Joan Heller Brown

Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.

Ca2+/Calmodulin-Dependent Kinase IIδC-Induced Chronic Heart Failure Does Not Depend on Sarcoplasmic Reticulum Ca2+ Leak

Nitric Oxide Modulates Ca ²⁺ Leak and Arrhythmias via S-Nitrosylation of CaMKII

RhoA signaling increases mitophagy and protects cardiomyocytes against ischemia by stabilizing PINK1 protein and recruiting Parkin to mitochondria

SiglecF(HI) Marks Late‐Stage Neutrophils of the Infarcted Heart: A Single‐Cell Transcriptomic Analysis of Neutrophil Diversification

SiglecF(HI) Marks Late‐Stage Neutrophils of the Infarcted Heart: A Single‐Cell Transcriptomic Analysis of Neutrophil Diversification

Hyperglycemia Acutely Increases Cytosolic Reactive Oxygen Species via <i>O</i> -linked GlcNAcylation and CaMKII Activation in Mouse Ventricular Myocytes

CaMKIIδC Drives Early Adaptive Ca ²⁺ Change and Late Eccentric Cardiac Hypertrophy

Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload

Inflammation in nonischemic heart disease: initiation by cardiomyocyte CaMKII and NLRP3 inflammasome signaling

Inflammation and NLRP3 Inflammasome Activation Initiated in Response to Pressure Overload by Ca ²⁺ /Calmodulin-Dependent Protein Kinase II δ Signaling in Cardiomyocytes Are Essential for Adverse Cardiac Remodeling

Chronic inhalation of e-cigarette vapor containing nicotine disrupts airway barrier function and induces systemic inflammation and multiorgan fibrosis in mice

CaMKIIδ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis

RhoA regulates Drp1 mediated mitochondrial fission through ROCK to protect cardiomyocytes

YAP and MRTF-A, transcriptional co-activators of RhoA-mediated gene expression, are critical for glioblastoma tumorigenicity

Sphingosine 1-phosphate receptor 3 and RhoA signaling mediate inflammatory gene expression in astrocytes

CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α

Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB

G Protein–Coupled Receptor and RhoA-Stimulated Transcriptional Responses: Links to Inflammation, Differentiation, and Cell Proliferation

Myocardin-Related Transcription Factor A and Yes-Associated Protein Exert Dual Control in G Protein-Coupled Receptor- and RhoA-Mediated Transcriptional Regulation and Cell Proliferation

CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca2+ leak and the pathophysiological response to chronic β-adrenergic stimulation

Mitochondrial Reprogramming Induced by CaMKIIδ Mediates Hypertrophy Decompensation

CaMKIIdelta subtypes: localization and function

CaMKII-dependent phosphorylation of cardiac ryanodine receptors regulates cell death in cardiac ischemia/reperfusion injury

Induction of the matricellular protein CCN1 through RhoA and MRTF-A contributes to ischemic cardioprotection

Epac2 Mediates Cardiac β1-Adrenergic–Dependent Sarcoplasmic Reticulum Ca ²⁺ Leak and Arrhythmia

Ca ²⁺ /Calmodulin-Dependent Protein Kinase II δ Mediates Myocardial Ischemia/Reperfusion Injury Through Nuclear Factor-κB

Akt regulates L-type Ca2+ channel activity by modulating Cavα1 protein stability

Phospholipase Cɛ links G protein-coupled receptor activation to inflammatory astrocytic responses

PLCε, PKD1, and SSH1L Transduce RhoA Signaling to Protect Mitochondria from Oxidative Stress in the Heart