A5029222524- Congenital heart defects research
- CRISPR and Genetic Engineering
- Congenital Heart Disease Studies
- Genomics and Chromatin Dynamics
- Protein Degradation and Inhibitors
- Developmental Biology and Gene Regulation
- Chromatin Remodeling and Cancer
- Cell Adhesion Molecules Research
- Chromosomal and Genetic Variations
- RNA modifications and cancer
- Genomic variations and chromosomal abnormalities
- Single-cell and spatial transcriptomics
- Cardiomyopathy and Myosin Studies
- Eicosanoids and Hypertension Pharmacology
- Renal and related cancers
- Pluripotent Stem Cells Research
- Retinopathy of Prematurity Studies
- Cardiac Fibrosis and Remodeling
- Epigenetics and DNA Methylation
- Nitric Oxide and Endothelin Effects
- Retinoids in leukemia and cellular processes
- Antioxidant Activity and Oxidative Stress
- Tissue Engineering and Regenerative Medicine
- Neuropeptides and Animal Physiology
- Peptidase Inhibition and Analysis
University of Helsinki
2019-2023
Gladstone Institutes
2009-2016
Max Planck Institute for Molecular Genetics
2003-2008
Max Planck Society
2003-2004
Deutsches Herzzentrum der Charité
2003
Deutsches Herzzentrum München
2003
Chromatin remodeling and histone modifications facilitate access of transcription factors to DNA by promoting the unwinding destabilization histone–DNA interactions. We present DPF3, a new epigenetic key factor for heart muscle development characterized double PHD finger. DPF3 is associated with BAF chromatin complex binds methylated acetylated lysine residues 3 4. Thus, may represent first plant homeodomains that bind lysines, feature previously only shown bromodomain. During Dpf3 expressed...
We present the first genome-wide cDNA array analysis of human congenitally malformed hearts and attempted to partially elucidate these complex phenotypes. Most congenital heart defects, which account for largest number birth defects in humans, represent genetic disorders. As a consequence malformation, abnormal hemodynamic features occur cause an adaptation process heart.The statistical our data suggests distinct gene expression profiles associated with tetralogy Fallot, ventricular septal...
Non-cell-autonomous signals often play crucial roles in cell fate decisions during animal development. Reciprocal signaling between endoderm and mesoderm is vital for embryonic development, yet the key mechanisms remain unclear. Here, we show that endodermal cells efficiently promote emergence of mesodermal neighboring population through containing an essential short-range component. The endoderm-mesoderm interaction promoted precardiac formation mouse stem involved production fibronectin....
Acute myeloid leukemia (AML) is characterized by several recurrent mutations that affect disease biology and phenotype, response to therapy risk of subsequent relapse. Though tyrosine kinase inhibitors have gained regulatory approval for the treatment AML, it unclear whether single drugs targeting a specific genomic alteration will be sufficient eradicate disease. Fortuitously, kinase/bromodomain allow downstream transcriptional effectors oncogenic pathways, allowing impediment drug...
Non-cell-autonomous signals often play crucial roles in cell fate decisions during animal development. Reciprocal signaling between endoderm and mesoderm is vital for embryonic development, yet the key mechanisms remain unclear. Here, we show that endodermal cells efficiently promote emergence of mesodermal neighboring population through containing an essential short-range component. The endoderm-mesoderm interaction promoted precardiac formation mouse stem involved production fibronectin....
Several vasoregulatory systems including the renin-angiotensin system, sympathetic vasoregulation, and cytokine release have been studied extensively. The aim of present study was to establish a physiogenomic screening model for differentially expressed genes in regulation blood pressure that might give hint as new mechanisms. We induced acute hypotension normotensive rats, assuming will counteract hypotension. Microarray transcriptome analysis performed from kidneys 6 h after induction...
Pharmacological modulation of cell fate decisions and developmental gene regulatory networks holds promise for the treatment heart failure. Compounds that target tissue-specific transcription factors could overcome non-specific effects small molecules lead to regeneration muscle following myocardial infarction. Due cellular heterogeneity in heart, activation programs representing specific atrial ventricular cardiomyocyte subtypes would be highly desirable. Chemical compounds modulate used...
Heart formation requires transcriptional regulators that underlie congenital anomalies and the fetal gene program activated during heart failure. Attributing effects of disease (CHD) missense variants to disruption specific protein domains allows for a mechanistic understanding CHDs improved diagnostics. A combined chemical genetic approach was employed identify novel CHD drivers, consisting screening pluripotent stem cell (PSC) differentiation, expression analyses native tissues primary...
Abstract Reliable in vitro models to assess developmental toxicity of drugs and chemicals would lead improvement fetal safety a reduced cost drug development. The validated embryonic stem cell test (EST) uses cardiac differentiation mouse cells (mESCs) predict vivo toxicity, but does not take into account the stage-specific patterning progenitor populations anterior (ventricular) posterior (atrial) compartments. In this study, we generated novel dual reporter mESC line with fluorescent...
Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, organ homeostasis. Additionally, metabolites of are utilized as differentiation agents in the treatment hematological cancers skin disorders, necessitating further study into effects both nutrient deficiency exogenous delivery its on cardiovascular phenotypes. Though vitamin A/retinoids well-known regulators cardiac formation, recent evidence has emerged supports their role...
The procholecystokinin (proCCK) gene encodes a secreted peptide known to regulate the digestive, endocrine, and nervous systems. Though recently proposed as biomarker for heart dysfunction, its physiological role in both embryonic adult is poorly understood, there are no reports of tissue-specific regulators cholecystokinin signaling or other tissues. In present study, mRNA proCCK was observed cardiac tissues during mouse development, establishing an early marker differentiated...
Zusammenfassung In einer genomweiten Genexpressionsstudie wurden normale und fehlgebildete menschliche Herzen mittels cDNS-Arrays untersucht. Statistische bioinformatische Methoden benutzt, um gewebe- krankheitsspezifische Genexpressionsmuster zu identifizieren funktionelle Genkategorien mit bestimmten Phänotypen assoziieren.