title: Maternal antibodies orchestrate the establishment of salivary and oral mucosal immunity

city: Jerusalem

first: Inbar

last: Plaschkes

address: The Hebrew University of Jerusalem - Ein Kerem

department: The Faculty of Medicine - Ein Kerem

country: Israel

institute: HUJI

summary: The establishment of mucosal homeostasis after birth involves mutual development of the microbiota and the immune system, with each mucosal barrier has specific mechanisms. Here, we show that in utero-delivered maternal IgG antibodies are translocated to the salivary glands and secreted to the neonatal saliva. As a result, the microbial burden of the neonate oral cavity and salivary glands is reduced. In the absence of maternal antibodies, oral dendritic cells migrate in higher frequencies to the salivary glands resulting in elevated activation of T and B cells, while dampening T regulatory cells. The IgG/IgA balance in the adult saliva was also dysregulated. The absence of maternal antibodies further regulates the adult gingival immunity, a key oral barrier, increasing alveolar bone loss during experimental periodontitis. This work reveals the importance of the salivary-oral axis during neonatal life via maternal antibodies, orchestrating local mucosal immunity and protecting against pathological damage in adulthood.

overall_design: B cell-deficient (JhT-/- ) females were crossed with wild-type (WT) males to generate offspring with intact B cells that were not exposed to mIg.

first: Reem

last: Naamneh

first: Avi-Hai

last: Hovav

first: Yasmin

last: Netanely

first: Shahd

last: Yacoub

last: Jaber


title: The impact of Pyruvate dehydrogenase kinase 4 knockout on the function of vascular smooth muscle cells

status: Public on Feb 22 2026

city: Guangzhou

first: Li

last: Zhao

state: Guangdong

address: 1838 North Guangzhou Avenue,

department: Department of Cardiovascular Surgery

country: China

institute: Nanfang Hospital, Southern Medical University

type: Expression profiling by high throughput sequencing

summary: This study investigated the impact of pyruvate dehydrogenase kinase 4 knockout on the function of vascular smooth muscle cells.

overall_design: Vascular smooth muscle cells were extracted from the abdominal aorta of Pdk4fl/fl and Pdk4SMKO mice. The expression of pyruvate dehydrogenase kinase 4 in vascular smooth muscle cells was detected using RT-qPCR, followed by transcriptomic sequencing to investigate the impact of pyruvate dehydrogenase kinase 4 on the function of vascular smooth muscle cells.

first: Xiu

last: Liu


title: RNA-seq of fresh apheresis human platelets and freeze dried platelets (Thrombosomes)

status: Public on Feb 23 2026

city: San Francisco

first: Huimin

last: Geng

state: CA

address: 513 Parnassus Ave., MSB HSW 1201

department: Department of Laboratory Medicine

country: USA

institute: UCSF

summary: To determine the transcriptomic (mRNA and microRNA) content present in fresh apheresis platelets and freeze dried platelets (Thrombosomes) we used RNA-Seq approach. The goal was to determine if the freeze drying process maintained the transcriptomic cargo of the fresh platelets.

overall_design: Genome-wide profiling of total RNA transcript levels in human Pletlet and Thrombosomes

first: Alpa

last: Trivedi

first: Shibani

last: Pati


title: IL2Ra-dependent feedback control of the B-cell receptor and its oncogenic mimics

summary: Human BCR-ABL1 ALL cells were sorted as CD25-positive and CD25-negative BCR-ABL1 ALL cells on three xenograft samples BLQ11, LAX9 and BLQ1. The expression profiles of CD25+ and CD25- BCR-ABL1 ALL cells were studied by Affymetrix Human Genome U133 Plus 2.0 Array.

overall_design: Human BCR-ABL1 ALL cells were sorted as CD25-positive and CD25-negative BCR-ABL1 ALL cells for microarray gene expression profiling.

first: Markus

last: Muschen


title: The impact of Pyruvate dehydrogenase kinase 4 overexpression on the function of vascular smooth muscle cells

summary: This study investigated the impact of pyruvate dehydrogenase kinase 4 overexpression on the function of vascular smooth muscle cells.

overall_design: Vascular smooth muscle cells were transduced with adenoviral vectors carrying pyruvate dehydrogenase kinase 4 overexpression plasmids or control plasmids. The expression of pyruvate dehydrogenase kinase 4 in vascular smooth muscle cells was detected using RT-qPCR, followed by transcriptomic sequencing to investigate the impact of pyruvate dehydrogenase kinase 4 on the function of vascular smooth muscle cells.


title: RNA-Seq profiling of blood and jejunal samples from subclinical Holstein cattle naturally infected with Mycobacterium avium subsp. paratuberculosis revealed host transcriptional adaptations to a latent MAP infection

status: Public on Feb 18 2026

city: Derio

first: Marta

last: Alonso-Hearn

state: Bizkaia

address: Berreaga 1

department: Animal Health

country: Spain

institute: NEIKER

summary: Bovine paratuberculosis (PTB), caused by Mycobacterium avium subsp. paratuberculosis (MAP), is a chronic granulomatous intestinal disease that leads to substantial economic losses in the global dairy industry. Current diagnostic tests have limited sensitivity, as they can reliably detect only animals that have advanced stages of disease characterized by diffuse lesions and with the presence of clinical signs, but fail to identify those in earlier or subclinical stages, with focal or multifocal lesions in gut tissues. Previous studies have suggested that multifocal granulomas prevent lesions progression, but the molecular mechanisms involved in the establishment and maintenance of a chronic MAP infection are not fully understood. This study aimed to compare the whole transcriptomic profiles of peripheral blood (PB), jejunum (JE), and jejunal lymph node (JELN) samples from Holstein cattle with multifocal lesions and those without lesions in gut tissues. Total RNA was extracted from samples from 11 cows with multifocal lesions and 4 control cows without lesions. RNA libraries were prepared using 250 ng of RNA with the Illumina NEBNext Ultra Directional RNA library preparation kit and sequenced on an Illumina NovaSeq sequencer. On average, 34.08, 33.85, and 36.92 million raw reads were sequenced from the PB, JE and JELN samples, respectively. In cows with multifocal lesions compared to controls, 1,272 differentially expressed (DE) genes were identified in PB, mainly linked to translation, RNA splicing, and mRNA processing. In JE, 7 genes were DE and related to metabolic processes, oxidative stress response, and granulocyte migration. In JELN, 18 genes were DE and associated with the mTOR signaling, response to reactive oxygen species and hypoxia, and regulation of autophagy. The protein-to-protein interaction (PPI) analysis revealed that several differentially expressed genes are highly interconnected and associated with pathways related to splicing and translation inhibition, as well as activation of a robust innate immune response in peripheral blood. Overall, this study demonstrates that MAP persistence with multifocal granulomas results from a complex interplay of host innate immune activation and regulation, autophagy suppression, translational reprogramming, and metabolic adaptation, providing new insights into MAP pathogenesis and identifying potential biomarkers or therapeutic targets.

overall_design: RNA-Seq libraries prepared from peripheral blood (PB), jejunum (Ty), and jejunal lymph node (Tg) samples from Holstein cattle with multifocal lesions (N = 11) and without lesions in gut tissues (N = 4).

first: Gerard

last: Badia-Bringué

first: Arrate

last: Prado-López


title: Transcripts identified by microarray analysis that were deregulated in E13.75+18h cultures of NMRI ureters upon treatment with NOGGIN.

city: Hannover

first: Mark-Oliver

last: Trowe

address: Carl-Neuberg-Str. 1

department: Molekularbiologie

country: Germany

institute: Medizinische Hochschule Hannover

summary: Evaluation of the transcriptional changes in E13.75+18h ureters upon treatment with NOGGIN.

overall_design: Ureters of E13.75 NMRI embryos were dissected and cultured for 18h in medium containing 10 µg/ml NOGGIN  (treated) or in medium without NOGGIN (control). Total RNA from these ureters was analyzed by microarray analysis.

first: Andreas

last: Kispert


title: Transcripts identified by microarray analysis that were deregulated in E14.5 Pax2-cre/+;Smad4(fl/fl) (Smad4cKO (UE)) ureters.

summary: Evaluation of the transcriptional changes in E14.5 ureters upon loss of Smad4 in the ureteric epithelium.

overall_design: Total RNA from dissected ureters of E14.5 Smad4cKO (UE) and control embryos was analyzed by microarray analysis.


title: Transcripts identified by microarray analysis that were deregulated in E14.5 Tbx18(cre/+);Bmp4(fl/fl) (Bmp4cKO) ureters.

summary: Evaluation of the transcriptional changes in E14.5 ureters upon loss of Bmp4 in the ureteric mesenchyme.

overall_design: Total RNA from dissected ureters of E14.5 Bmp4cKO and control embryos was analyzed by microarray analysis.


title: RNA-seq profiling of Siniperca chuatsi MFF-1 cells under hypoxic conditions

status: Public on Feb 16 2026

city: Zhuhai

first: Mincong

last: Liang

address: No. 2 Daxue Road

department: School of Marine Sciences

institute: Sun Yat-sen University

summary: To investigate the molecular mechanisms underlying hypoxia adaptation in mandarin fish (Siniperca chuatsi), bulk RNA sequencing was performed on MFF-1 cells. The study compares the transcriptomic profiles of cells cultured under normoxic conditions (21% O2) versus those subjected to hypoxic stress (3% O2) for 72 hours.

overall_design: The experimental variable was the oxygen concentration in the culture environment: normoxia (21% O2) versus hypoxia (3% O2). Cells were maintained under these specific conditions for 72 hours prior to RNA extraction. Three biological replicates were generated for each condition to allow for statistical analysis of differential gene expression.

first: Yang

last: Yu

first: Shaoping

last: Weng

first: Jian

last: He

first: Jianguo

first: Changjun

last: Guo


title: An atlas of primate insular cortex reveals a signal-processing strategy in von Economo neurons [Patch-seq]

first: Ruifeng

state: Guangdong province

address: Jinsui Road, 7#

department: Zhongshan Ophthalmic Center

summary: The anterior insular cortex (AIC) is a critical hub integrating exteroceptive and interoceptive information into high-order cognition, yet its neural basis remains incompletely understood. Here, by combining whole-cell-based single-cell transcriptomics with Patch-seq recordings, we resolved and characterized 78 detailed cell types in the macaque AIC, revealing the diversity and specialization of this region in cell type, connectivity profile, signal-processing strategy, and metabolic characteristics. Among these, we identified two transcriptomically and morphoelectrically defined von Economo neuron (VEN) subtypes, DSG2-expressing VEN-L and POC5-expressing VEN-S, transcriptomically relating to extratelencephalic and corticothalamic projection neurons, respectively. We also uncovered a previously underappreciated signal-processing strategy in VENs, whereby the geometry of the dendrite-originating axon initial segment (AIS) reshapes action potential dynamics and enhances somatic responsiveness to deep-layer synaptic inputs. Together, this multimodal atlas establishes a molecular and functional framework for investigating the circuit principles underlying deep-layer projection neurons in the primate AIC.

overall_design: Here we employed a massively parallel 10X genomics single cell RNA-sequencing (scRNA-seq) analysis of the AIC to derive a molecular classification and then related each molecularly distinct cell type to well-established AIC cell types via Patch-seq.

first: Sheng

first: Mengyao

last: Huang

first: Yuhui

last: Shen

first: Mingting

last: Shao


title: Transcriptome data of larval zebrafish exposed to continuous sub- and supra-MCL sodium arsenite and depleted uranium

city: Flagstaff

first: Phillip

middle: Hua

last: Kalaniopio

state: Arizona

address: 617 S Beaver St.

department: Department of Biological Sciences

institute: Northern Arizona University

summary: Depleted uranium (DU) and arsenic (As) are both ubiquitous contaminants in the American southwest, posing risks to indigenous tribes, wildlife, and the environment. DU’s chronic effects and mechanisms of toxicity are poorly elucidated. Concomitant mixture exposure studies with geographically relevant environmental contaminants including both DU and As are also not available. Continuous low-dose (UL, AsL), high-dose (UH, AsH), and concomitant (AsU) exposures are investigated using the larval zebrafish (Danio rerio), with exposure paradigms lasting from embryo collection at 2-3 hours post fertilization until harvest at 5 days post fertilization. Herein, we describe differential gene expression analyses including gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment statistics.

overall_design: RNA-seq profiling of larval (5 days post-fertilization) zebrafish continuously exposed to: 1 or 10 µM sodium arsenite, 30 or 300 µg/L uranyl nitrate, or 1 µM sodium arsenite and 30 µg/L uranyl nitrate in combination.

first: Kalaniopio

middle: H

last: Phillip

first: Allen

middle: S

last: Ronald

first: Salanga

middle: C

last: Matthew


title: Impact of Alzheimer’s disease risk factors and local neuromelanin content on the transcriptomic landscape of the human locus coeruleus

city: Baltimore

first: Keri

last: Martinowich

state: Maryland

address: 855 N Wolfe St Suite 300

institute: Lieber Institute for Brain Development

summary: The locus coeruleus (LC) is a small noradrenergic nucleus in the dorsal pons that sends projections widely across the brain to regulate multiple functions including  sleep, memory, arousal, and cognition. The LC has several unique cellular features including the presence of neuromelanin (NM) and its accumulation of a precursor to Alzheimer’s Disease (AD) pathology, soluble phospho-tau (pTau), in virtually all individuals by adulthood. NM increases in LC during early life, plateauing in middle age, and eventually dissipating, coinciding with LC neuron degeneration, a process which is observed in healthy aging but accelerated in AD. NM-sensitive neuroimaging predicts clinical severity and future progression of AD. While these findings suggest an etiologic role for the LC in AD, data describing the molecular landscape of the LC in middle age,  preceding the clinical manifestation of sporadic AD, is lacking. Understanding the molecular state of the LC during this time period is critical to developing interventions that preserve this brain region and the cognitive functions it supports. Here, we performed Visium spatial transcriptomics on 85 tissue sections of human postmortem LC from a cohort of 33 middle-aged, neurotypical donors, balanced for epidemiologic AD risk factors including sex, African or European ancestry, and APOE genotypes (carriers of the E4/risk or E2/protective alleles). We find an unexpected male-bias in LC expression of cholesterol synthesis pathway genes, suggesting that intrinsic neuronal cholesterol synthesis may be protective against AD. Comparing across APOE genotypes, astrocytic gene expression differs in the immediate vicinity of LC neurons. Finally, we leverage histological images captured from the profiled tissue to associate gene expression to NM abundance, finding that APOE expression is associated with reduced NM content, and that NM-associated genes are enriched for aging-related pathways. These findings provide important information about how AD risk factors and NM content impact molecular correlates of resilience/susceptibility of the aging LC to degeneration. Data are freely available, including through visualization browsers to enable wide utilization of these tools for understanding LC biology in AD and other LC-related neurodegenerative disorders, including Parkinson’s disease.

overall_design:
We obtained tissue blocks of postmortem human brain containing locus coeruleus (LC) from 33 neurotypical adult brain donors, balanced for age, sex, APOE2 and APOE4 carrier status (all donors had at least one copy of one of the two alleles), and predominant genomic ancestry (African Ancestry or European Ancestry). We used the 10x Genomics Visium platform to generate spatial transcriptomics from two sequential tissue sections containing LC for each donor, with a second pair of tissue sections collected for a subset of donors. Data were integrated and clustered, defining a robust LC cluster, two mixed non-LC neuron clusters, and several clusters labeling spots with mixed glial types contents. 77 samples from 30 donors with substantial LC content (≥10 spots per tissue section) were retained for downstream analyses. Differential expression (DE) analyses were then performed for the 5 clusters (of 9 total) with adequate count data, including LC, comparing expression between groups for each Alzheimer's risk variable of interest (sex, genomic ancestry, and APOE genotype). Additional analyses were performed for: 1) spatially variable expression within spots of the LC cluster; 2) comparing neuromelanin (NM)containing LC spots NM-negative LC spots; 3) modeling spot-level NM relationships to spot-level gene expression; 4) nonnegative matrix factorization of LC cluster gene expression to identify discrete expression programs; 5) gene set enrichment analyses of DE genes, NM-associated genes, and factorization-identfied LC gene groups.

***************************************************************
Raw files for human/patient samples are being made available in dbGaP (https://www.ncbi.nlm.nih.gov/gap/) for controlled access to the personally identifiable sequence data.
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first: Bernard

last: Mulvey

first: Heena R

last: Divecha

first: Madhavi

last: Tippani

first: Svitlana V

last: Bach

first: Rahul

last: Bharadwaj

first: Ishbel

last: del Rosario

first: Sarah

last: Maguire

first: Ryan A

last: Miller

first: Aaron J

last: Salisbury

first: Atharv

last: Chandra

first: Beau A

last: Oster

first: Kelsey D

last: Montgomery

first: Sang Ho

last: Kwon

first: Haya

last: Algrain

first: Alexis

last: Papariello

first: Joel E

last: Kleinman

first: Leonardo

last: Collado-Torres

first: Thomas M

last: Hyde

first: Shizhong

last: Han

first: Daniel R

last: Weinberger

first: Stephanie C

last: Hicks

first: Stephanie

last: Cerceo Page

first: Kristen R

last: Maynard


title: Simultaneous profiling of native-state proteomes and transcriptomes of neural cell types using proximity labeling

city: Atlanta

first: Christina

last: Ramelow

address: 615 Michael St RM 375

institute: Emory University

type: Non-coding RNA profiling by high throughput sequencing

summary: Phenotyping cells at transcriptomic and proteomic levels is an essential step to understanding cellular contributions to development, aging, injury, and disease. Since proteome and transcrip-tome level abundances modestly correlate, complementary profiling of both is needed. We report a method called simultaneous protein and RNA -omics (SPARO) to capture the cell type-specific transcriptome and proteome simultaneously in vitro and in vivo. SPARO leverages TurboID to biotinylate RNA-interacting cytosolic proteins, enabling enrichment of proteins for proteomics and protein-associated RNA for transcriptomics. We validate SPARO first using well-controlled in vitro systems to verify that the proteomes and transcriptomes obtained reflect the global proteo-mes and transcriptomes. The effect of neuroinflammatory activation by lipopolysaccharide is al-so faithfully captured. We apply SPARO to obtain native-state proteomes and transcriptomes from astrocytes and neurons, thereby validating the approach in vivo. We interrogate mRNA-protein concordance and discordance, providing insights into molecular processes that exhibit uniform or cell type-specific patterns.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Cell type-specific transcriptomes of BV2-microglia and HEK293 cells in vitro and Aldh1l1-expressing astrocytes and Camk2a-expressing neurons in vivo were obtained using the proximity labeling enzyme, TurboID, that biotinylates proteins that interact with RNA (e.g., ribosomal and RNA-binding proteins). Following streptavidin or A/G bead affinity purification, RNA was extracted and sent for RNA-sequencing. HEK293 cells expressing TurboID with and without a nuclear export sequence were contrasted. The TurboID-enriched and RiboTag-enriched astrocyte in vivo transcriptomes were also compared. MicroRNA-sequencing from cortical Aldh1l1-expressing astrocytes and the bulk cortex in vivo was also completed.

first: Srikant

last: Rangaraju

first: Steven

middle: A

last: Sloan


title: Follicular mural granulosa cells stockpile glycogen to fuel corpus luteum pre-vascularization

status: Public on Feb 14 2026

city: Wuhan

first: changjiu

last: he

state: Hubei

address: 1 Shizishan street, Hongshan District

department: College of Animal Science and Technology

institute: Huazhong Agricultural University

summary: The differentiation of follicular mural granulosa cells (fGCs) into luteal cells involves a rapid progesterone synthesis surge and the vascular network development. However, progesterone elevation occurs before vascularization, leaving luteinizing fGCs temporarily devoid of blood supply. The mechanism of how fGCs fuel increased progesterone synthesis during this avascular phase remains unclear. Our research, utilizing single-cell RNAseq and in vivo/ex vivo experiments, revealed that upon receiving the ovulatory/luteinization signal, fGCs transition to a low-energy state, reducing metabolic activity and storing glucose as glycogen.

overall_design: Ovaries were collected at 0 (H0), 1 (H1), and 6 hours (H6) post-hCG injection for single-cell RNA-seq.

first: Changjiu

last: He

first: Jianning

last: Liao


title: Distinct roles of tip progenitor subpopulation in shaping the murine lung

status: Public on Feb 13 2026

first: Pao-Tien

last: Chuang

address: 555 Mission Bay Blvd. South

institute: University of California, San Francisco

summary: A gradient SOX9+ distal progenitor cell differentiation impacts the patterning of the lung during branching morphogenesis. Although the heterogeneity of this population has been suggested, the specific roles of these subgroups still largely obscure. Here, we explore at least two distinct functional subgroups: the tip progenitors residing at the tips are critical for bud extension and cell allocation, while the transition progenitors sitting immediately to them are indispensable for cell transition. It’s suggested Hippo pathway could regulate the gradient cell differentiation during lung branching. We observed the Cre recombinase driving by Sftpc promoter couldn’t delete Lats1/2 floxed alleles in majority of the tip of SOX9+ distal region, even though the Cre was activated in all the conducting airway. Genetic evidence implied the distal tip progenitors alone is sufficient to help construct the comparable lung structures, while cells at transition stage contributed to the conducting airways. At the expense of themselves, the distal tip progenitors would quickly switch to the transition state when activate YAP via LATS1/2 perturbation. The increasing of cells at transition state results in aggregation of AT1 cells and missing of AT2 cells. Lacking Lats1/2 in SOX9+ distal progenitors in 3D culture could also promote the cell differentiation toward the transition state. Thus, a lower YAP activity is benefit for tip progenitor cell reservation.

overall_design: Examine the difference of gene expression between Lats1/2 -deficient and their littermate control lungs

first: Kuan

last: Zhang

first: Madhuri

last: Basak

first: Erica

last: Yao


title: Reduced IP6K levels impair life-cycle transitions and intracellular development of Trypanosoma cruzi within human cardiomyocytes

city: São Paulo

first: Eduardo

middle: Moraes

last: Reis

state: SP

address: Av. Prof. Lineu Prestes, 748

department: Biochemistry

country: Brazil

institute: University of São Paulo

summary: Trypanosoma cruzi is the etiological agent of Chagas disease (CD). During its life cycle, T. cruzi undergoes several key differentiation processes that are essential for its survival. The precise mechanisms that regulate these processes remain elusive, and any interference in this cycle would represent a breakthrough in the development of effective therapy against CD. Here we show that key differentiation processes of T. cruzi (metacyclogenesis, amastigogenesis and trypomastigogenesis) are profoundly impaired in response to low inositol hexakisphosphate kinase (IP6K) levels. Epimastigote forms of IP6K-deficient T. cruzi exhibit morphological alterations and reduced metacyclogenesis. IP6K-deficient metacyclic forms show reduced infective potential in human cardiomyocytes. IP6K-deficient amastigote forms present impaired ability to transform into trypomastigotes, with most of the population egressing from human cardiomyocytes without completing trypomastigogenesis. Although IP6K catalyzes the formation of inositol pyrophosphates (IP7), the levels of this metabolite do not undergo significant reduction in response to low IP6K levels, suggesting that this kinase sustains the T. cruzi life cycle through non-canonical functions. Since total depletion of IP6K is lethal and the primary structure of IP6K shares only ~25% similarity with its human homolog, this kinase emerges as a promising target for drug development against CD.

overall_design: RNA-seq profiling of control T. cruzi (CL Brener) lineage (parental T7/Cas9) and its IP6K single-knockout lineage (using epimastigotes and trypomastigotes forms).

first: Bryan

middle: E

last: Abuchery

first: Thaise

middle: L

last: Teixeira

first: Vitor

last: da Silva

first: Rauni

middle: B

last: Marques

first: Fernanda

middle: M

last: Gerolamo

first: A

last: Shukla

first: Carolina

last: Catta-Preta

first: Bruno

last: Santarossa

first: Marija

last: Krasilnikova

first: Craig

last: Lepslay

first: Yete

middle: G

last: Ferri

first: Maria Cristina

last: Motta

first: Samuel

first: Miguel

last: Chiurrilo

first: Noelia

last: Lander

first: Simone

last: Calderano

first: Henning

middle: J

last: Jessen

first: Richard

last: McCulloch

first: Marcelo


title: Fibrillarin-mediated 2'-O-methylation serves as a translation brake on uncapped enterovirus RNA

status: Public on Jul 03 2026

first: Zhang

last: Kui

address: Jinlong Avenue, Jiangxia District     Wuhan Institute of Virology, Chinese Academy of Sciences     Wuhan, Hubei 430200     China

institute: Wuhan Institute of Virology

summary: 2′-O-methylation (Nm) is a key epitranscriptomic mark across diverse RNAs, yet its role in antiviral defense remains largely unexplored. To systematically investigate the landscape and functional significance of internal Nm modifications on enterovirus RNAs, a sensitive sequencing method termed RACE-Nm was established, in combination with the machine learning–based predictor NanoNm, to map Nm sites on low-abundance RNAs at single-nucleotide resolution. A conserved Nm site was identified at nucleotide 307C within the viral internal ribosome entry site (IRES), which was catalyzed by the methyltransferase FBL. The 2′-O-methylation at 307C caused steric hindrance that disrupted PCBP2 recruitment to the IRES and repressed cap-independent translation. Consequently, FBL-mediated suppression of IRES activity limited the production of the viral RNA polymerase 3D, which in turn prevented the upregulation of a set of pro-viral host genes, including FOSL1, ITGB3, KCNQ4, and TFPI2. The physiological importance of this defense mechanism was further demonstrated in vivo, as EV71 mutant lacking the 307C site showed markedly enhanced replication, aggravated tissue damage, and increased lethality in mouse model. Our study establishes FBL-mediated internal Nm modification as a novel host defense pathway that directly targets cap-independent translation to restrict enteroviral infection, highlighting the epitranscriptomic regulation of host–virus interactions.

sample_organism:
Homo sapiens
Chlorocebus sabaeus

platform_organism:
Homo sapiens
Chlorocebus sabaeus

overall_design: This study integrates four experimental modules: (1) Time-course transcriptomic profiling of host gene expression in RD cells at 0, 6, and 24 hours post EV71 infection using RNA-seq on the DNBSEQ platform. (2) RNA-seq analysis of EV71-infected RD cells following siRNA-mediated knockdown of FBL to assess its functional role in infection. (3) Nm site mapping on EV71 RNA by sequencing cDNA termination products from low-dNTP primer extension, followed by targeted RACE-PCR and Illumina sequencing. (4) Direct RNA sequencing of poly(A)-selected EV71 RNA using Oxford Nanopore technology, followed by genome-wide identification of Nm modification sites via machine learning-based (NanoNm) analysis.

first: Kui

last: Zhang

first: Lishi

last: Liu

first: Haibin

first: Wuxiang

last: Guan


title: Thyroid cancer-associated EZH1 Q571R mutation drives chromatin compaction and H3K27me3 invasion into active chromatin

city: Seoul

first: Hanbyeol

last: Kim

address: Daehak-ro 103

country: South Korea

institute: Seoul National University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Dysregulation of Polycomb Repressive Complex 2 (PRC2) contributes to cancer. Of its catalytic subunits, Enhancer of Zeste (EZH) 1 and EZH2, EZH2 mutations are extensively studied, but the role of EZH1 in cancer remains largely unexplored. Here, we investigate the thyroid cancer-associated EZH1 Q571R mutation and uncover a mechanism that extends beyond catalytic gain of function. Using biochemical, single-molecule, epigenomic, and transcriptomic analyses, we demonstrated that EZH1 Q571R significantly enhances chromatin compaction and stimulates PRC2-EZH1 catalytic activity, thereby rewiring PRC2 chromatin interactions. This altered engagement enables PRC2 activity within H3K36me2-marked chromatin typically refractory to H3K27 methylation, leading to widespread epigenetic and transcriptional reprogramming. Notably, enhanced chromatin compaction is observed with EZH1 Q571R but not with the corresponding EZH2 Q570R mutation, indicating an EZH1-specific mechanism. Functionally, EZH1 Q571R accelerated tumor growth in vivo and induced pronounced micronuclei formation ex vivo, reflecting aberrant chromatin compaction and genome instability. Together, our study demonstrates that EZH1 Q571R promotes a permissive epigenomic landscape for the progression of follicular thyroid cancer.

overall_design: CUT&Tag for H3K27me3 in Nthy cells expressing EZH1 WT, EZH1 Q571R, EZH1 Y727D, EZH1 Q571R;Y727D, EZH2 WT, EZH2 Q570R. Additionally, H3K36me2 CUT&Tag in Nthy cells expressing EZH1 WT or EZH1 Q571R.

first: Chul-Hwan

last: Lee


title: Pro-inflammatory signaling originates from epicardium-derived fibroblasts in a PKP2 deficient model of arrhythmogenic cardiomyopathy

status: Public on Feb 12 2026

city: Rochester

first: Cameron

last: Baker

state: NY

address: 601 Elmwood Ave

institute: University of Rochester

summary: Introduction: Arrhythmogenic Cardiomyopathy (AC) is an inherited disease that is caused by desmosome protein mutation with plakophilin 2 (PKP2) mutation being most common. AC is known to cause sporadic ventricular arrhythmias, myocyte damage, and subepicardial fibrosis. Given the origin of fibrosis from epicardium, we wanted to understand how epicardium-derived cells (EDCs) contribute to the AC pathogenesis. Hypothesis: EDCs propagate the pro-inflammatory signaling that contributes to AC pathogenesis. Methods: We developed transgenic mice that lack PKP2 in cardiomyocytes (PKP2-cKO) or in both cardiomyocyte and epicardial cells (PKP2-ceKO) via the tissue-specific expression of tamoxifen-inducible Cre recombinase. Tamoxifen injected mice expressing Cre in cardiomyocytes, but with no floxed PKP2 gene, was used as a control. EDCs were traced with Cre-dependent Green Fluorescence Protein (GFP). Non-myocyte populations were isolated 21 days post-tamoxifen injection for single cell RNA-sequencing (scRNA-seq) using 10X Genomics platform. Perfused hearts were separated into left and right ventricle for qRT-PCR. Immunohistochemistry was used for cardiac structure and cellular composition. Echocardiography was performed to measure cardiac physiology.  Results: The scRNA-seq analysis identified an epicardium-derived fibroblast population that secretes pro-inflammatory cytokines, including CCL2, CCL7, Thbs1, and PTX3. While pro-inflammatory EDCs are found in both PKP2-cKO and PKP2-ceKO mice, they were most numerous in PKP2-ceKO mice. Importantly, macrophages and B cells accumulated in both PKP2-cKO and PKP2-ceKO mice compared to controls. qRT-PCR confirmed that the expression of genes encoding fibrosis markers (POSTN, Col1A1, Col1A2, and Col3A1), pro-inflammatory fibroblast markers (CCL2, CCL7, Thbs1, PTX3), macrophage markers (F4/80, Cx3cr1, Spp1, Trem2, and CCR2), and B cell markers (CD19 and CD79b) were significantly enriched in both PKP2-cKO and PKP2-ceKO mice compared to control. Our expression and histologic data also revealed an exaggerated pro-inflammatory response in PKP2-ceKO mice, that progresses from the right to bi-ventricular predominance. However, echocardiography showed no significant difference in cardiac function between PKP2-cKO and PKP2-ceKO, and B cell depletion did not alter disease progression. Conclusion: A subset of epicardium-derived fibroblasts in PKP2 KO mice secretes pro-inflammatory cytokines that contributes to cardiomyocyte damage and cardiac fibrosis in AC.

first: Daniel

last: Han

first: Alan

last: Brooks

first: John

last: Ashton

first: Mario

last: Delmar

first: Eric

last: Small


title: RNA sequencing datasets generated from murine CD8-positive T cells

city: Tsukiji

first: Yuki

last: Okuhiro

state: Tokyo-to

country: Japan

institute: National cancer center research institute

summary: This repository contains raw bulk and single-cell RNA sequencing reads generated from mouse T lymphocyte samples. Libraries were prepared and sequenced using standard protocols.

overall_design: RNA-seq profiling of murine naive CD8+ T cells from splenocytes of C57BL/6 mice after 48 hours of stimulation with anti-CD3 and anti-CD28 monoclonal antibodies in the presence of either DMSO (control) or 10 nM ponatinib.

first: Yasuhiro

last: Kojima

first: Hiroyoshi

last: Nishikawa


title: Age-stratified transcriptomic profiling reveals biologically distinct molecular phenotypes across pediatric, adolescent, and adult osteosarcoma

status: Public on Feb 11 2026

city: Beijing

first: Jichuan

last: Wang

state: Beijing

address: No. 11 Xizhimen South St.

institute: Peking University People's Hospital

summary: Osteosarcoma exhibits a bimodal age distribution with distinct clinical behaviors between pediatric and adult patients. In this study, bulk RNA sequencing was performed on tumor specimens from 70 osteosarcoma patients stratified into pediatric (14 years and younger), adolescent (15 to 18 years), and adult (19 years and older) groups. Differential expression, functional enrichment, and immune infiltration analyses were conducted to characterize age-associated transcriptional differences. Pediatric tumors exhibited a hyperproliferative phenotype, adolescent tumors showed enhanced immune-related signatures, and adult tumors displayed activation of osteogenic differentiation programs. A characteristic pediatric-specific gene signature was further identified, providing insights into age-related molecular heterogeneity in osteosarcoma.

overall_design:
Tumor specimens from 70 osteosarcoma patients were analyzed by bulk RNA sequencing to investigate age-associated transcriptional differences among pediatric, adolescent, and adult groups.

***************************************************************
Due to limitations in data archiving and long-term storage, the raw sequencing data are currently unavailable.
***************************************************************

first: Li

last: Hu

first: Feiyang

last: Qi

first: Huimin


title: A Single-Cell Bioprinting Approach with Subcellular Resolution to Reconstruct Native Cellular Microenvironments and Interrogate Spatial Biology

city: Portland

first: Luiz

last: Bertassoni

state: OR

address: 2720 S Moody Ave

department: Knight Cancer Institute

institute: Oregon Health and Science University

summary: Tissue development, function, and disease are largely driven by the spatial organization of individual cells and their interactions within a complex and heterogeneous cellular microenvironment. Engineered tissue models provide a controllable platform to dissect these spatially driven processes. However, strategies to fabricate tissues that replicate near-exact spatial organization and cellular composition of native microenvironments, necessary to faithfully recapitulate in vivo spatial relationships, have remained elusive to date. Here we present a precision bioprinting approach capable of generating high-fidelity replicas of patient biopsies that preserve complex cellular organization and heterogeneity with subcellular resolution. We demonstrate spatial placement of individual cells with down to ~3 µm spatial precision and up to eight cell types per bioprint. Using this approach, we demonstrate for the first time that altering the microscale spatial organization of tumor microenvironments of similar cellular composition can significantly alter transcriptomic programs of cell response. The ability to engineer and manipulate native cellular microenvironments with single-cell resolution marks a significant advancement toward understanding the critical influence of spatial biology on complex biological systems, such as the tumor microenvironment and organogenesis.

overall_design: A combination of MCF10A, MCF7, and primary human fibroblasts cells were single-cell bioprinted onto a collagen coated glass microscope slide either in a patterened or randomly deposited arrangement. The cells were cultured in M87 media for 24 hours before being fixed with 4% PFA and permeabilized with 100% methanol. The Visium HD spatial transcriptomics protocol was then followed to generate the data deposited here. Complete protocol for sample preparation through library preparation can be found at: Helms HR and Bertassoni LE. Single-cell spatial transcriptomic profiling of cultured cells and engineered tissues without embedding or sectioning. STAR Protocols. 2025. DOI: 10.1016/j.xpro.2025.104074

first: Haylie

middle: R

last: Helms


title: An atlas of primate insular cortex reveals a signal-processing strategy in von Economo neurons [scRNA-seq]

status: Public on Feb 20 2026

first: Ruifeng

last: Liu

first: Sheng

first: Rui-Feng

first: Mengyao

last: Huang

first: Yuhui

last: Shen

first: Mingting

last: Shao


title: A novel Adnp frameshift variant disrupts Wnt signaling leading to chromatocytoskeletal defects and autism-related behavior in mice

city: Edegem

first: Dale

middle: John

last: Annear

state: Antwerpen

address: Prins Boudewijnlaan 43/6

department: Center of Medical Genetics

country: Belgium

institute: University of Antwerp

summary: Background: Heterozygous de novo variants in the transcription factor Activity-Dependent Neuroprotective Protein (ADNP) cause a severe neurodevelopmental disorder, termed the Helsmoortel-Van der Aa syndrome (HVDAS), that is characterized by autism, intellectual delay, and malfunctions in several other organ systems. The ADNP gene is essential for embryonic development and interacts with components of several chromatin remodeling complexes, though the exact pathophysiological mechanisms remain hidden.  Methods: We used CRISPR/Cas9 genome editing to create a 14-base pair deletion in the murine Adnp gene to study the effects of the variant in a heterozygous disease-relevant mouse model.  Results: Heterozygous mice carrying the c.2463_2476del (p.Leu822Hisfs*6) deletion are viable and fertile. Introduction of the 14-base pair deletion reduced cellular Adnp levels in the brain as well as its associations to chromatin, paralleled by a genome-wide increase in chromatin accessibility. Morphology analysis showed mild neuroanatomical changes in brain regions related to cognition, memory and learning, and motor skills. Behavioral testing in heterozygous Adnp mice confirmed cognitive defects in the Morris water maze test, increased anxiety in the elevated plus maze test, repetitive behavior after marble burying, and impaired social interactions. Transcriptome sequencing of the frontal cortex, an essential region involved in executive functions, cognition, and motor control, showed predominant downregulation of the Wnt signaling pathway. Cytoskeletal abnormalities were further coupled to synaptic plasticity deficits with dysregulated transcription factors implicated in lineage specification, as well as alterations in neuronal cell numbers. Adnp can also directly regulated mechanisms of synaptic plasticity by interacting with Camk2a and Dbn1. The frameshift variant interfered with these complexes and caused aberrant Camk2a phosphorylation at synapses. Mass spectrometry of the frontal cortex of heterozygous Adnp mice identified changes of multiple chromatin interacting proteins and cytoskeletal components, confirming chromatocytoskeletal dysregulations detected in the bulk transcriptome. Ultimately, Hi-C analysis detected fine-scale, locus-specific differences in 3D genome architecture in the heterozygous Adnp 14-base pair deletion mice, which are associated with transcriptional changes.  Conclusions: We generated a disease-relevant heterozygous Adnp mouse model that parallels many of the molecular and behavioral aspects observed in Helsmoortel-Van der Aa patients. We demonstrate that Adnp has a primary nuclear role involving Wnt signaling coupled with cytoskeletal deficits. Our novel mouse model is thus a valuable model to study the human disorder and may be used for preclinical studies.

overall_design: RNAseq of the frontal cortex in adolescent WT and HET littermates. Differential gene expression seven WT and seven HET mice was analyzed 13,383 expressed genes.

first: Claudio Peter

last: D’Incal

first: Elisa

last: Cappuyns

first: Flora

last: Paldi

first: Mathijs

last: van der Lei

first: Dale John

first: Clara

last: Milián Alastruey

first: Frank

last: Kooy


title: Single-cell RNA sequencing of non-cardiomyocytes obtained from wild-type mouse hearts 20 days after transverse aortic constriction or sham surgery

city: bad nauheim

first: Stefan

last: Günther

address: ludwigtr. 43

institute: MPI for heart and lung research

overall_design: The non-cardiomyocyte population was isolated from mouse hearts obtained 20 days after sham ("Sham") or transverse aortic constriction ("TAC")

first: Haruya

last: Kawase

first: Nina

last: Wettschureck

last: Guenther


title: Transcripts identified by microarray analysis that were deregulated in E12.5+18h cultures of NMRI ureters upon treatment with NOGGIN.

first: Mark-Oliver

last: Trowe

summary: Evaluation of the transcriptional changes in E12.5+18h ureters upon treatment with NOGGIN.

overall_design: Ureters of E12.5 NMRI embryos were dissected and cultured for 18h in medium containing 10 µg/ml NOGGIN  (treated) or in medium without NOGGIN (control). Total RNA from these ureters was analyzed by microarray analysis.

first: Andreas

last: Kispert


title: Targeting the lipid metabolism proteins FASN and GPAM in alveolar type II cells decreases lung metastasis

status: Public on Feb 10 2026

city: London

first: Mariia

last: Yuneva

address: 1 Midland Road

country: United Kingdom

institute: The Francis Crick Institute

summary: Cancer cells that seed in the lung require lipids, which are mostly produced by alveolar type II (AT2) cells. However, whether overt metastases depend on AT2 cell-derived lipids and whether AT2 cells can be targeted to reduce metastasis growth remains unknown. We discovered that metastases stimulate the proliferation of AT2 cells in their vicinity and reprogram them into lipid feeder cells in mice and patients with breast cancer using spatial mass spectrometry imaging combined with immunohistochemistry and spatial transcriptomics. Mechanistically, we find that the secretome of the metastases contains IL-6 and formate, which increase the activity of the transcription factor sterol regulatory element-binding transcription factor 1 (SREBP-1). This in turn enhances the expression of key de novo lipid synthesis genes including fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase 1 (GPAM). Deleting Fasn selectively in AT2 cells or targeting FASN and GPAM systemically is sufficient to impair breast cancer-derived metastasis growth in mice. In summary, we discovered that overt metastases reprogram AT2 cells and that targeting the lipid metabolism of AT2 cells impairs metastasis growth.

overall_design: 6–8-week-old female Balb/c mice were inoculated with 4T1 (1 x 10^6) cells in the mammary fat pad. Mice were euthanized after 21-23 days. Lungs from either tumour-bearing or control mice were taken for the analysis. Visium spatial transcriptomics analysis was carried out according to the manufacturer’s instructions (10x Genomics) with the following parameters: Fresh-frozen mouse either control or metastatic lung tissues derived from 4T1 m.f.p. injection model was processed for spatial gene expression profiling using the 10x Genomics Visium Spatial Gene Expression platform (Visium Slide PN-2000233, SN: V13J17-305). Tissue sections were mounted on a Visium Spatial Gene Expression Slide with four capture areas, each containing ~5,000 spatially barcoded spots. Following fixation and hematoxylin and eosin (H&E) staining, tissue permeabilization was performed for 18 minutes—a duration determined through prior tissue optimization using the 10x Genomics Tissue Optimization protocol (CG000238). mRNA released from permeabilized tissue was hybridized to oligonucleotides on the slide, and reverse transcription was carried out in situ to generate spatially barcoded cDNA. Subsequent library preparation followed the manufacturer's protocol (Visium Spatial Gene Expression Reagent Kits User Guide, CG000239 Rev F), including second-strand synthesis, cDNA amplification, enzymatic fragmentation, end repair, adaptor ligation, and sample index PCR. Libraries were sequenced on an Illumina platform (NovaSeq 6000) using paired-end sequencing (Read 1: 28 bp, Read 2: 90 bp) at a target depth of (50k reads per cell/spot).

first: Weigang

last: Cai

first: Yulia

last: Panina

first: Jiadong

last: Mao

first: Juan

last: Fernández-García

first: Xiao-Zheng

last: Liu

first: Robert

last: Gunn

first: Marg

last: Crawford

first: Sarah-Maria

last: Fendt


title: Transcripts identified by microarray analysis that were deregulated in E14.5 Tbx18(cre/+);Smad4(fl/fl) (Smad4cKO (UM)) ureters.

address: Carl-Neuberg-Str. 1

institute: Medizinische Hochschule Hannover

summary: Evaluation of the transcriptional changes in E14.5 ureters upon loss of Smad4 in the ureteric mesenchyme.

overall_design: Total RNA from dissected ureters of E14.5 Smad4cKO (UM) and control embryos was analyzed by microarray analysis.


title: PRMT5 Inhibition Promotes Cross-Species Spermatogonia Expansion and Suppresses Differentiation

city: guangzhou

first: kang

last: Tang

address: No. 1023 South Shatai Road, Baiyun District, Guangzhou, Guangdong, China

institute: Southern Medical University

summary: Spermatogonial stem cells (SSCs) hold great promise for treating male infertility, but their clinical translation is impeded by the lack of optimal conditions to maintain their undifferentiated state in vitro. In this study, we focused on epigenetic regulators upregulated during differentiation as potential targets. Through a small-molecule screen targeting such conserved regulators, we found that PRMT5 inhibition suppressed mouse SSC differentiation and enhanced their proliferation in a GDNF-deficient, differentiation-prone microenvironment in vitro. Using SSC transplantation assays, we confirmed that EPZ015666-treated SSCs retained their spermatogonial identity. This differentiation-inhibitory effect was reversible upon EPZ015666 withdrawal, allowing for the restoration of normal spermatogenesis. Notably, EPZ015666 also inhibited differentiation and promoted the proliferation of human and non-human primate spermatogonia in vitro. Mechanistically, EPZ015666 exerted this effect by inhibiting the enzymatic active site of PRMT5. These findings suggest that PRMT5 inhibition could provide a novel strategy for culturing human SSCs in vitro.

overall_design: To address this, we generated Prmt5-knockout mouse cultured SSCs from Prmt5 flox/flox; Rosa26-CreERT2 mice by treating them with 1 µM 4-hydroxytamoxifen (4OHT) in vitro (Dong et al, 2021). Compared to the ethanol-treated (EtOH) control group, the expression level of PRMT5 and DMRT1 dramatically reduced in these knockout SSCs treated with 4OHT


title: Single cell sequencing of bladder cancer patients

city: Chongqing

first: Li

middle: qiu

address: No. 10, Changjiang Road, Daping, Yuzhong District, Chongqing

institute: Chongqing Daping Hospital

summary: To achieve a more profound comprehension of the bladder tumor microenvironment, we have meticulously curated single-cell samples from 11 patients diagnosed with bladder cancer. Our comprehensive analysis not only elucidates the intricate heterogeneity among distinct cellular subpopulations within the tumor but also uncovers the underlying cellular interactions. These findings collectively serve as an invaluable asset, paving the way for the development of innovative and targeted therapeutic strategies for bladder cancer.

overall_design: We performed single-cell sequencing on samples derived from five patients. Initial data processing involved stringent quality control to exclude low-quality cells. This included filtering based on thresholds for unique molecular identifiers (nUMI), expressed genes (nGene), and mitochondrial gene content. We also applied a doublet removal step. The resulting high-quality gene expression matrix is provided to facilitate studies on tumor microenvironment heterogeneity, immune cell composition in bladder cancer.

first: Qiuli

first: Weihua

last: Lan

first: Jun

last: Jiang

first: Weiming

last: Luo


title: Impact of ATEVs and EV-DNA on transcriptional profile of DC2.4 cells

city: New Ypok

first: Mengying

last: Hu

state: New York

address: 413 E 69th St, New York, NY 10021

institute: Weill Cornell Medical College

summary: Antigen processing and presentation (APP) is essential for adaptive immunosurveillance in all nucleated cells. Here we describe a novel mechanism through which secreted factors other than cytokines, specifically extracellular vesicles (EVs) released from activated T cells (ATEVs) drive a positive feedback loop that enhances antigen presentation and immune responses in normal physiology and cancer. ATEV-induced immunogenicity relies on extravesicular double-stranded DNA (EVDNA) and granzyme B (Gzmb). ATEV-DNA is notably abundant, primarily consisting of genomic DNA enriched in copies of specific genes, including numerous APP machinery genes. Mechanistically, ATEV transfer of APP machinery genes to recipient dendritic or tumor cells is facilitated by Gzmb disruption of recipient cell nuclear integrity. DNAse treatment of ATEVs removed the majority of EVDNA, preventing APP machinery upregulation in recipient cells, which in turn failed to recruit T lymphocytes into tumors. Notably, ATEVs hold promise as an immune-boosting therapeutic, particularly in restoring MHC-I antigen processing and presentation, and synergize with checkpoint blockade therapy in several immunotherapy-refractory tumors. Collectively, our findings uncover a novel mechanism through which ATEVs boost APP and anti-tumor immunity. Gzmb-mediated nuclear transfer opens new avenues for non-viral gene delivery, offering potential for enhanced intranuclear gene transport and expression efficiency.

overall_design: RNAseq profiling of DC2.4 cells after being treated with PBS, ATEVs, NTEVs (non-activated T cell-derived EVs), and DNAse-pretreated ATEVs in vitro


title: DLEU2 promotes cell motility and immune infiltration in cervical squamous cell carcinoma through reciprocal feed-forward activation of E2F1

first: Chuntao

last: Tao

state: State...

address: China

institute: Chongqing Medical University

summary: Cancer metastasis is the primary cause of high mortality in patients with cervical squamous cell carcinoma (CESC). The invasive ability of cancer cells is enhanced by increased cell motility, which contributes to their distant metastasis. The oncogenic lncRNA DLEU2, implicated in tumor progression and prognosis, remains understudied in CESC. This study investigated how DLEU2 enhances cell motility and regulates immune infiltration in CESC. We found that DLEU2 was upregulated in CESC tissues and correlated with poor prognosis in advanced-stage patients. Functionally, DLEU2 knockdown suppressed cell migration and invasion, while its overexpression enhanced motility. Mechanistically, DLEU2 knockdown altered the expression of downstream genes related to cell motility and adhesion. An interaction between DLEU2 and E2F1 protein was confirmed by RNA pulldown assay. E2F1 expression was downregulated or upregulated after DLEU2 knockdown or overexpression, respectively, while DLEU2 expression was also upregulated after E2F1 overexpression. Therefore, DLEU2 may form a regulatory loop with E2F1 to activate the transcription of downstream genes related to cell motility and adhesion. Additionally, E2F1 expression strongly correlated with immune infiltration levels (e.g., T cells, Tregs, monocytes, mast cells), and DLEU2 exhibited a parallel immune cell abundance pattern,  suggesting indirect immunomodulatory effects via E2F1. These findings propose that the DLEU2-E2F1 axis promotes CESC metastasis by dual mechanisms: enhancing tumor cell motility and reshaping the immune microenvironment. The study highlights DLEU2 as a potential therapeutic target to disrupt metastatic pathways and immune evasion in CESC. Further validation is needed to explore clinical applications of targeting this regulatory network.

overall_design: 7 unique pairs of biopsy and surgical resection specimens and 1 pairs of cell lines samples were sequenced and profiled.

first: Min

last: He


title: Peripheral blood mononuclear cells single-cell landscape of newly diagnosed NK/T cell lymphoma patients

status: Public on Feb 07 2026

city: Shanghai

first: Xiaozhen

last: Liang

address: Life Science Research Building 320 Yueyang Road, Xuhui District

institute: Shanghai Institute of Materia Medica Chinese Academy of Sciences

summary: Natural killer/T cell lymphoma (NKTCL) is a rare and aggressive form of non-Hodgkin's lymphoma associated with Epstein-Barr Virus (EBV) infection.The recent advancement of multi-omics technologies has significantly enhanced our understanding of NKTCL disease biology, including genetics, transcription landscape, variations of EBV strain, and microenvironments. Emerging evidence suggests that immunoprofiling of peripheral blood mononuclear cells (PBMCs) is associated with the treatment response of cancer patients and can be used to guide clinical trials and therapy. In this study, we utilized single-cell RNA sequencing (scRNA-seq) to comprehensively characterize the phenotypic landscape of PBMCs in newly diagnosed patients with NKTCL. This research offers a valuable peripheral blood-based signature for newly diagnosed NKTCL, which could be a crucial resource for further investigations into the pathogenesis of NKTCL and the optimization of therapeutic regimens.

overall_design: scRNA-seq profiling of PBMCs from healthy donors and newly diagnosed NKTCL patients

first: Rong

first: Ran

last: Jia

first: Chuanxu


title: Impact of ATEVs and EV-DNA on transcriptional profile of a pancreatic cancer cell line with poor immunogenicity

overall_design: RNAseq profiling of a low immunogenic pancreatic cancer cell clone isolated from KPCY (KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre; Rosa26YFP/YFP) mice, after being treated with PBS, ATEVs, NTEVs (non-activated T cell-derived EVs), and DNAse-pretreated ATEVs in vitro


title: Adaptive immune responses to vaccination reflect social status at first exposure in rhesus macaques

status: Public on Feb 06 2026

city: Chicago

first: Joao

last: Barroso-Batista

state: IL

address: The University of Chicago, KCBD room 9220E, 900 E 57th Street

institute: The University of Chicago

summary: Social gradients are consistently associated with variation in health outcomes, including infectious disease. However, distinguishing between social gradients in antigen exposure versus susceptibility remains challenging. Here, we use a nonhuman primate model for chronic social stress to investigate how social status influences the influenza vaccine-induced adaptive immune response. We manipulated the social status of female rhesus macaques to test the response to influenza antigens in naïve individuals and after secondary exposure. Higher social status at the time of first exposure, but not at the time of secondary exposure, predicted stronger antibody responses to both exposures. Social status also drove gene expression differences for adaptive immune pathways, and genes that predict the magnitude of the antibody response overlap with those linked to social status. Thus, social gradients shape the adaptive immune response in a temporally dependent manner, with particular sensitivity at the time of initial antigen exposure.

overall_design: RNA-seq profiling of PBMCsfrom rhesus macaques before (day 0) and 1, 3 or 7 days following influenza vaccination

first: C. Ryan

last: Campbell

first: Luis B.

last: Barreiro

first: Jenny

last: Tung


title: Thyroid cancer-associated EZH1 Q571R mutation drives chromatin compaction and H3K27me3 invasion into active chromatin

first: Hanbyeol

last: Kim

overall_design: ChIP-seq for EZH1 in Nthy cells expressing EZH1 WT, EZH1 Q571R, EZH1 Y727D, EZH1 Q571R;Y727D, EZH2 WT, or EZH2 Q570R.

first: Chul-Hwan

last: Lee


title: RNA-SEQ of HRECs depleted with Norrin/beta-catenin signaling components or KIF11 or PRDX1

city: Chengdu

first: Shujin

last: Li

state: Sichuan

address: Chengdu, Sichuan province, China, first-ring road, No.34

institute: Sichuan Provincial People's Hospital, Sichuan Academy of Medical Sciences

summary: We performed RNA-Seq on human microvascular endothelial cells (HRECs) with lentivirus-mediated knockdown of CTNNB1, LRP5, FZD4, TSPAN12, KIF11, and PRDX1. This dataset includes the gene expression profiles that reveal the specific gene expression changes that occur in HRECs following the knockdown of these key genes implicated in FEVR.

overall_design: Processed RNA-seq data were generated from human retinal endothelial cells (HRECs) that had been depleted of CTNNB1, LRP5, FZD4, TSPAN12, KIF11, or PRDX1. A shared control group was used for the CTNNB1, LRP5, FZD4, and TSPAN12 knockdown groups, while the KIF11 and PRDX1 knockdown groups each had their own control group.


title: Single-Cell transcriptomic profiling of mouse retinal vascular cells reveals mechanisms of familial exudative vitreoretinopathy.

summary: Familial Exudative Vitreoretinopathy (FEVR) is a rare, inherited disorder characterized by a failure of peripheral retinal blood vessels to develop fully.To investigate the pathogenic mechanisms of FEVR, we conducted single-cell RNA-sequencing of retinal vascular cells from two distinct mouse models: Tspan12 knockout mice and mice with an endothelial-specific conditional knockout of Ctnnb1, which encodes β-catenin. Our analysis of the cellular and molecular profiles of these cells provides unprecedented insight into how disruption of key components of the Norrin/β-catenin pathway contributes to the pathology of FEVR.

overall_design: Three samples from  wild-type (WT) mice, Tspan12 knockout (KO) mice, and Ctnnb1 conditional knockout (cKO) mice.


title: Neutrophils and CD8+ T cells in Muscle-invasive Bladder Cancer (MIBC)

city: Houston

first: Stephen

middle: Qi Rong

last: Wong

state: Texas

address: 6670 Bertner Ave

institute: Houston Methodist

summary:
Biopsies in FFPE blocks from MIBC patients who responded (Responded) or did not respond (Non-Responder) to gemcitabine-cisplatin neoadjuvant chemotherapy were subject to Xenium spatial transcriptomics analysis.
While local immunological effects of chemotherapy-induced tumor cell death are well studied, its systemic impact on distant bone marrow—a site essential for immune cell maturation—remains underexplored. Here, we show that gemcitabine chemotherapy induces inflammatory caspase-1 activation in epithelial cancer cells (epiCaspase-1), triggering pyroptotic cell death. Despite its inflammatory nature, epiCaspase-1 mediated cell death is non-immunogenic. Clinically, cancer patients with high expression of a newly derived epiCaspase-1 gene signature show poorer outcomes. Mechanistically, epiCaspase-1 induces noncanonical release of IL-1α through NINJ1 lytic pores, which remotely skews bone marrow hematopoiesis towards granulocyte-monocyte progenitors and mature neutrophil output. This systemic alteration leads to a heightened neutrophil-to-lymphocyte ratio (NLR) in both peripheral blood and the tumor microenvironment. Notably, pharmaceutic inhibition of caspase-1 blocks this cascade, normalizes hematopoiesis, and recalibrates NLR to favor intratumoral CD8+ T cell infiltration and activation—ultimately improving chemotherapeutic efficacy. These findings underscore that inflammatory pyroptosis is not inherently immunogenic, instead, it reshapes systemic immune landscape towards neutrophil-dominant inflammation in the chemotherapy context.

overall_design: Patient FFPE blocks were sectioned and processed for downstream Xenium spatial transcriptomics according to manufacturer's protocol.

first: Yung Hsing

last: Huang

middle: Q

first: Ethan

last: Subel

first: Hongbo

last: Gao

first: Fotis

last: Nikolos

first: Keith

last: Chan


title: Inflammatory epiCaspase-1 dampens immunogenic cell death by remotely skewing bone marrow hematopoiesis to drive systemic neutrophil-dominant inflammation

summary: While local immunological effects of chemotherapy-induced tumor cell death are well studied, its systemic impact on distant bone marrow—a site essential for immune cell maturation—remains underexplored. Here, we show that gemcitabine chemotherapy induces inflammatory caspase-1 activation in epithelial cancer cells (epiCaspase-1), triggering pyroptotic cell death. Despite its inflammatory nature, epiCaspase-1 mediated cell death is non-immunogenic. Clinically, cancer patients with high expression of a newly derived epiCaspase-1 gene signature show poorer outcomes. Mechanistically, epiCaspase-1 induces noncanonical release of IL-1α through NINJ1 lytic pores, which remotely skews bone marrow hematopoiesis towards granulocyte-monocyte progenitors and mature neutrophil output. This systemic alteration leads to a heightened neutrophil-to-lymphocyte ratio (NLR) in both peripheral blood and the tumor microenvironment. Notably, pharmaceutic inhibition of caspase-1 blocks this cascade, normalizes hematopoiesis, and recalibrates NLR to favor intratumoral CD8+ T cell infiltration and activation—ultimately improving chemotherapeutic efficacy. These findings underscore that inflammatory pyroptosis is not inherently immunogenic, instead, it reshapes systemic immune landscape towards neutrophil-dominant inflammation in the chemotherapy context.

overall_design: Mouse hematopoetic progenitor cells were isolated by immunomagnetic separation from bone marrow preparations of different treatment groups

first: Kazukuni

last: Hayashi


title: Single-cell transcriptomic landscape of epithelial heterogeneity in metastatic hormone-naïve prostate cancer

status: Public on Feb 05 2026

city: Suita

first: Daisuke

last: Motooka

state: Osaka

address: 3-1, Yamadaoka

institute: NGS core facility, Research Institute for Microbial Diseases, Osaka University

summary: Single-cell transcriptomic profiling was performed on diagnostic prostate biopsy specimens from patients with metastatic hormone-naïve prostate cancer to characterize epithelial tumor heterogeneity at diagnosis. Integrated and case-specific analyses revealed that tumors are composed of heterogeneous epithelial cell populations, including basal-associated and epithelial–mesenchymal transition–related transcriptional states, in addition to conventional luminal epithelial cells. No discrete epithelial cluster with high expression of canonical neuroendocrine markers was detected at baseline. These data provide a single-cell–level resource describing epithelial transcriptional states in treatment-naïve metastatic prostate cancer.

overall_design: Diagnostic prostate biopsy specimens from five patients with metastatic hormone-naïve prostate cancer were subjected to single-cell RNA sequencing using the 10x Genomics Fixed RNA Profiling (Flex) platform. The study was designed to characterize epithelial tumor heterogeneity at diagnosis using integrated and case-specific single-cell transcriptomic analyses.

first: Ryuta

last: Watanabe

first: Noriyoshi

last: Miura

first: Tadahiko

last: Kikugawa

first: Takashi

last: Saika


title: Gene expression profile at single cell level of Merkel cells from embryonic, neonatal and postnatal mouse skin

city: Bethesda

first: Lingling

last: Miao

state: MD

address: 9000 Rockville Pike

department: NIAMS

institute: National Institutes of Health

summary: Merkel cells (MCs) are neuroendocrine touch sensors in the epidermis. We used single cell RNA sequencing (scRNA-seq) to analyze the differentiation of MCs in mouse skin.

overall_design: GFP-expressing cells including MCs were isolated from the skin of Sox2-GFP and Gfi1-GFP reporter mice by Fluorescence-activated cell sorting (FACS) and analyzed using scRNAseq.

first: Isaac

last: Brownell


title: Self-clustering of three CBX2 molecules drives PRC2 to promote facultative heterochromatinization of Polycomb target genes [RNA-Seq]

city: Aurora

first: Srinivas

last: Ramachandran

state: CO

department: Biochemistry and Molecular Genetics

institute: University of Colorado School of Medicine

summary: Phase separation is increasingly recognized in facultative heterochromatinization of Polycomb target genes; however, the underlying mechanisms remain obscure. Using single-molecule imaging and tracking, we show that individual condensates in mESCs contain approximately 3 CBX2 molecules and numerous PRC1 and PRC2 subunits and indicate that the composition and dynamics of condensates are developmentally regulated. We reveal that CBX2 clusters PRC2 and controls the spatial distribution of both PRC2 and H3K27me3. Using genomic approaches, we demonstrate that CBX2 binds condensate initiation sites enriched for PRC2 nucleation sites. CBX2 deletion causes PRC2 and H3K27me3 to redistribute from their regular targets. By developing a separate-of-function variant, we determine that CBX2 relies on its self-clustering ability to function. These findings collectively support a novel phase-separation model driven by nucleation and bridging, in which low-abundance proteins self-cluster to initiate condensate assembly, a process tightly coupled to function.

overall_design: CUT&RUN of tagged CBX2 and EZH2 in CBX2fl/fl-HaloTag EZH2-Venus-dTag, CUT&RUN of tagged CBX2-PSM-HT  in CBX2fl/fl-HaloTag & Parental Cells,  CUT&Tag of H3K27me3 in mESCs (CBX2 WT, CBX2 KO, CBX2 PSM, and PGK12.1) in two biological replicates.

first: Steven

last: Ingersoll

first: Abby

last: Trouth

first: J. Carlos

last: Angel

first: Xinlong

last: Luo

first: Axel

last: Espinoza

first: Joey

last: Wen

first: Chengjie

last: Zhu

first: Joseph

last: Tucker

first: Kalkidan

last: Astatike

first: Christopher

last: Phiel

first: Hatim

last: Sabaawy

first: Tatiana

last: Kutateladze

first: Tao

last: P. Wu

first: Tingting

last: Yao

first: Chao

last: Lu

first: Xiaojun

last: Ren


title: Predictability of progression free survival in ovarian cancer

status: Public on Feb 17 2026

first: Benjamin

last: Bitler

state: Colorado

address: CU Anschutz Research Complex II  12700 East 19th Avenue  3400D

department: Cancer Biology

institute: University of Colorado-Anschutz

summary: Given the interrelated mechanisms by which changes to the tumor microenvironment (TME) may drive disease recurrence, we test a novel machine learning approach to identifying key genes that may be involved in the likelihood of recurrence. The ability to compare pre- and post- NACT samples from the same patient shows how chemotherapy drives changes in the TME. We also had the opportunity to employ machine learning methods to investigate whether patient progression-free survival can be prediced from the impact of chemotherapy on the tumor microenvironment.

overall_design:
83 patients with high grade serous ovarian cancer were included in this study. Matched tumor samples from treatment naive biopsies and interval debulking surgery following neoadjuvant chemotherapy (NACT) were obtained from each patients with appropriate clinical information. 95 of these samples were analyzed using the raw (RCC) files provided in GEO series accession numbers GSE201600 and GSE181597. These 166 matched samples were used to capture the gene expression changes that occur after treatment. NanoStriing nCounter Human PanCancer IO360 panel was used to analyze the tumor RNA for 750 genes associated with the tumor microenvironment for all samples. All raw RCC files (of new and previously published data) were analyzed together as described in the data processing steps below.

***************************************************************
see 'GSE319500_reanalysis_samples.xlsx' for GEO accessions reused/reanalyzed for this study.
***************************************************************

first: Lucy

last: Kleunen

first: Grace

last: Bowman

first: Sarah

last: Stockman

first: Logan

last: Barrios

first: Hope

last: Townsend

first: Kimberly

last: Jordan

first: Rebecca

last: Wolsky

first: Kian

last: Behbakht

first: Matthew

last: Sikora

first: Aaron

last: Clauset


title: Self-clustering of three CBX2 molecules drives PRC2 to promote facultative heterochromatinization of Polycomb target genes

first: Srinivas

last: Ramachandran

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

overall_design: Refer to individual Series


title: scRNAseq analysis of 8 week-old KPPC WT, MAP3K7ff   KPPC and MAP3K7fwt KPPC mice pancreatic tumor

city: ST LOUIS

first: KIAN

middle: HUAT

last: LIM

state: MO

address: 660 S. Euclid Avenue  Campus Box 8069, St. Louis

department: internal Medicine

institute: WashU

summary: We pooled three 8 week-old KPPC WT (n=3), MAP3K7ff KPPC (n=3) and MAP3K7fwt KPPC (n=3) mice pancreatic tumor respectively into one sample, prepared single cell suspension and performed 10X genomics scRNASeq to assess transcriptomic changes all cell populations

first: Kian-Huat

last: Lim

first: Sapana

last: Bansod


title: 6 week old KPPC mice treated with vehicle or Takinib (50mg/kg) for 14 days

summary: We pooled three KPPC mice tumors into one sample for vehicle (n=3) or Takinib (n=3), prepared single cell suspension and performed  10X genomics scRNASeq to assess transcriptomic changes all cell populations

overall_design: scRNAseq analysis of KPPC tumors treated with vehcile or  takinib


title: KPPC cells cells treated with EphA2 inhibitor

first: SAPANA

middle: PRAKASHRAO

last: BANSOD

address: 4482 LINDELL BLVD, 608

department: INTERNAL MEDICINE

institute: WASHINGTON UNIVERSITY, ST LOUIS

summary: We treated KPPC cells with DMSO and EphA2 inhibitor for 24 hours and performed bulk RNAseq to assess transcriptomic changes KPPC cells

overall_design: Bulk RNAseq analysis of KPPC cells after DMSO and EphA2 inhibitor treatment


title: Sparse CBX2 nucleates many Polycomb proteins to promote facultative heterochromatinization of Polycomb target genes

summary: Facultative heterochromatinization of genomic regulators by Polycomb repressive complex (PRC) 1 and 2 is essential in development and differentiation; however, the underlying molecular mechanisms remain obscure. Using genetic engineering, molecular approaches, and live-cell single-molecule imaging, we quantify the number of proteins within condensates formed through liquid-liquid phase separation (LLPS) and find that in mouse embryonic stem cells (mESCs), approximately 3 CBX2 proteins nucleate many PRC1 and PRC2 subunits to form one non-stoichiometric condensate. We demonstrate that sparse CBX2 prevents Polycomb proteins from migrating to constitutive heterochromatin, demarcates the spatial boundaries of facultative heterochromatin, controls the deposition of H3K27me3, regulates transcription, and impacts cellular differentiation. Furthermore, we show that LLPS of CBX2 is required for the demarcation and deposition of H3K27me3 and is essential for cellular differentiation. Our findings uncover new functional roles of LLPS in the formation of facultative heterochromatin and unravel a new mechanism by which low-abundant proteins nucleate many other proteins to form compartments that enable them to execute their functions.

overall_design: CUT&RUN of tagged CBX2 and Ezh2, and CUT&Tag of H3K27me3 in mESCs (WT and CBX2 KO) in two biological replicates.

first: Steven

last: Ingersoll

first: Abby

last: Trouth

first: Xinlong

last: Luo

first: Axel

last: Espinoza

first: Joey

last: Wen

first: Joseph

last: Tucker

first: Kalkidan

last: Astatike

first: Christopher

last: Phiel

first: Tatiana

last: Kutateladze

first: Tao

middle: P

last: Wu

first: Xiaojun

last: Ren


title: E96A baseline transcriptional changes

status: Public on Feb 04 2026

city: Indianapolis

first: Kelley

last: Mark

state: Indiana

institute: Herman B Wells Center for Pediatric Research

summary: APE1/Ref-1 is the primary apurinic/apyrimidinic endonuclease in the base excision repair pathway. To define baseline transcriptional changes resulting from loss of APE1 endonuclease activity, RNA-seq was performed on Pa03C pancreatic ductal adenocarcinoma cell lines engineered to carry a homozygous E96A mutation and on matched Cas9 controls. Cells were cultured under untreated conditions. This dataset provides gene expression profiles associated with impaired APE1 endonuclease function in PDAC cells.

overall_design: Pa03C pancreatic ductal adenocarcinoma (PDAC) cell lines were engineered to carry a homozygous APE1 E96A endonuclease-deficient mutation or a matched Cas9 control allele. Cells were cultured under standard growth conditions without drug treatment. RNA-seq was then performed on Pa03C Cas9 and Pa03C E96A PDAC cell lines under untreated conditions. The study aims to capture baseline transcriptional consequences of impaired APE1 endonuclease activity

first: Mahmut

last: Mijit

first: Eyram

last: Kpenu

first: Mark

last: Kelley


title: Single cell mRNA sequencing on esophageal cells of human biopsies coming from subtotal esophagectomy

status: Public on Feb 03 2026

city: Anderlecht

first: Louison

last: Descampe

address: Route de Lennik 808

department: IRIBHM

institute: Université Libre de Bruxelles

summary: In our study, we used single-cell RNA sequencing to characterize epithelial cell populations in the human esophagus in control condition compared to Barrett esophagus condition.

overall_design: Oesophageal single cell mRNA profiles of control and Barret biopsies from patient by deep sequencing using 10x genomic.

first: Benjamin

last: Beck


title: Intrinsic mechanisms and microenvironmental cues fine-tune plasticity of esophageal progenitors


title: Single cell mRNA sequencing on esophageal cells of WT and Krt5-CreERT2:R26SmoM2/EYFP (K5:Smo) mice 5 days after Tamoxifen administration

summary: In our study, we used single-cell RNA sequencing to investigate the early effects of Hedgehog signaling pathway activation in esophageal progenitors.

overall_design: Esophageal single cell mRNA profiles of WT and Krt5-CreERT2:R26SmoM2/EYFP mice by deep sequencing using 10x genomic.


title: mRNA sequencing on esophageal cells of Krt5-CreERT2:R26SmoM2/EYFP (K5:Smo) mice, untreated and treated with ibuprofen

summary: In our study, we used mRNA sequencing to investigate the effect of ibuprofen on the transcriptome of esophageal epithelial cells of K5:Smo mice.

overall_design: Oesophageal mRNA profiles of Krt5-CreERT2:R26SmoM2/EYFP mice, 12 weeks after tamoxifen administration, untreated and treated with ibuprofen by deep sequencing using Illumina

last: Dassy

first: Alizée

last: Vercauteren Drubbel


title: mRNA sequencing on esophageal organoids derived from wild-type mice

summary: In our study, we used mRNA sequencing to investigate the effect of 3 days-treatment with TGFb1, BMP4 alone or in combination on the squamous and columnar differentiation.

overall_design: mRNA profiles of esophageal organoids derived from wild-type mice treated for 72h with TGFb inhibitor / BMP4 / TGFb / TGFb + BMP4 by deep sequencing using Illumina


title: Single cell mRNA sequencing on esophageal cells of Krt5-CreERT2:R26SmoM2/EYFP (K5:Smo) mice untreated and treated with ibuprofen

summary: In our study, we used single-cell RNA sequencing to investigate the effect of ibuprofen on cell-mediated communication between esophageal epithelial cells and their microenvironment in K5:Smo mice.

overall_design: Oesophageal single cell mRNA profiles of Krt5-CreERT2:R26SmoM2/EYFP mice by deep sequencing using 10x genomic.


title: Comprehensive Characterization of the Human Neural Stem Cell Line HNSC.100 as a Versatile Model for Neurobiological Research

status: Public on Feb 02 2026

city: Ulm

first: Estera

middle: Anna

last: Jeruzalska

address: James-Franck-Ring N27

department: Institute of Pharmaceutical Biotechnology

institute: Ulm University

summary: Studying neural-related questions is inherently challenging due to the limited number of suitable cell models. Here, we characterize a previously reported immortalized human neural stem cell line, HNSC.100, serving as a robust model for a wide range of neurobiological research questions. The cell line expresses key neural stem cell markers, including SOX2, vimentin, nestin, and allows for efficient genetic manipulation. Furthermore, HNSC.100 cells can be differentiated into neurons, astrocytes and oligodendrocytes, thereby covering a wide spectrum of major neural cell types. We established a comprehensive panel of molecular markers to validate successful differentiation, enabling precise characterization of the resulting cell population. In addition, we provide a complete dataset of RNA expression levels for all detectable genes in HSNC.100 cells. Based on this dataset, we assembled a list of expressed genes implicated in neural disorders that can be studied with this cell line. Together, we present a detailed characterization of the HNSC.100 cell line and provide new tools and reference data to facilitate its use. This resource enables researchers to evaluate the line's suitability for specific applications and to rapidly integrate HNSC.100 cells into their experimental workflows.

overall_design: RNA sequencing of untreated HNSC.100 cells for expression analysis in this cell line

first: Carolin

last: Ketteler

first: Elisa

last: Stuetzenberger

first: Sandra

last: Burczyk

first: Larissa

last: Moeller

first: Dierk

last: Niessing


title: NanoString PanCancer IO 360 expression profiling of histologically normal breast lobules from NHBW and NHWW donors (IO360)

city: Jacksonville

first: Derek

middle: Charles

last: Radisky

state: Florida

address: 4500 San Pablo Road

institute: Mayo Clinic

summary: Histologically normal breast lobules were obtained from non-Hispanic Black women (NHBW) and non-Hispanic White women (NHWW) (n=10 per group) matched by age, BMI, and parity. RNA extracted from FFPE sections was profiled using the NanoString PanCancer IO 360 CodeSet to characterize transcriptional programs associated with group differences in benign breast epithelium.

overall_design: Twenty histologically normal breast lobule samples (10 NHBW, 10 NHWW) were profiled on the NanoString PanCancer IO 360 panel. Raw RCC files are provided along with normalized expression values.

first: Joshua

middle: W

last: Ogony

middle: C


title: Chemotherapy-induced reactive myelopoiesis leads to expansion of immunosuppressive neutrophil-like monocytes in mice and humans

city: Augusta

first: Huidong

last: Shi

state: GA

department: Georgia Cancer Center

institute: Augusta University


title: Chemotherapy-induced reactive myelopoiesis leads to expansion of immunosuppressive neutrophil-like monocytes in mice and humans [scRNA-Seq]

summary: Cytotoxic chemotherapy primarily targets rapidly proliferating cancer cells but also depletes normal myeloid cells. The resulting cell loss triggers reactive myelopoiesis, a compensatory process in which hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM) regenerate myeloid lineages. We previously showed that the alkylating agent cyclophosphamide (CTX) induces myelopoiesis leading to the expansion of immunosuppressive monocytes in mice. However, the molecular features and clinical relevance of these cells remain poorly understood. Here, we report the emergence of immunosuppressive monocytes in the peripheral blood of lymphoma patients receiving CTX-containing chemotherapy. To gain mechanistic insight into CTX-induced myelopoiesis, we performed single-cell RNA sequencing (scRNA-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) on BM monocytes from CTX-treated mice. These analyses revealed a heterogeneous monocyte population and demonstrated that CTX skews myelopoiesis toward the generation of neutrophil-like monocytes (NeuMo). Moreover, CTX-induced NeuMo cells, enriched within the CXCR4⁺CX3CR1⁻ monocyte subset, exhibited potent T-cell suppressive activity. Using the NeuMo gene signature, reanalysis of public scRNA-seq datasets identified a transcriptionally similar monocyte subset in chemotherapy-treated cancer patients. Collectively, our findings suggest that the expansion of NeuMo-like cells following chemotherapy represents a conserved immunoregulatory feedback mechanism with potential impact on tumor response to chemoimmunotherapy.

overall_design: For scRNA-seq of whole bone marrow cells, bone marrows were collected from cyclophosphamide-treated mice on day 2 (CTX_D2) and day 7 (CTX_D7). Bone marrows from untreated mice were used as the control (naïve). Live cells were enriched using the EasySep Dead Cell Removal kit (Stemcell Technologies). Equal numbers of cells from three individual mice under each condition were mixed and the pooled samples were used for downstream sequencing. For scRNA-seq of pre-enriched monocytes, bone marrow cells were stained with anti-CD11b and anti-Ly6C antibodies and sorted for CD11b+Ly6Chi monocytes by Bigfoot Spectral Cell Sorter. The purity of sorted monocytes was greater than 98%. Freshly isolated whole bone marrow cells or monocytes (CD11b+Ly6Chi) were processed for scRNA-seq libraries using the Chromium Controller (10X Genomics).

first: Gang

last: Zhou

first: Zhichun

last: Ding


title: Chemotherapy-induced reactive myelopoiesis leads to expansion of immunosuppressive neutrophil-like monocytes in mice and humans [ATAC-seq]

overall_design: Nuclei were prepared from freshly isolated monocytes (CD11b+Ly6Chi) by fluorescence-activated cell sorting (FACS) and used for the ATAC-seq library construction. The differential analysis was used to detect the changes in the chromatin accessibility after CTX treatment in monocytes.


title: Gene silencing of ANGPTL3 suppresses α1-antitrypsin and lectin mannose-binding 1 expression in the hepatoma Huh7 cell line

city: Padova

first: Giulio

last: Ceolotto

address: Via Orus 2B

department: Medicine

country: Italy

institute: University of Padova

summary: Background: Angiopoietin-like 3 (ANGPTL3) is a hepatokine acting as negative regulator of hepatic and endothelial lipases. Vupanorsen, an antisense oligonucleotide targeting ANGPTL3, reduced triglycerides up to 60% in a phase 2b trial, but caused dose-dependent increases in hepatic fat fraction. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plasma levels also correlates with liver fat accumulation. Methods: To further elucidate the biological activity of ANGPTL3 on lipid metabolism in the liver we performed a RNAseq analysis from human hepatoma Huh7 cells transfected with siRNA-ANGPTL3, siRNA-PCSK9 and double siRNA-ANGPTL3/PCSK9. Results: RNA-seq analysis detected 192 genes out of 13,945 transcripts differential ex-pressed in response to ANGPTL3-siRNA compared to scramble-siRNA controls. In cells transfected with PCSK9-siRNA, 88 genes were differentially expressed, while dual transfection with both ANGPTL3- and PCSK9-siRNA resulted in 219 differentially ex-pressed genes. When ANGPTL3 gene expression was silenced we observed a compensa-tory induction of proprotein convertase subtilisin/kexin type 9 (PCSK9) mRNA and pro-tein expression. Moreover, PCSK9 silencing increased ANGPTL3 mRNA expression. Bi-oinformatic analysis revealed that gene silencing of ANGPTL3 or both ANGPTL3/PCSK9 suppresses SERPINA1, gene encoding α1-antitrypsin, and lectin mannose-binding 1 ex-pression (LMAN1). These data were confirmed by western blot and qRT-PCR analysis. Conclusions: Our data identified two key genes SERPINA1 and LMAN1, involved in endoplasmic reticulum stress, lipid accumulation and liver damage, that are downregu-lated in response to gene silencing of ANGPTL3 in Huh7 hepatoma cell line.

overall_design: Huh7 cells transfected with siRNA-ANGPTL3, siRNA-PCSK9 and double siRNA-ANGPTL3/PCSK9 for 48 hours

first: Ilaria

last: Rossi

first: Enidia

last: Hazizaj

first: Maria Giovanna

last: Lupo

first: Giorgia

last: Marodin

first: Stjin

last: Cos

first: Alessandra

last: Giannella

first: Nicola

last: Ferri


title: Characterization of a Novel Transmembrane Activating STING Agonist using Genetically Humanized Mice

city: Beaverton

first: Victor

middle: Robert

last: DeFilippis

state: Oregon

address: 505 NW 185th Ave.

department: Vaccine and Gene Therapy Institute

institute: Oregon Health and Science University

summary: Transcriptome analysis of bone marrow derived dendtitic cells from C57Bl/6 parental and genetically humanized STING (huSTING) mice treated ex vivo with two STING agonists and LPS

overall_design: We analyzed RNA harvested from BMDC treated for 6 hours in duplicate treatments using the Affymetrix Clariom S platform. Array data was processed by Trancriptome Analysis Console (Affymetrix).

first: Nobuyo

last: Mizuno

first: Jinu

last: Abraham

first: Ian

last: Rose

first: Laura

last: Springgay

first: Kevin

last: Jimenez-Perez

first: Omer

last: Rasheed

first: David

last: Burkhart

first: Shannon

last: Miller

first: Dylan

last: Boehm

first: Takeshi

last: Ando

first: Daniel

last: Streblow

first: Janine

last: Ward

first: Elias

last: Haddad

first: Roshell

last: Muir

last: Joyner

first: Uddav

last: Pandey

first: Ahmad

last: Junaid


title: Cup-like nuclei is a hallmark of IGH:DUX4 acute lymphoblastic leukemia and reveals cytoplasmic mitochondria accumulation

city: Paris

first: Hélène

last: CAVE

state: France

address: 48 Bd sérurier

department: Genetics

country: France

institute: APHP Hôpital Robert Debré

summary: Cup-like nuclei are a distinctive morphological feature observed in certain cases of acute lymphoblastic leukemia (ALL). We provide evidence that they characterize DUX4-rearranged ALL independently of IKZF1 deletion, and reveal marked mitochondrial accumulation in this ALL subset. We provide here the RNAseq data from DUX4 rearranged ALL and non-DUX4 rearranged ALL which revealed DUX4-rearranged distinct transcriptional mitochondrial signature.

overall_design: RNAseq data on mononucleated cells from 19 DUX4r and 67 non-DUX4r pediatric ALL cases

first: Chloé

last: Arfeuille

first: Hugo

last: Roux

first: Yoann

last: Vial

first: Aurélie

last: Caye

last: Cavé

first: Marion

last: Strullu

first: Alexia

last: Kinoo


title: Blocking Host Factors IAP and DDX3 Reverse HIV-1 Latency and Restore Apoptosis Vulnerability of the HIV-1 reservoir

status: Public on Feb 01 2026

city: Amsterdam

first: Neeltje

last: Kootstra

address: Meibergdreef 9

country: Netherlands

institute: AmsterdamUMC

summary: Antiretroviral therapy (ART) effectively suppresses HIV-1 replication but does not purge the latent HIV-1 reservoir. Strategies aimed at HIV-1 latency reversal and subsquent elimination of infected cells are being explored. Targeting the inhibitor of apoptosis proteins (IAP) and DEAD-box polypeptide 3 (DDX3) RNA helicase reduce the HIV-1 reservoir ex vivo. However, mechanisms driving elimination of HIV-1 infected cells remain unclear. Here we uncovered the mechanism regarding latency reversal and induction of cell death specific for HIV-1 infected cells. Inhibition of IAP by second mitochondrial-derived activator of caspases mimetic (SMACm; AZD5582) resulted in activation of non-canonical NF-κB that induced HIV-1 transcription also in combination with a DDX3 inhibitor (DDX3i; FH1321). Transcriptome analysis revealed that HIV-1 actively suppressed apoptosis-related genes. SMACm treatment resulted in a broad induction of these genes irrespective of infection. Notably, DDX3 inhibition specifically restored the expression of the majority of HIV-1 suppressed genes, and when combined with SMACm restored almost all HIV-1 downregulated genes, thereby rendering HIV-1 infected cells vulnerable to apoptosis. Thus, our data strongly suggest that inhibition of host factors IAP and DDX3 not only induces latency reversal but also restores HIV-1 induced suppression of apoptotic processes in infected cells leading to reservoir elimination.

overall_design: The combination of SMACm and DDX3i induces cell death specifically of HIV-1 infected but not uninfected PBMCs from PWH. To explore the underlying mechanism, we analyzed the gene expression during HIV-1 infection and assessed the effect of the different compounds using a survival/apoptosis pathway qPCR array. After 48 hours of infection of SUPT1-CCR5 cells with HIV-1 NL4-3BaL, cells were treated with DDX3i, SMACm, or their combination and after 6 hours, transcription of survival and apoptosis genes was analyzed by qPCR array.

first: Jade

last: Jansen

first: Shirley

last: Man

first: Fenna

first: Ad

last: van Nuenen

first: Karel

middle: A

last: van Dort

first: Claudi

last: Zamperini

first: Conraed

last: Houck

first: Teunis

middle: B

last: Geijtenbeek


title: Effect of intrauterine growth restriction on the chromatin accessibility of microglia in hippocampus

status: Public on Jan 30 2026

city: Shanghai

first: Zhu

last: wei

address: siping road 1239

institute: tongji university

summary: Early-life exposures (spanning from the gamete stage to childhood) to adverse environmental factors can exert long-term effects on offspring health through epigenetic modifications, significantly increasing susceptibility to chronic diseases such as neuropsychiatric disorders in adulthood. Previous studies have shown that fetal growth restriction can lead to excessive activation of microglia in the individual's brain, but there is still a lack of research on its epigenetic mechanisms. Our data supplements the changes in chromatin accessibility of microglia in the hippocampus of individuals with fetal growth restriction, and explores the epigenetic basis of microglial activation

overall_design: ATAC-seq profiling of hippocampus microglia in control and FGR mice at postpartum three week


title: Autophagy enhancement ameliorates tau burden and neurofilament pathology in sporadic PSP-RS neurons

city: Catanzaro

first: Barbara

last: Puccio

address: Viale Europa

department: Dept of Surgical and Medical Sciences

institute: Magna Graecia University of Catanzaro

summary: Progressive supranuclear palsy, Richardson’s syndrome subtype (PSP-RS), is a tauopathy marked by early axonal pathology and neurodegeneration. Modeling sporadic PSP-RS in human neurons remained a major challenge. Here, we generated midbrain dopaminergic (mDA) neurons from induced pluripotent stem cells (iPSCs) derived from idiopathic PSP-RS patients and healthy controls. Combined transcriptomic and proteomic analysis revealed reduced dopaminergic differentiation and synaptic function, alongside increased phosphorylated and oligomeric Tau, neurofilament accumulation, axonal swelling, and endoplasmic reticulum disorganization. These alterations coincided with impaired autophagic flux and elevated levels of phosphorylated mTOR. Pharmacological inhibition of mTOR restored autophagy and reduced neurofilament and tau pathology. Collectively, our findings implicate mTOR-dependent autophagy dysfunction as a key driver of early axonal pathology of PSP-RS and highlight autophagy modulation as a promising therapeutic avenue.

overall_design: RNA-seq profiling of iPSC-derived dopaminergic neurons from pHC and spPSP at DIV60

first: Raffaele

last: Covello

first: Giorgia Lucia

last: Benedetto

first: Stefania

last: Scalise

first: Caterina

last: Gabriele

first: Desirèe

last: Valente

first: Clara

last: Zannino

first: Pietro Hiram

last: Guzzi

first: Andrea

last: Quattrone

first: Marco

last: Gaspari

first: Aldo

first: Elvira Immacolata

last: Parrotta

first: Giovanni

last: Cuda


title: Caspase inhibition restores dopaminergic identity through the PKA–CREB–BDNF axis in Parkinson’s disease neurons

summary: The progressive loss of dopaminergic identity in midbrain neurons is a hallmark of Parkinson’s disease (PD), contributing to synaptic dysfunction and neurodegeneration. While a subset of PD cases is linked to genetic mutations, the majority are sporadic (sPD) and of unknown etiology. Current therapies offer only symptomatic relief and do not prevent neurodegeneration, underscoring the urgent need for disease-modifying strategies targeting actionable molecular pathways. Here, we used human induced pluripotent stem cell (hiPSC)-derived midbrain dopaminergic neurons (mDAs) from sporadic PD patients to investigate early alterations in neuronal identity, plasticity, and survival. We found that PD-derived mDAs exhibit upregulation of phosphorylated α-synuclein, marked reductions in dopaminergic markers (TH, NURR1), deficient dopamine handling, and impaired synaptogenesis. Transcriptomic and protein analyses revealed sustained activation of apoptotic caspases (caspase-3, -7) and downregulation of the PKA–CREB–BDNF signaling axis, which underpins dopaminergic differentiation and synaptic maturation. Pharmacological inhibition of caspases with Q-VD-OPh restored pCREB, BDNF, and downstream dopaminergic markers, leading to morphological recovery and functional synaptic rescue. Inhibition of PKA with H89 abrogated these effects, positioning the caspase–PKA–CREB cascade as a critical regulator of dopaminergic identity in PD neurons. These findings define a novel non-apoptotic role for caspases in disrupting the transcriptional program of mDAs and identify a druggable pathway capable of rescuing key aspects of dopaminergic function in a patient-derived cellular model. This work provides a mechanistic rationale for targeting caspase signaling in early-stage PD.

overall_design: RNA-seq profiling of iPSC-derived dopaminergic neurons from pHC and spPD at DIV60

first: Pierangelo

last: Veltri

first: Verdon

last: Taylor


title: Role lymphatic-derived neurotensin in pressure overload-induced cardiac damage

city: bad nauheim

first: Stefan

last: Günther

address: ludwigtr. 43

institute: MPI for heart and lung research

summary: Neuropeptide neurotensin (NTS) was found to be upregulated after induction of cardiac injury in cardiac lymphatic endothelial cells (LEC). We generated tamoxifen-inducible, LEC-specific NTS knockout mice and used scRNA-seq to understand the consequences of LEC-specific NTS deletion on cardiac remodeling 7 days after induction of pressure overload by transverse aortic constriction.

overall_design: Non-cardiomyocyte population was isolated from control (3) and Nts KO (4) mice after 7 days of pressure overload (TAC model).

first: Niharika

last: Shiva

first: Haruya

last: Kawase

first: Nina

last: Wettschureck

last: Guenther