نتایج جستجو برای: camkii

تعداد نتایج: 2543  

Journal: :Endocrine-related cancer 2010
Maria Rosaria Rusciano Marcella Salzano Sara Monaco Maria Rosaria Sapio Maddalena Illario Valentina De Falco Massimo Santoro Pietro Campiglia Lucio Pastore Gianfranco Fenzi Guido Rossi Mario Vitale

RET/papillary thyroid carcinoma (PTC), TRK-T, or activating mutations of Ras and BRaf are frequent genetic alterations in PTC, all leading to the activation of the extracellular-regulated kinase (Erk) cascade. The aim of this study was to investigate the role of calmodulin-dependent kinase II (CaMKII) in the signal transduction leading to Erk activation in PTC cells. In normal thyroid cells, Ca...

Journal: :Molecular pharmacology 1999
G H Fan L Z Wang H C Qiu L Ma G Pei

Learning and memory have been suggested to be important in the development of opiate addiction. Based on the recent findings that calcium/calmodulin-dependent protein kinase II (CaMKII) is essential in learning and memory processes, and morphine treatment increases CaMKII activity in hippocampus, the present study was undertaken to examine whether inhibition of hippocampal CaMKII prevents morph...

Journal: :Circulation research 2009
Mark E Anderson

The multifunctional Ca 2 and calmodulin dependent protein kinase (CaMK)II is a serine threonine kinase that plays increasingly evident and important roles in regulating ion channels in heart and other excitable tissues. CaMKII activation initially requires an increase in intracellular Ca that leads to binding of calcified calmodulin (Ca /CaM) to the CaMKII regulatory domain. This activating Ca ...

2012
Steven J. Coultrap Kelsey Barcomb K. Ulrich Bayer

BACKGROUND Autophosphorylation of the Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) at T286 generates partially Ca(2+)/CaM-independent "autonomous" activity, which is thought to be required for long-term potentiation (LTP), a form of synaptic plasticity thought to underlie learning and memory. A requirement for T286 autophosphorylation also for efficient Ca(2+)/CaM-stimulated CaM...

Journal: :American journal of physiology. Heart and circulatory physiology 2006
Olaia Colinas Mónica Gallego Raúl Setién José Ramón López-López M Teresa Pérez-García Oscar Casis

In this work we have combined biochemical and electrophysiological approaches to explore the modulation of rat ventricular transient outward K(+) current (I(to)) by calmodulin kinase II (CaMKII). Intracellular application of CaMKII inhibitors KN93, calmidazolium, and autocamtide-2-related inhibitory peptide II (ARIP-II) accelerated the inactivation of I(to), even at low [Ca(2+)]. In the same co...

Journal: :The Journal of physiology 1999
S D Koh B A Perrino W J Hatton J L Kenyon K M Sanders

1. The kinetics of inactivation of delayed rectifier K+ current in murine colonic myocytes differed in amphotericin-permeabilized patch and conventional patch clamp. The difference was accounted for by Ca2+ buffering. 2. Calcium-calmodulin-dependent protein kinase II (CaMKII) inhibitors increased the rate of inactivation and slowed recovery from inactivation of the outward current. This was see...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2003
Heather L Hinds Ivan Goussakov Kazu Nakazawa Susumu Tonegawa Vadim Y Bolshakov

A significant fraction of the total calciumcalmodulin-dependent protein kinase II (CaMKII) activity in neurons is associated with synaptic connections and is present in nerve terminals, thus suggesting a role for CaMKII in neurotransmitter release. To determine whether CaMKII regulates neurotransmitter release, we generated and analyzed knockout mice in which the dominant alpha-isoform of CaMKI...

Journal: :Neuron 2015
Frédéric J. Hoerndli Rui Wang Jerry E. Mellem Angy Kallarackal Penelope J. Brockie Colin Thacker David M. Madsen Andres V. Maricq

Excitatory glutamatergic synaptic transmission is critically dependent on maintaining an optimal number of postsynaptic AMPA receptors (AMPARs) at each synapse of a given neuron. Here, we show that presynaptic activity, postsynaptic potential, voltage-gated calcium channels (VGCCs) and UNC-43, the C. elegans homolog of CaMKII, control synaptic strength by regulating motor-driven AMPAR transport...

2013
Mei-ling Anne Joiner

Ca2+–Calmodulin (CaM) kinase II (CaMKII) activation depends predominantly on modifications of amino acids within the regulatory domain on this multidomain kinase. A number of mechanisms of activation have been described since the original mode of activation, via Ca2+–CaM binding and phosphorylation of a threonine residue in the regulatory domain of CaMKII, was demonstrated. Gutierrez et al. pro...

Journal: :Journal of neurophysiology 2010
Shangyou Zeng William R Holmes

Activation of calcium-calmodulin dependent protein kinase II (CaMKII) during induction of long-term potentiation (LTP) is a series of complicated stochastic processes that are affected by noise. There are two main sources of noise affecting CaMKII activation within a dendritic spine. One is the noise associated with stochastic opening of N-methyl-d-aspartate (NMDA) receptor channels and the oth...

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