Sympathetic Stimulation Upregulates the Ca(2+) Channel Subunit CaValpha2delta1 via the beta1 and ERK 1/2 Pathway in Neonatal Ventricular Cardiomyocytes.
beta1-adrenergic receptor but not beta2 mediates osteogenic differentiation of bone marrow mesenchymal stem cells in normotensive and hypertensive rats.
O-GlcNAc transferase affects the signal transduction of beta1 adrenoceptor in adult rat cardiomyocytes by increasing the O-GlcNAcylation of beta1 adrenoceptor.
These results showed that prolonged action of adrenoceptor beta 1- autoantibodys significantly reduced the autophagy of myocardial tissues and H9c2 cardiomyocytes and endoplasmic reticulum stress and its related apoptotic pathways were significantly activated.
The authors demonstrate that endogenous beta1-adrenergic receptors at the Golgi apparatus in cardiac myocytes are required to stimulate hypertrophic Epac/PLCe-dependent phosphatidylinositol 4-phosphate hydrolysis at the Golgi and that these intracellular beta1-adrenergic receptors can be accessed by physiological neurotransmitters and synthetic b-blockers and agonists.
lower b1-adrenoreceptor expression was significantly associated with increased lymph node metastasis. Reduced b2-adrenoreceptor staining proportion was significantly associated with worse histological grade. Furthermore the proportion of b2-adrenoreceptor staining was significantly lower in tumors with diffuse-type histology than those with intestinal-type histology.
beta-AR stimulation affects post-translational modifications of NF2 via the involvement beta1-AR/PKA/cAMP pathway and NF2 plays a pro-apoptotic role in beta-AR-stimulated myocyte apoptosis via the phosphorylation (inactivation) of YAP and involvement of mitochondrial death pathway
Despite enhanced agonist-mediated downregulation of hepatic beta-ARs preferentially affecting the beta2-AR subtype increased generation of both receptor subtypes during aging augments the pool of plasma membrane-bound beta-ARs coupled to adenylyl cyclase in hepatocytes.
beta-AR stimulation induces HDAC5 nuclear accumulation in cardiomyocytes by a mechanism that is protein kinase A-dependent but requires B55alpha-PP2A-mediated dephosphorylation of Ser259/Ser498.
Data reveal essential roles of beta-arrestin 2 and PDE4D in a common mechanism for heterologous desensitization of cardiac beta adrenergic receptors under hormonal stimulation which is associated with impaired cardiac function during the development of pathophysiological conditions.
Data show that beta1-Adrenoceptor stimulation triggers the production of the second messenger cAMP which activates the Rap guanine nucleotide exchange factor Epac and the protein kinase A (PKA).
Chronic bilateral renal denervation reduces cardiac hypertrophic remodelling but not beta-adrenergic responsiveness in hypertensive type 1 diabetic rats.
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