Associate Professor of Pediatrics, Boston Children's Hospital
Pediatric Cardiology
Dr. William T. Pu, MD
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Doctor William T. Pu, MD works in the field of Pediatric Cardiology. He went to Harvard Medical School. Harvard Medical School is a top medical college. Harvard Medical School is ranked 1/12 in Research/PrimaryCare. William T. Pu is also a published doctor. He has 90 paper published. The most recent paper is: pICln binds to a mammalian homolog of a yeast protein involved in regulation of cell morphology.
Publications
- Pi3kcb links Hippo-YAP and PI3K-AKT signaling pathways to promote cardiomyocyte proliferation and survival.
- Releasing YAP from an α-catenin trap increases cardiomyocyte proliferation.
- Cellular origin and developmental program of coronary angiogenesis.
- Introduction to the special issue on Heart regeneration and rejuvenation.
- Strategies for Cardiac Regeneration and Repair.
- Notching up vascular regeneration.
- GATA4 represses an ileal program of gene expression in the proximal small intestine by inhibiting the acetylation of histone H3, lysine 27.
- Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and Heart-on-chip technologies.
- Hippo activation in arrhythmogenic cardiomyopathy.
- Modified mRNA directs the fate of Heart progenitor cells and induces vascular regeneration after myocardial infarction.
- Interrogating translational efficiency and lineage-specific transcriptomes using ribosome affinity purification.
- Timing of myocardial trpm7 deletion during cardiogenesis variably disrupts adult ventricular function, conduction, and repolarization.
- The mysterious origins of coronary vessels.
- mir-17-92 Cluster is Required for and Sufficient to Induce Cardiomyocyte Proliferation in Postnatal and Adult Hearts.
- A dynamic H3K27ac signature identifies VEGFA-stimulated endothelial enhancers and requires EP300 activity.
- Targeted and genome-wide sequencing reveal single nucleotide variations impacting specificity of Cas9 in human stem cells.
- Insights into the Genetic Structure of Congenital Heart Disease from Human and Murine Studies on Monogenic Disorders.
- Optimization of Genome Engineering Approaches with the CRISPR/Cas9 System.
- Dynamic GATA4 enhancers shape the chromatin landscape central to heart development and Disease.
- Diagnosis and management of agenesis of the right lung and left Pulmonary artery sling.
- UvrABC incision of N-methylmitomycin A-DNA monoadducts and cross-links.
- Dimerization of leucine zippers analyzed by random selection.
- Uracil interference, a rapid and general method for defining protein-DNA interactions involving the 5-methyl group of thymines: the GCN4-DNA complex.
- Evaluation of the role of I(KACh) in Atrial fibrillation using a mouse knockout model.
- The leucine zipper symmetrically positions the adjacent basic regions for specific DNA binding.
- Mutations in the bZIP domain of yeast GCN4 that alter DNA-binding specificity.
- Highly conserved residues in the bZIP domain of yeast GCN4 are not essential for DNA binding.
- Therapeutic neovascularization for peripheral arterial Diseases: advances and perspectives.
- Chaperoning of estrogen receptor and induction of mammary gland proliferation by neuronal protein synuclein gamma.
- Transcription factors and Heart failure: does the stressed Heart need a hand?
- pICln inhibits snRNP biogenesis by binding core spliceosomal proteins.
- pICln binds to a mammalian homolog of a yeast protein involved in regulation of cell morphology.
- ICln is essential for cellular and early embryonic viability.
- Conditional ablation of Gata4 and Fog2 genes in mice reveals their distinct roles in mammalian sexual differentiation.
- Mesenchymal stem/stromal cells (MSC) transfected with stromal derived factor 1 (SDF-1) for therapeutic neovascularization: enhancement of cell recruitment and entrapment.
- Impaired mesenchymal cell function in Gata4 mutant mice leads to diaphragmatic hernias and primary lung defects.
- YAP1, the nuclear target of Hippo signaling, stimulates Heart growth through cardiomyocyte proliferation but not hypertrophy.
- Isolation and characterization of embryonic and adult epicardium and epicardium-derived cells.
- PRC2 directly methylates GATA4 and represses its transcriptional activity.
- Polycomb repressive complex 2 regulates normal development of the mouse Heart.
- Adult cardiac-resident MSC-like stem cells with a proepicardial origin.
- Epicardial epithelial-to-mesenchymal transition in injured Heart.
- Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes.
- miR-155 inhibits expression of the MEF2A protein to repress skeletal muscle differentiation.
- Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.
- WT1 regulates epicardial epithelial to mesenchymal transition through ?-catenin and retinoic acid signaling pathways.
- De novo cardiomyocytes from within the activated adult Heart after injury.
- Adult mouse epicardium modulates myocardial injury by secreting paracrine factors.
- Co-occupancy by multiple cardiac transcription factors identifies transcriptional enhancers active in Heart.
- A Tbx1-Six1/Eya1-Fgf8 genetic pathway controls mammalian cardiovascular and craniofacial morphogenesis.
- Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac Valve development. [corrected]
- Septum transversum-derived mesothelium gives rise to hepatic stellate cells and perivascular mesenchymal cells in developing mouse liver.
- Reprogramming fibroblasts into cardiomyocytes.
- CompleteMOTIFs: DNA motif discovery platform for transcription factor binding experiments.
- Genome-wide location analysis by pull down of in vivo biotinylated transcription factors.
- Synergistic effects of the GATA-4-mediated miR-144/451 cluster in protection against simulated ischemia/reperfusion-induced cardiomyocyte death.
- Conditional Gata4 deletion in mice induces bile acid absorption in the proximal small intestine.
- Dissecting spatio-temporal protein networks driving human heart development and related Disorders.
- Expression and function of microRNAs in heart Disease.
- Heart failure-associated changes in RNA splicing of sarcomere genes.
- Genetic fate mapping demonstrates contribution of epicardium-derived cells to the annulus fibrosis of the mammalian Heart.
- Inducible cardiomyocyte-specific gene disruption directed by the rat Tnnt2 promoter in the mouse.
- Identification of a cardiac Disease modifier gene using forward genetics in the mouse.
- Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse Heart.
- MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes.
- Platelet-derived growth factor receptor beta signaling is required for efficient epicardial cell migration and development of two distinct coronary vascular smooth mus...
- Reassessment of Isl1 and Nkx2-5 cardiac fate maps using a Gata4-based reporter of Cre activity.
- More than a cover: epicardium as a novel source of cardiac progenitor cells.
- Nkx2-5- and Isl1-expressing cardiac progenitors contribute to proepicardium.
- GATA4 is a direct transcriptional activator of cyclin D2 and Cdk4 and is required for cardiomyocyte proliferation in anterior Heart field-derived myocardium.
- Epicardial progenitors contribute to the cardiomyocyte lineage in the developing Heart.
- Altered microRNA expression in human heart Disease.
- Endothelial-to-mesenchymal transition contributes to cardiac fibrosis.
- Spectrum of heart Disease associated with murine and human GATA4 mutation.
- Uncoupling protein 2 modulates cell viability in adult rat cardiomyocytes.
- Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced Heart failure.
- Gata4 is essential for the maintenance of jejunal-ileal identities in the adult mouse small intestine.
- Development of heart Valves requires Gata4 expression in endothelial-derived cells.
- A multivariate approach for integrating genome-wide expression data and biological knowledge.
- Overexpression of HAX-1 protects cardiac myocytes from apoptosis through caspase-9 inhibition.
- Dilated cardiomyopathy resulting from high-level myocardial expression of Cre-recombinase.
- Transcription factor gata4 regulates cardiac BCL2 gene expression in vitro and in vivo.
- Morphogenesis of the right ventricle requires myocardial expression of Gata4.
- GATA4 is a dosage-sensitive regulator of cardiac morphogenesis.
- Developmental changes in ventricular diastolic function correlate with changes in ventricular myoarchitecture in normal mouse embryos.
- NFAT transcription factors are critical survival factors that inhibit cardiomyocyte apoptosis during phenylephrine stimulation in vitro.
- Structural characterization of the mouse Girk genes.
- Epicardium is required for cardiac seeding by yolk sac macrophages, precursors of resident macrophages of the adult Heart.
- Recounting Cardiac Cellular Composition.
Schools
Harvard Medical School
Children39s Hospital
Procedures Preformed
- Cardiac Imaging
Conditions Treated
- Aortic Aneurysm
- Aortic Valve Disease
- Arrhythmias (incl. Atrial Fibrillation)
- Cardiomegaly
- View All
Doctors Specialties
- Cardiology
- Pediatric Cardiology
Accepted Insurances
Education
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Boston Children's Hospital -
Harvard Medical School
Hospital
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Boston Children's Hospital
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