atrial fibrillation/phosphatase

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Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.

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Protein phosphatase 1 (PP1) is a key regulator of important cardiac signaling pathways. Dysregulation of PP1 has been heavily implicated in cardiac dysfunctions. Accordingly, pharmacological targeting of PP1 activity is considered for therapeutic intervention in human cardiomyopathies. Recent

Increased open probability of single cardiac L-type calcium channels in patients with chronic atrial fibrillation. role of phosphatase 2A.

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BACKGROUND The L-type calcium channel (LCC) plays a crucial role in the electrical remodeling of atrial fibrillation (AF). AF is associated with reduction of L-type calcium current density, due to a transcriptional downregulation of the pore forming alpha(1c)-subunit of LCC. However, it is unclear,

Alterations in the interactome of serine/threonine protein phosphatase type-1 in atrial fibrillation patients.

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BACKGROUND Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, yet current pharmacological treatments are limited. Serine/threonine protein phosphatase type-1 (PP1), a major phosphatase in the heart, consists of a catalytic subunit (PP1c) and a large set of regulatory

Serine/Threonine Phosphatases in Atrial Fibrillation.

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Serine/threonine protein phosphatases control dephosphorylation of numerous cardiac proteins, including a variety of ion channels and calcium-handling proteins, thereby providing precise post-translational regulation of cardiac electrophysiology and function. Accordingly, dysfunction of this

High Serum Alkaline Phosphatase Levels in Relation to Multi-Cerebral Microbleeds in Acute Ischemic Stroke Patients with Atrial Fibrillation and/or Rheumatic Heart Disease.

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Elevated alkaline phosphatase (ALP) levels are associated with cerebral small vascular diseases, such as silent brain infarction and cerebral white matter hyperintensity (cWMH), but few prospective data are available for cerebral microbleeds (CMBs). The aim of the study was to investigate

Loss of Protein Phosphatase 1 Regulatory Subunit PPP1R3A Promotes Atrial Fibrillation.

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BACKGROUND

Abnormal calcium (Ca²⁺) release from the sarcoplasmic reticulum (SR) contributes to the pathogenesis of atrial fibrillation (AF). Increased phosphorylation of 2 proteins essential for normal SR-Ca²⁺ cycling, the type-2 ryanodine receptor (RyR2)

Impaired local regulation of ryanodine receptor type 2 by protein phosphatase 1 promotes atrial fibrillation.

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OBJECTIVE Altered Ca(2+) handling in atrial fibrillation (AF) has been associated with dysregulated protein phosphatase 1 (PP1) and subcellular heterogeneities in protein phosphorylation, but the underlying mechanisms remain unclear. This is due to a lack of investigation into the local, rather than

Increased Serum Alkaline Phosphatase as a Predictor of Symptomatic Hemorrhagic Transformation in Ischemic Stroke Patients with Atrial Fibrillation and/or Rheumatic Heart Disease.

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OBJECTIVE Elevated alkaline phosphatase (ALP) is considered as a marker of liver function in clinical practice. Furthermore, it has been identified that liver function can contribute to hemorrhagic transformation (HT). However, whether ALP levels play a role in HT after stroke remains an open

L-type Ca2+ current downregulation in chronic human atrial fibrillation is associated with increased activity of protein phosphatases.

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BACKGROUND Although downregulation of L-type Ca2+ current (I(Ca,L)) in chronic atrial fibrillation (AF) is an important determinant of electrical remodeling, the molecular mechanisms are not fully understood. Here, we tested whether reduced I(Ca,L) in AF is associated with alterations in

Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.

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Affinity proteomics for phosphatase interactions in atrial fibrillation.

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[Morphological remodeling in atrial fibrillation].

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In the recent years, a tremendous amount has been learned about the pathophysiology of atrial fibrillation (AF). AF induces electrophysiological changes in the atria causing a perpetuation of the arrhythmia ("electrical remodeling"). Besides such AF-induced electrophysiological changes, which

[Pulmonary valve endocarditis and atrial fibrillation].

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A 61-year-old man became ill with a fever of 39.4 degrees C, decreased exercise tolerance and headache as well as chest pain. Physical examination 3 weeks after the onset of symptoms merely revealed irregular heart rate at 100 beats/min. Erythrocyte sedimentation rate was increased (30/61 mm), as

Differential phosphorylation-dependent regulation of constitutively active and muscarinic receptor-activated IK,ACh channels in patients with chronic atrial fibrillation.

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OBJECTIVE In chronic atrial fibrillation (cAF) the potassium current IK,ACh develops agonist-independent constitutive activity. We hypothesized that abnormal phosphorylation-dependent regulation underlies the constitutive IK,ACh activity. METHODS We used voltage-clamp technique and biochemical

Regulating the regulator: Insights into the cardiac protein phosphatase 1 interactome.

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Reversible phosphorylation of proteins is a delicate yet dynamic balancing act between kinases and phosphatases, the disturbance of which underlies numerous disease processes. While our understanding of protein kinases has grown tremendously over the past decades, relatively little is known

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