William T. Pu

Structural characterization of the mouse Girk genes.

NFAT transcription factors are critical survival factors that inhibit cardiomyocyte apoptosis during phenylephrine stimulation in vitro.

Developmental changes in ventricular diastolic function correlate with changes in ventricular myoarchitecture in normal mouse embryos.

GATA4 is a dosage-sensitive regulator of cardiac morphogenesis.

Morphogenesis of the right ventricle requires myocardial expression of Gata4.

Transcription factor gata4 regulates cardiac BCL2 gene expression in vitro and in vivo.

Dilated cardiomyopathy resulting from high-level myocardial expression of Cre-recombinase.

Overexpression of HAX-1 protects cardiac myocytes from apoptosis through caspase-9 inhibition.

A multivariate approach for integrating genome-wide expression data and biological knowledge.

Development of heart valves requires Gata4 expression in endothelial-derived cells.

Gata4 is essential for the maintenance of jejunal-ileal identities in the adult mouse small intestine.

Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced heart failure.

Impaired mesenchymal cell function in Gata4 mutant mice leads to diaphragmatic hernias and primary lung defects.

Uncoupling protein 2 modulates cell viability in adult rat cardiomyocytes.

Spectrum of heart disease associated with murine and human GATA4 mutation.

Endothelial-to-mesenchymal transition contributes to cardiac fibrosis.

Altered microRNA expression in human heart disease.

Epicardial progenitors contribute to the cardiomyocyte lineage in the developing heart.

GATA4 is a direct transcriptional activator of cyclin D2 and Cdk4 and is required for cardiomyocyte proliferation in anterior heart field-derived myocardium.

Nkx2-5- and Isl1-expressing cardiac progenitors contribute to proepicardium.

More than a cover: epicardium as a novel source of cardiac progenitor cells.

Reassessment of Isl1 and Nkx2-5 cardiac fate maps using a Gata4-based reporter of Cre activity.

Platelet-derived growth factor receptor beta signaling is required for efficient epicardial cell migration and development of two distinct coronary vascular smooth muscle cell populations.

MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes.

Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart.

Identification of a cardiac disease modifier gene using forward genetics in the mouse.

Inducible cardiomyocyte-specific gene disruption directed by the rat Tnnt2 promoter in the mouse.

Genetic fate mapping demonstrates contribution of epicardium-derived cells to the annulus fibrosis of the mammalian heart.

Heart failure-associated changes in RNA splicing of sarcomere genes.

Expression and function of microRNAs in heart disease.

Dissecting spatio-temporal protein networks driving human heart development and related disorders.

Conditional Gata4 deletion in mice induces bile acid absorption in the proximal small intestine.

Synergistic effects of the GATA-4-mediated miR-144/451 cluster in protection against simulated ischemia/reperfusion-induced cardiomyocyte death.

Genome-wide location analysis by pull down of in vivo biotinylated transcription factors.

CompleteMOTIFs: DNA motif discovery platform for transcription factor binding experiments.

Reprogramming fibroblasts into cardiomyocytes.

Septum transversum-derived mesothelium gives rise to hepatic stellate cells and perivascular mesenchymal cells in developing mouse liver.

Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac valve development. [corrected]

A Tbx1-Six1/Eya1-Fgf8 genetic pathway controls mammalian cardiovascular and craniofacial morphogenesis.

Co-occupancy by multiple cardiac transcription factors identifies transcriptional enhancers active in heart.

Adult mouse epicardium modulates myocardial injury by secreting paracrine factors.

De novo cardiomyocytes from within the activated adult heart after injury.

WT1 regulates epicardial epithelial to mesenchymal transition through β-catenin and retinoic acid signaling pathways.

Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.

miR-155 inhibits expression of the MEF2A protein to repress skeletal muscle differentiation.

Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes.

Epicardial epithelial-to-mesenchymal transition in injured heart.

Adult cardiac-resident MSC-like stem cells with a proepicardial origin.

Polycomb repressive complex 2 regulates normal development of the mouse heart.

PRC2 directly methylates GATA4 and represses its transcriptional activity.

Isolation and characterization of embryonic and adult epicardium and epicardium-derived cells.

Transcription factor GATA4 is activated but not required for insulin-like growth factor 1 (IGF1)-induced cardiac hypertrophy.

YAP1, the nuclear target of Hippo signaling, stimulates heart growth through cardiomyocyte proliferation but not hypertrophy.

CIP, a cardiac Isl1-interacting protein, represses cardiomyocyte hypertrophy.

Cardiac expression of ms1/STARS, a novel gene involved in cardiac development and disease, is regulated by GATA4.

Regulation of GATA4 transcriptional activity in cardiovascular development and disease.

Equal modulation of endothelial cell function by four distinct tissue-specific mesenchymal stem cells.

Congenital heart disease-causing Gata4 mutation displays functional deficits in vivo.

Endocardial and epicardial epithelial to mesenchymal transitions in heart development and disease.

Endostatin lowers blood pressure via nitric oxide and prevents hypertension associated with VEGF inhibition.

Mature cardiomyocytes recall their progenitor experience via polycomb repressive complex 2.

Genetic and environmental risk factors in congenital heart disease functionally converge in protein networks driving heart development.

Myocardial regeneration: expanding the repertoire of thymosin β4 in the ischemic heart.

Genetic Cre-loxP assessment of epicardial cell fate using Wt1-driven Cre alleles.

A dynamic H3K27ac signature identifies VEGFA-stimulated endothelial enhancers and requires EP300 activity.

Timing of myocardial trpm7 deletion during cardiogenesis variably disrupts adult ventricular function, conduction, and repolarization.

The mysterious origins of coronary vessels.

A simple method for deriving functional MSCs and applied for osteogenesis in 3D scaffolds.

HCN4 charges up the first heart field.

Interrogating translational efficiency and lineage-specific transcriptomes using ribosome affinity purification.

Modified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarction.

Developing insights into cardiac regeneration.

WT1 maintains adrenal-gonadal primordium identity and marks a population of AGP-like progenitors within the adrenal gland.

Peritruncal coronary endothelial cells contribute to proximal coronary artery stems and their aortic orifices in the mouse heart.

GATA factors promote ER integrity and β-cell survival and contribute to type 1 diabetes risk.

Hippo activation in arrhythmogenic cardiomyopathy.

Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies.

Yap1 is required for endothelial to mesenchymal transition of the atrioventricular cushion.

Cardiac-Specific YAP Activation Improves Cardiac Function and Survival in an Experimental Murine MI Model.

Notching up vascular regeneration.

Harnessing Hippo in the heart: Hippo/Yap signaling and applications to heart regeneration and rejuvenation.

Strategies for cardiac regeneration and repair.

Vessel formation. De novo formation of a distinct coronary vascular population in neonatal heart.

Optimization of genome engineering approaches with the CRISPR/Cas9 system.

Dynamic GATA4 enhancers shape the chromatin landscape central to heart development and disease.

Pi3kcb links Hippo-YAP and PI3K-AKT signaling pathways to promote cardiomyocyte proliferation and survival.

Epicardium-to-fat transition in injured heart.

Insights into the genetic structure of congenital heart disease from human and murine studies on monogenic disorders.

Introduction to the special issue on heart regeneration and rejuvenation.

Releasing YAP from an α-catenin trap increases cardiomyocyte proliferation.

Cellular origin and developmental program of coronary angiogenesis.

Novel Roles of GATA4/6 in the Postnatal Heart Identified through Temporally Controlled, Cardiomyocyte-Specific Gene Inactivation by Adeno-Associated Virus Delivery of Cre Recombinase.

Trbp regulates heart function through microRNA-mediated Sox6 repression.

Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis.

Nuclear receptor RORα regulates pathologic retinal angiogenesis by modulating SOCS3-dependent inflammation.

Regional differences in WT-1 and Tcf21 expression during ventricular development: implications for myocardial compaction.

SOCS3 in retinal neurons and glial cells suppresses VEGF signaling to prevent pathological neovascular growth.

Cardiomyocyte-enriched protein CIP protects against pathophysiological stresses and regulates cardiac homeostasis.

Recounting Cardiac Cellular Composition.

Epicardium is required for cardiac seeding by yolk sac macrophages, precursors of resident macrophages of the adult heart.

Comprehensive analysis of promoter-proximal RNA polymerase II pausing across mammalian cell types.

Long non-coding RNAs link extracellular matrix gene expression to ischemic cardiomyopathy.

Acetylation of VGLL4 Regulates Hippo-YAP Signaling and Postnatal Cardiac Growth.

An IGF1R-Dependent Pathway Drives Epicardial Adipose Tissue Formation After Myocardial Injury.

Modeling Inherited Arrhythmia Disorders Using Induced Pluripotent Stem Cell-Derived Cardiomyocytes.

Efficient, footprint-free human iPSC genome editing by consolidation of Cas9/CRISPR and piggyBac technologies.