M
Michael H. Nathanson
Researcher at Yale University
Publications - 166
Citations - 8030
Michael H. Nathanson is an academic researcher from Yale University. The author has contributed to research in topics: Receptor & Calcium signaling. The author has an hindex of 49, co-authored 159 publications receiving 7271 citations. Previous affiliations of Michael H. Nathanson include University Hospitals of Cleveland & Salisbury University.
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Mechanisms and regulation of bile secretion.
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Regulation of calcium signals in the nucleus by a nucleoplasmic reticulum
TL;DR: The findings show that the nucleus contains a nucleoplasmic reticulum with the capacity to regulate calcium signals in localized subnuclear regions and provides a potential mechanism by which calcium can simultaneously regulate many independent processes in the nucleus.
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Type III InsP3 receptor channel stays open in the presence of increased calcium
TL;DR: It is found that type III InsP3R forms Ca2+ channels with single-channel currents that are similar to those of type I InsP4,5-trisphosphate receptor; however, the open probability of type IIIinsp3R isoform increases monotonically with increased cytoplasmic Ca2- concentration, whereas the type I isoform has a bell-shaped dependence on cytopalasmicCa2+.
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Isolated rat hepatocytes can signal to other hepatocytes and bile duct cells by release of nucleotides
TL;DR: Mechanical stimulation of isolated hepatocytes, including by microinjection, can evoke [Ca2+]i signals in the stimulated cell as well as in neighboring noncontacting hepatocytes and bile duct epithelia, suggesting a novel paracrine signaling pathway for epithelIA, which previously were thought to communicate exclusively via gap junctions.
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Role in host cell invasion of Trypanosoma cruzi-induced cytosolic-free Ca2+ transients.
TL;DR: Results indicate that a trypomastigote membrane factor triggers cytosolic-free Ca2+ transients in host cells through a G-protein-coupled pathway that may promote invasion through modulation of the host cell actin cytoskeleton.