未登录

T

Tatiana M. Vinogradova

Vanderbilt University

H指数:29

被引数:4,933

个人简介

暂无内容

教育背景

暂无内容

工作经历

暂无内容

荣誉奖项

暂无内容

Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) Regulates Basal Cardiac Pacemaker Function: Pros and Cons

IF5.2

2024-12-250

OAAI

Phosphoprotein Phosphatase 1 but Not 2A Activity Modulates Coupled-Clock Mechanisms to Impact on Intrinsic Automaticity of Sinoatrial Nodal Pacemaker Cells

IF5.2

2021-11-108

OAAI

Ca2+ and Membrane Potential Transitions During Action Potentials Are Self-Similar to Each Other and to Variability of AP Firing Intervals Across the Broad Physiologic Range of AP Intervals During Autonomic Receptor Stimulation

FRONTIERS IN PHYSIOLOGY

IF3.4

2021-09-0810

OAAI

Rhythm and Rate of Action Potential Firing of Single Cardiac Pacemaker Cells Emerge from Concordant Beat to Beat Variability of Coupled Calcium and Membrane Potential Functions

BIOPHYSICAL JOURNAL

IF3.1

2019-02-010

OAAI

The Anti-Cancer Drug Vatalanib (Ptk787/Zk222584) Suppresses Normal Spontaneous Firing of Rabbit Sinoatrial Node Cells (SANC)

BIOPHYSICAL JOURNAL

IF3.1

2019-02-010

OAAI

Dual Activation of Phosphodiesterases 3 and 4 Regulates Basal Spontaneous Beating Rate of Cardiac Pacemaker Cells: Role of Compartmentalization?

磷酸二酯酶3和4的双重激活调节心脏起搏细胞的基础自发搏动率: 区室化的作用？

FRONTIERS IN PHYSIOLOGY

IF3.4

2018-10-0916

OAAI

Basal Spontaneous Firing of Rabbit Sinoatrial Node Cells Is Regulated by Dual Activation of PDEs (Phosphodiesterases) 3 and 4

CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY

IF9.8

2018-06-0122

OAAI

Concurrent PDE3 and PDE4 Activation Suppresses Local Ca2+ Releases (LCR) to Regulate Normal Spontaneous Firing of Sinoatrial Node Cells (SANC)

BIOPHYSICAL JOURNAL

IF3.1

2016-02-010

OAAI

Basal Activity of Epidermal Growth Factor Receptor (EGFR) and Phospholipase C (PLC) are Required to Sustain Spontaneous Beating of Cardiac Pacemaker Cells

BIOPHYSICAL JOURNAL

IF3.1

2015-01-010

OAAI

Microtubule network asymmetry in motile cells Role of Golgi-derived array

IF3.4

2014-10-3183

OAAI

Sarcoplasmic reticulum Ca2+ cycling protein phosphorylation in a physiologic Ca2+ milieu unleashes a high-power, rhythmic Ca2+ clock in ventricular myocytes: Relevance to arrhythmias and bio-pacemaker design

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY

IF4.7

2014-01-0122

OAAI

Ca2+-Dependent Phosphorylation of Ca2+ Cycling Proteins Generates Robust Rhythmic Local Ca2+ Releases in Cardiac Pacemaker Cells

SCIENCE SIGNALING

IF6.6

2013-01-2937

OAAI

CaMKII-Dependent Phosphorylation Modulates Ca2+ Cycling in Sinoatrial Node Cells to Regulate Cardiac Pacemaker Function

BIOPHYSICAL JOURNAL

IF3.1

2013-01-010

OAAI

Concerted effort of centrosomal and Golgi-derived microtubules is required for proper Golgi complex assembly but not for maintenance

MOLECULAR BIOLOGY OF THE CELL

IF2.7

2012-03-0171

OAAI

Basal PKC Activity Regulates Spontaneous Firing of Cardiac Pacemaker Cells

BIOPHYSICAL JOURNAL

IF3.1

2012-01-010

OAAI

An Inherent Ability of Ventricular Myocytes to Self-Organize Spontaneous RyRs Activation that Generate Synchronized Local Ca2+ Releases is Physiologically Suppressed by Constitutive Phosphodiesterase and Protein Phosphatase Activity

BIOPHYSICAL JOURNAL

IF3.1

2012-01-010

OAAI

A full range of mouse sinoatrial node AP firing rates requires protein kinase A-dependent calcium signaling

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY

IF4.7

2011-11-0127

OAAI

Study of Receptor-Chaperone Interactions Using the Optical Technique of Spectroscopic Ellipsometry

BIOPHYSICAL JOURNAL

IF3.1

2011-07-0113

OAAI

Sarcoplasmic Reticulum Ca2+ Pumping Kinetics Regulates Timing of Local Ca2+ Releases and Spontaneous Beating Rate of Rabbit Sinoatrial Node Pacemaker Cells

CIRCULATION RESEARCH

IF16.2

2010-09-1768

OAAI

A Coupled SYSTEM of Intracellular Ca2+ Clocks and Surface Membrane Voltage Clocks Controls the Timekeeping Mechanism of the Heart's Pacemaker

CIRCULATION RESEARCH

IF16.2

2010-03-05534

OAAI