Publications by authors named "K A Zuhlke"
Background: The β-adrenergic augmentation of cardiac contraction, by increasing the conductivity of L-type voltage-gated Ca1.2 channels, is of great physiological and pathophysiological importance. Stimulation of β-adrenergic receptors (βAR) activates protein kinase A (PKA) through separation of regulatory (PKAR) from catalytic (PKAC) subunits.
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- Phosphodiesterase 3A gain-of-function mutations lead to hypertension and stroke, but surprisingly do not cause cardiac hypertrophy or heart failure in affected patients, suggesting a potential protective mechanism in the heart.* -
- Researchers used CRISPR-Cas9 models and human stem cells to analyze the effects of these mutations, observing that new mutations could enhance enzyme activity and self-assembly while preserving normal heart structure despite high blood pressure.* -
- In their experiments, cardiac responses in mutant models showed adaptive changes in calcium cycling and similarities in heart function to normal (wild-type) rats, indicating the mutations might lead to beneficial heart adaptations under certain conditions.*
The cAMP-dependent aquaporin-2 (AQP2) redistribution from intracellular vesicles into the plasma membrane of renal collecting duct principal cells induces water reabsorption and fine-tunes body water homeostasis. However, the mechanisms controlling the localization of AQP2 are not understood in detail. Using immortalized mouse medullary collecting duct (MCD4) and primary rat inner medullary collecting duct (IMCD) cells as model systems, we here discovered a key regulatory role of Aurora kinase A (AURKA) in the control of AQP2.
View Article and Find Full Text PDFBackground: High blood pressure is the primary risk factor for cardiovascular death worldwide. Autosomal dominant hypertension with brachydactyly clinically resembles salt-resistant essential hypertension and causes death by stroke before 50 years of age. We recently implicated the gene encoding phosphodiesterase 3A (); however, in vivo modeling of the genetic defect and thus showing an involvement of mutant PDE3A is lacking.
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