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Targeted deletion of ROCK1 protects the heart against pressure overload by inhibiting reactive fibrosis
Results indicate that ROCK1 contributes to the development of cardiac fibrosis and induction of fibrogenic cytokines in cardiomyocytes in response to pathological stimuli.
Live-cell analysis of endogenous GFP-RPB1 uncovers rapid turnover of initiating and promoter-paused RNA Polymerase II
This study generated GFP-RPB1 knockin cells and developed photobleaching of endogenous Pol II combined with computational modeling to study the in vivo dynamics of Pol II in real time and suggests that the continuous release and reinitiation of promoter-bound Pol II is an important component of transcriptional regulation.
Hsp20 Functions as a Novel Cardiokine in Promoting Angiogenesis via Activation of VEGFR2
Hsp20 serves as a novel cardiokine in regulating myocardial angiogenesis through activation of the VEGFR signaling cascade, and is identified through exosomes, independent of the endoplasmic reticulum-Golgi pathway.
Inhibitory Cardiac Transcription Factor, SRF-N, Is Generated by Caspase 3 Cleavage in Human Heart Failure and Attenuated by Ventricular Unloading
Caspase 3 activation in heart failure sequentially cleaved SRF and generated a dominant-negative transcription factor, which may explain the depression of cardiac-specific genes, and caspase3 activation may be reversible in the failing heart with ventricular unloading.
NFATc4 is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression.
It is determined that NFATc4, a hypertrophy-associated mediator, is negatively regulated by miR-133a, and the negative regulation of NFAT c4 expression contributes to miR -133a-mediated hypertrophic repression.
Activation of Rho-associated coiled-coil protein kinase 1 (ROCK-1) by caspase-3 cleavage plays an essential role in cardiac myocyte apoptosis
Data suggest an obligatory role for ROCK-1 cleavage in promoting apoptotic signals in myocardial hypertrophy and/or failure in human heart failure.
SENP5, a SUMO isopeptidase, induces apoptosis and cardiomyopathy.