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Atsuko Yatani

Researcher at University of Medicine and Dentistry of New Jersey

Publications -  130
Citations -  9892

Atsuko Yatani is an academic researcher from University of Medicine and Dentistry of New Jersey. The author has contributed to research in topics: G protein & Adenylyl cyclase. The author has an hindex of 50, co-authored 130 publications receiving 9718 citations. Previous affiliations of Atsuko Yatani include Kyushu University & Baylor College of Medicine.

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A G protein directly regulates mammalian cardiac calcium channels.

TL;DR: G proteins are now known to directly gate two classes of membrane ion channels, and in addition to regulating calcium channels indirectly through activation of cytoplasmic kinases, they can regulate calcium channels directly.
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cAMP-Dependent Regulation of Cardiac L-Type Ca2+ Channels Requires Membrane Targeting of PKA and Phosphorylation of Channel Subunits

TL;DR: The PKA-mediated regulation of L-type Ca2+ channels is critically dependent on a functional AKAP and phosphorylation of the alpha1C subunit at Ser1928, demonstrating that the events observed in the heterologous expression system reflect those occurring in the native system.
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Direct activation of mammalian atrial muscarinic potassium channels by GTP regulatory protein Gk

TL;DR: Potassium channels in isolated, inside-out patches of membranes from atrial cells now are shown to be activated by a purified pertussis toxin-sensitive G protein of subunit composition alpha beta gamma, with an alpha subunit of 40,000 daltons, indicating proteins other than enzymes can be under control of receptor coupling G proteins.
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Early and Delayed Consequences of β2-Adrenergic Receptor Overexpression in Mouse Hearts Critical Role for Expression Level

TL;DR: These data demonstrate that the heart tolerates enhanced contractile function via 60-fold beta(2)AR overexpression without detriment for a period of >/=1 year and that higher levels of expression result in either aggressive or delayed cardiomyopathy.
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Rapid beta-adrenergic modulation of cardiac calcium channel currents by a fast G protein pathway

TL;DR: The presence of a fast pathway in the heart can explain what the slow pathway cannot account for: the ability of cardiac sympathetic nerves to change heart rate within a single beat.