Tabea L. Stephan

ORCID: 0000-0003-3636-0510
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About
Contact & Profiles
Research Areas
  • Pancreatic function and diabetes
  • Epigenetics and DNA Methylation
  • Cancer-related molecular mechanisms research
  • Diabetes Management and Research
  • Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
  • Liver physiology and pathology
  • Genomics and Chromatin Dynamics
  • Congenital heart defects research
  • Chromatin Remodeling and Cancer
  • Diabetes and associated disorders
  • Pediatric Hepatobiliary Diseases and Treatments
  • Hippo pathway signaling and YAP/TAZ
  • Cancer-related gene regulation
  • Cancer Genomics and Diagnostics
  • MicroRNA in disease regulation

University of British Columbia
2020-2024

Terry Fox Research Institute
2019-2024

Cell‐fate determination is influenced by interactions between master transcription factors (TFs) and cis‐regulatory elements. Hepatocyte nuclear factor 4 alpha (HNF4A), a liver‐enriched TF, acts as controller in specification of hepatic progenitor cells regulating network TFs to control onset hepatocyte cell fate. Using analysis genome‐wide histone modifications, DNA methylation, hydroxymethylation mouse hepatocytes, we show that HNF4A occupies active enhancers hepatocytes essential for...

10.1002/hep.30631 article EN Hepatology 2019-04-01

Abstract The transcription factor SOX9 is activated at the onset of endothelial-to-mesenchymal transition (EndMT) during embryonic development and in pathological conditions. Its roles regulating these processes, however, are not clear. Using human umbilical vein endothelial cells (HUVECs) as an EndMT model, we show that expression alone sufficient to activate mesenchymal genes steer towards a fate. By genome-wide mapping chromatin landscape, displays features pioneer factor, such opening...

10.1093/nar/gkac652 article EN cc-by Nucleic Acids Research 2022-07-29

Abstract Hepatocyte nuclear factor 4A (HNF4A/NR2a1), a transcriptional regulator of hepatocyte identity, controls genes that are crucial for liver functions, primarily through binding to enhancers. In mammalian cells, active and primed enhancers marked by monomethylation histone 3 (H3) at lysine 4 (K4) (H3K4me1) in cell type-specific manner. How this modification is established maintained connection with transcription factors (TFs) remains unknown. Using analysis genome-wide modifications,...

10.1038/s42003-024-05835-0 article EN cc-by Communications Biology 2024-01-31

During pancreas development, endocrine progenitors differentiate into the islet cell subtypes, which undergo further functional maturation in postnatal development. In β-cells, genes involved glucose-stimulated insulin secretion are activated, and glucose exposure increases response as β-cells mature. We investigated role of H3K4 trimethylation differentiation by disrupting TrxG complex histone methyltransferase activity mouse progenitors. embryo, genetic inactivation component Dpy30...

10.2337/db20-1214 article EN Diabetes 2021-08-10

Abstract Hepatocellular carcinoma (HCC) is the most common liver cancer and arises from malignant transformation of hepatocytes. HCC tumors often express genes critical for hepatocyte development but regulatory mechanisms driving aberrant expression remain unclear. Recent evidence indicates that epigenetic alterations contribute to progression with nearly 50% cases associated mutations in chromatin modifiers. Thus, it imperative understand how altered identify DNA sequences tumorigenesis....

10.1158/1538-7445.am2024-4412 article EN Cancer Research 2024-03-22

Summary During pancreas development, endocrine progenitors differentiate into the islet-cell subtypes, which undergo further functional maturation in postnatal islet development. In β-cells, genes involved glucose-stimulated insulin secretion are activated and glucose exposure increases response as β-cells mature. Here, we investigated role of H3K4 trimethylation cell differentiation by disrupting TrxG complex histone methyltransferase activity mouse progenitors. embryo, genetic inactivation...

10.1101/2020.11.29.402990 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-11-30

Abstract The transcription factor SOX9 is expressed in multiple tissues during embryogenesis and directs developmental processes. activated upon endothelial-to-mesenchymal transition (EndMT) the developing heart, but its role regulating this process less clear. Using human umbilical vein endothelial cells as an EndMT model, we show that expression alone sufficient to activate mesenchymal enhancers steer towards a fate. By genome-wide mapping of chromatin landscape, acts pioneer factor,...

10.1101/2020.09.11.293993 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-09-11

During pancreas development, endocrine progenitors differentiate into the islet-cell subtypes, which undergo further functional maturation in postnatal islet development. In b-cells, genes involved glucose-stimulated insulin secretion are activated and glucose exposure increases response as b-cells mature. Here, we investigated role of H3K4 trimethylation cell differentiation by disrupting TrxG complex histone methyltransferase activity mouse progenitors. embryo, genetic inactivation...

10.2337/figshare.15124854 preprint EN cc-by-nc-sa 2021-08-10
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