Area of research
Cardiology and Cardiovascular Medicine · Molecular Biology
Research interest
Research focused on Angiotensin-converting enzyme and Genetics, with related work in Lung, Epitope, ACE inhibitor. Notable publications include 'Unique Toll-Like Receptor 4 Activation by NAMPT/PBEF Induces NFκB Signaling and Inflammatory Lung Injury', 'Gene Therapy by Targeted Adenovirus-mediated Knockdown of Pulmonary Endothelial Tph1 Attenuates Hypoxia-induced Pulmonary Hypertension', and 'A Novel Splice-Site Mutation in Angiotensin I-Converting Enzyme (ACE) Gene, c.3691+1G>A (IVS25+1G>A), Causes a Dramatic Increase in Circulating ACE through Deletion of the...'.
Carriers of Heterozygous Loss-of-Function ACE Mutations Are at Risk for Alzheimer’s Disease
Effect of ACE mutations on blood ACE phenotype parameters
Predictive potential of ACE phenotyping in extrapulmonary sarcoidosis
Phenotyping Angiotensin-Converting Enzyme in Blood: A Necessary Approach for Precision Medicine
Epitope mapping of novel monoclonal antibodies to human angiotensin I‐converting enzyme
Novel ACE mutations mimicking sarcoidosis by increasing blood ACE levels
Tissue ACE phenotyping in lung cancer
ACE phenotyping in Gaucher disease
ACE phenotyping in human heart
ACE Phenotyping as a Guide Toward Personalized Therapy With ACE Inhibitors
The Splicing Factor hnRNPA1 Regulates Alternate Splicing of the <i>MYLK</i> Gene
Lysozyme and bilirubin bind to ACE and regulate its conformation and shedding
Mechanical Stress and Single Nucleotide Variants Regulate Alternative Splicing of the <i>MYLK</i> Gene
Unique Toll-Like Receptor 4 Activation by NAMPT/PBEF Induces NFκB Signaling and Inflammatory Lung Injury
Tissue Specificity of Human Angiotensin I-Converting Enzyme
Renin-Angiotensin Activation and Oxidative Stress in Early Heart Failure with Preserved Ejection Fraction
A Novel Angiotensin I-Converting Enzyme Mutation (S333W) Impairs N-Domain Enzymatic Cleavage of the Anti-Fibrotic Peptide, AcSDKP
A Novel Splice-Site Mutation in Angiotensin I-Converting Enzyme (ACE) Gene, c.3691+1G>A (IVS25+1G>A), Causes a Dramatic Increase in Circulating ACE through Deletion of the Transmembrane Anchor
Gene Therapy by Targeted Adenovirus-mediated Knockdown of Pulmonary Endothelial Tph1 Attenuates Hypoxia-induced Pulmonary Hypertension
Conformational Changes of Blood ACE in Chronic Uremia