chihiro

last: Nakayama

first: Yasukazu

last: Daigaku

first: Yuki

last: Aoi

first: Qi

last: Fang

first: Hiroshi

last: Kimura

first: Ali

last: Shilatifard

first: Takayuki

last: Nojima


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells

first: Michael

last: Tellier

summary:
Regulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognised role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer.

This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series

first: Shoko

last: Ito

first: Mami

last: Takahashi

first: Reo

last: Shimatani

first: Tamiko

last: Minamisawa

first: Yagiz

last: Ozturk


title: NELF prevents widespread transcriptional readthrough into DNA replication zones of cancer cells [ATAC-seq]

overall_design: ATAC-seq in biological replicates in DLD-1 NELFC-AID cells treated with DMSO or auxin (IAA) for 4 hours or 24 hours.


title: Stealth replication of SARS-CoV-2 Omicron in the nasal epithelium at physiological temperature

city: Gothenburg

first: Roshan

last: Vaid

state: Västra Götalands län [SE-14]

address: Bruna Stråket 16,

department: Department of Laboratory Medicine

country: Sweden

institute: GOTEBORGS UNIVERSITET

summary: The COVID-19 pandemic was marked by successive waves of SARS-CoV-2 variants with distinct properties. The Omicron variant that emerged in late 2021 showed a major antigenic shift and rapidly spread worldwide. Since then, Omicron-derived variants have maintained their global dominance, for reasons that remain incompletely understood. We report that the original Omicron variant BA.1 evolved several traits that converged in facilitating viral spread. First, Omicron displayed an early replicative advantage over previous variants when grown in a reconstructed nasal epithelium model based on primary human cells. The increase in Omicron replication was more marked at the 33°C temperature characteristic of human nasal passages, resulting in a physiologically relevant advantage. Omicron also caused a decrease in epithelial integrity, as measured by transepithelial electrical resistance and caspase-3 activation. Furthermore, Omicron caused a more marked loss of motile cilia at 33°C than other variants, suggesting a capacity to impair mucociliary clearance. RNAseq analysis showed that Omicron induced a broad transcriptional downregulation of ciliary genes but only a limited upregulation of host innate defense genes at 33°C. The lower production of type I and type III interferons in epithelia infected by Omicron compared to those infected by the Delta variant, at 33°C as well as 37°C, confirmed the increased capacity of Omicron to evade the innate antiviral response. Thus, Omicron combined replication speed, motile cilia impairment, and limited induction of innate antiviral responses when propagated in reconstructed nasal epithelia at physiological temperature. Omicron has the capacity to propagate efficiently but stealthily in the upper respiratory tract, which likely contributed to the evolutionary success of this SARS-CoV-2 variant.

overall_design: Examination of bulk RNA-seq from Human Nasal Epithelial Cells (HNEC) infected with various SARS-CoV-2 variants at 33 ºC  and 37 ºC temperatures.

first: Barbara

last: Fonseca

first: Rémy

last: Robinot

first: Vincent

last: Michel

first: Akram

last: Mendez

first: Samuel

last: Lebourgeois

first: Chloé

last: Chivé

first: Raphaël

last: Jeger-Madiot

first: Nikaïa

last: Smith

last: Bondet

first: Elizabeth

last: Maloney

first: Florence

last: Guivel-Benhassine

first: Olivier

last: Schwartz

first: Darragh

last: Duffy

first: Tanmoy

last: Mondal

first: Samy

last: Gobaa

first: Lisa

last: Chakrabarti


title: NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_2.

status: Public on Dec 12 2025

city: Liverpool

first: Sonia

last: Rocha

address: Crown Street

institute: University of Liverool

summary: Sequencing study was performed to elucidate the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

overall_design: AC16 cells were plated and cultured with DMSO (vehicle control), 100 nM CDDO-Me for 24 h or 100 nM CDDO for 72 h. RNA-seq was performed to measure differential transcript expression.

first: James

last: Roberts

first: Mihcael

last: Batie

first: Parveen

last: Sharma


title: NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

overall_design: AC16 cells were plated and cultured with DMSO (vehicle control), 100 nM CDDO-Me + 100 nM doxorubicin for a total of 72 h. RNA-seq was performed to measure differential transcript expression.


title: Gene Expression changes in the lung post pneumococcal infection of Myeloid Specific Zip8KO mice

city: Omaha

first: Sankarasubramanian

last: Jagadesan

state: NE

address: 42end and Emile st

department: Department of Genetics, Cell Biology & Anatomy

institute: University of Nebraska Medical Center

summary: We have used single cell sequencing approach using 10xGenomic using scRNA-seq to evaluate the changes in lung cells post pneumococcal infection in WT and Zip8KO mouse model.

overall_design: WT and Zip8KO non-infected and post 72 hour pneumococcal infection, whole lungs were harvested. Following enzymatic digestion, RBC lysis,  and dead cell removal, lung homogenates were submitted for scRNA-seq analysis.

first: Daren Knoell

last: PhamD

first: Derrick

last: Samuelson


title: Immunosuppressive monocytes are enriched in hepatocellular carcinoma patients with liver dysfunction in a phase II trial of combination sorafenib and nivolumab

city: San Francisco

first: Bridget

middle: P

last: Keenan

state: CA

address: 505 PARNASSUS AVE

institute: University of California San Francisco

summary: Background and aims: Immune checkpoint inhibition (ICI) and anti-angiogenic therapies are active in hepatocellular carcinoma (HCC), although patients with impaired hepatic function have worse outcomes. Methods: We conducted a multi-center, open-label phase II clinical trial to assess the safety and efficacy of the multikinase inhibitor, sorafenib, combined with nivolumab, in patients with advanced or unresectable HCC and varying liver function. In a Part 1 safety lead-in, we investigated the primary endpoint of the maximum-tolerated dose (MTD) of the combination in patients with Child-Pugh A or B7 HCC. In Part 2, we enrolled patients with Child-Pugh B HCC with the primary endpoint of grade >/=3 treatment-related adverse events (TRAE) incidence. Exploratory endpoints included immunologic biomarkers. Results: Overall, 25 patients were consented and 16 eligible patients enrolled. In Part 1, dose-limiting toxicity occurred in 1 of 6 patients in Dose Level -1, and 2 of 5 patients in Dose Level 1; Dose Level -1 was determined to be the MTD. In total, 69% of patients experienced a Grade >/=3 TRAE, with similar distribution for patients with Child-Pugh A and B liver function (70%, 95% CI: 0.35, 0.93 vs 66.7%, 95% CI: 0.22, 0.96). The objective response rate was 6%. We found that patients with Child-Pugh B liver disease harbored more circulating suppressive CD14+ monocytes at baseline. Conclusions: While the combination of sorafenib and nivolumab demonstrated acceptable safety at the MTD in both Child-Pugh subgroups, the objective response rate was below the pre-specified threshold to be declared worthy of further exploration. A distinct immune cell profile in Child-Pugh B patients may define mechanisms of resistance and potential therapeutic targets in this population with unmet clinical need

overall_design: This was a single-arm, multicenter, investigator-initiated pilot study to evaluate the safety and efficacy of sorafenib and nivolumab for the treatment of patients with advanced unresectable HCC, without prior systemic therapy, with Child-Pugh A or B liver function. The study was registered at Clinicaltrials.gov as NCT#03439891. Part 1 of the pilot study was designed to first determine the maximum tolerated dose (MTD) of sorafenib in combination with nivolumab in an Escalation Cohort with 3+3 design. Due to the mid-study regulatory approvals of other combination immunotherapy regimens for patients with advanced HCC and Child-Pugh A liver function, the Part 2 Expansion Cohort of this study was amended to restrict eligibility to Child-Pugh B liver function to address the unmet clinical need in this population. Peripheral blood mononuclear cells (PBMC) were obtained from patients pre- and on-treatment for the subset of patients treated at the UCSF study site.

first: Keenan

last: Bridget P.

first: Fan

last: Zenghua

first: Le

last: Bryan Khuong

first: Harris

last: Quincy

first: Chen

last: Jocelin

first: Clark

last: Matthew

first: Lea

last: Averey

first: Zhang

last: Li

first: Cheung

last: Alexander

first: Lara

last: Frances

first: Gordan

last: John D.

first: Bracci

last: Paige

first: Behr

last: Spencer C.

first: Fong

last: Lawrence

first: Venook

last: Alan P.

first: Kim

last: Edward J.

first: Kelley

last: Robin K.


title: NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

first: Sonia

last: Rocha

summary: Elucidation of the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

overall_design: AC16 cells were plated and cultured with DMSO (vehicle control) or 100 nM doxorubicin for 48 h. RNA-seq was performed to measure differential transcript expression.

first: James

last: Roberts

first: Mihcael

last: Batie

first: Parveen

last: Sharma