Argyris Papantonis

This paper identifies senescence-induced CTCF clusters (SICCs) and shows they sustain the senescence splicing program by repurposing nuclear speckle components.

This study shows that variant U1 snRNAs affect gene expression and cell cycle in human iPS cells through alternative splicing changes.

This study shows that nanotopography regulates pluripotency in mESCs by altering chromatin state through the mechanosensitive demethylase KDM3A.

LoopBin classifies chromatin loops using a VaDE neural network, identifying distinct functional subgroups from 3D genomics data with minimal input.

The paper identifies two chromatin modules, ACs and DCs, that regulate proinflammatory gene expression through distinct mechanisms in human endothelial cells.

This study shows that epigenetic editing at age-associated CpGs can modulate the epigenetic aging landscape, affecting epigenetic clocks and inducing non-random bystander modifications.

The paper identifies >350 p65/RELA interactors and reveals gene regulatory networks controlled by RELA and its interactors in the IL-1 response.

The paper shows that CTCF depletion disrupts chromatin hub formation but not enhancer-promoter interactions, which still drive gene expression during differentiation.

This study maps epigenetic and transcriptional changes in myeloma progression from precursor to advanced stages, identifying key transcription factors involved in disease development.

This paper presents chromosome-scale genome assemblies and regulatory element annotations for planarians, revealing conservation of regulatory regions despite rapid structural divergence.

The paper develops a single-nucleus full-length RNA-sequencing approach to identify intronic variants linked to mis-splicing in pancreatic cancer.

This study shows MPO enters endothelial cell nuclei, binds chromatin non-enzymatically, and regulates EndMT and EC fate through chromatin remodeling and interaction with ILF3.

This study uses a small molecule inhibitor to rapidly and synchronously induce senescence-like features in human cells, enabling analysis of its core regulatory program without paracrine effects.

The paper presents the first nuclear and mitochondrial genome sequences of Ranunculus, along with plastome evolution, using efficient assembly strategies for non-model plants.

The paper maps structural variants and neoloops in glioblastoma stem cells to show how they sustain tumor-specific transcriptional programs and identify patient-specific vulnerabilities.

The paper investigates the role of RNAPII in chromatin loop formation and shows that enhancer-promoter contacts are selectively lost upon RNAPII depletion, repressing gene expression.

This study identifies aging-associated increases in transcriptional elongation speed across multiple species and shows that reducing this speed extends lifespan.

The paper identifies circRAB3IP as a circRNA that modulates cell proliferation by altering gene expression and mRNA processing through interactions with SF3B1 in a paracrine manner.

The paper shows RNA polymerase II is necessary for spatial chromatin reorganization after mitosis, as demonstrated by Hi-C and in silico modeling.

This study shows human brain organoids can form bilateral optic vesicles with cellular diversity and functionality, including light-responsive photoreceptors and neuronal networks.

This study identifies HMGB1 as an RNA-binding protein that coordinates chromatin folding and RNA homeostasis in senescence through interactions with other RBPs and regulation of SASP-related transcripts.

This study identifies DNA methylation changes during long-term cell culture that resemble epigenetic drift, linked to chromatin conformation changes.

The paper shows that RBPMS controls mRNA translation in pluripotent hESCs to preset cardiac fate competence, which is critical for cardiogenesis.

Bloom is a method for analyzing 3C-type data that retrieves hidden interaction patterns and detects enhancer-promoter interactions with a frequency score, enabling the decoding of regulatory landscapes.

The paper identifies HMGB2 loss as an early event in senescence that disrupts chromatin organization by inducing CTCF clustering across multiple human cell types.