A5019878993- Genetic and Kidney Cyst Diseases
- Renal and related cancers
- Epigenetics and DNA Methylation
- Genetic Syndromes and Imprinting
- Kidney Stones and Urolithiasis Treatments
- Biomedical Research and Pathophysiology
- Tea Polyphenols and Effects
- Pancreatic function and diabetes
- Liver Disease Diagnosis and Treatment
- Prenatal Screening and Diagnostics
- Genomics and Chromatin Dynamics
- Genetics and Neurodevelopmental Disorders
- RNA modifications and cancer
- Metabolomics and Mass Spectrometry Studies
Xuzhou Medical College
2025
Tianjin Medical University
2019-2024
Second Hospital of Tianjin Medical University
2022
Pharmacological induction of NRF2 restores redox homeostasis and slows cystogenesis in mouse models polycystic kidney disease.
Emerging evidence indicates that epigenetic modulation of gene expression plays a key role in the progression autosomal dominant polycystic kidney disease (ADPKD). However, molecular basis for how altered epigenome modulates transcriptional responses, and thereby ADPKD, remains largely unknown.Kidneys from control ADPKD mice were examined CDYL histone acylations. its correlation with severity analyzed cohort patients ADPKD. Cdyl transgenic crossed Pkd1 knockout to explore CDYL's progression....
Abstract During the formation of kidney stones, interaction between crystals and tubular epithelial cells (TECs) leads to injury dysfunction, which in turn promote stone formation. However, molecular mechanisms underlying these changes TECs remain elusive. Drug screening revealed that JQ1 inhibited adhesion calcium oxalate (CaOx) TECs. Its therapeutic effect is further confirmed a glyoxylic acid‐induced CaOx crystal deposition mouse model. Utilizing epigenomic transcriptomic profiling,...
P-TEFb activation by cAMP-PKA signaling promotes cystogenic gene transcription elongation and disease progression in ADPKD.
Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during cell fate decisions, but the underlying mechanisms are not fully understood. Here we discover an HRP2-DPF3a-BAF epigenetic pathway that coordinates methylated H3 lysine 36 (H3K36me) ATP-dependent to regulate dynamics gene transcription myogenic differentiation. Using siRNA screening targeting modifiers, identify hepatoma-derived growth...
Prevailing strategies directing early-phase drug discovery heavily rely on equilibrium-based metrics such as affinity, which overlooks the kinetic process of a molecule interacting with its target. Herein, we developed number vasopressin V2 receptor (V2R) antagonists divergent binding affinities and kinetics for autosomal dominant polycystic kidney disease (ADPKD). Surprisingly, residence time V2R antagonists, but not their was correlated efficacy in both ex vivo models ADPKD. We envision...
Formation of biomolecular condensates by phase separation has recently emerged as a new principle for regulating gene expression in response to extracellular signaling. However, the molecular mechanisms underlying coupling signal transduction and activation through condensate formation, how dysregulation these contributes disease progression, remain elusive. Here, authors report that CREB-regulated transcription coactivator 2 (CRTC2) translocates nucleus forms phase-separated upon cAMP They...
Genome-wide mapping of transcription factor (TF) binding sites is essential to identify a TF's direct target genes in kidney development and diseases. However, due the cellular complexity limited numbers given cell type, it has been challenging determine TF vivo. cAMP response element-binding protein (CREB) phosphorylated hyperactive autosomal dominant polycystic disease (ADPKD). We focus on CREB as an example profile genomic loci bound by its using low specific cells.Cleavage under targets...
<title>Abstract</title> During the formation of kidney stones, interaction between stone crystals and tubular epithelial cells (TECs) leads to injury dysfunction, triggering osteogenic transformation inflammatory responses. However, molecular mechanisms underlying these changes in TECs remain elusive. Through high-throughput drug screening, we identified JQ1, an enhancer targeting epigenetic drug, effectively inhibiting adhesion calcium oxalate (CaOx) primary TECs. We further confirmed its...
cAMP-Induced Nuclear Condensation of CRTC2 Biomolecular condensates play key roles in controlling gene expression response to internal and external signals. In article number 2104578, Yupeng Chen co-workers elucidate a mechanism by which CREB-regulated transcription coactivator 2 (CRTC2) nuclear condensation conveys cAMP signaling promote elongation cystogenesis autosomal dominant polycystic kidney disease (ADPKD). The cover illustrates that upon activation (represented as turning on the...