The use of Chinese hamster ovary (CHO) cells in the study of ion channels (Q46464395)

22 December 2017

title

The use of Chinese hamster ovary (CHO) cells in the study of ion channels (English)

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22 December 2017

author

Nikita Gamper

series ordinal

1

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22 December 2017

author name string

James D Stockand

series ordinal

2

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22 December 2017

Mark S Shapiro

series ordinal

3

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22 December 2017

publication date

23 March 2005

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22 December 2017

Journal of Pharmacological and Toxicological Methods

published in

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22 December 2017

volume

51

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22 December 2017

issue

3

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22 December 2017

page(s)

177-185

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22 December 2017

Intracellular Ca2+ buffers disrupt muscarinic suppression of Ca2+ current and M current in rat sympathetic neurons.

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K+ channel activation by all three isoforms of serum- and glucocorticoid-dependent protein kinase SGK

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IGF-1 up-regulates K+ channels via PI3-kinase, PDK1 and SGK1.

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Calmodulin mediates Ca2+-dependent modulation of M-type K+ channels

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Differential tetraethylammonium sensitivity of KCNQ1-4 potassium channels

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The alpha subunit of Gq contributes to muscarinic inhibition of the M-type potassium current in sympathetic neurons

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Disruption of the m1 receptor gene ablates muscarinic receptor-dependent M current regulation and seizure activity in mice

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KCNQ4, a K+ channel mutated in a form of dominant deafness, is expressed in the inner ear and the central auditory pathway.

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KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness

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Molecular cloning and functional expression of KCNQ5, a potassium channel subunit that may contribute to neuronal M-current diversity

7 January 2021

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Biophysical properties of ClC-3 differentiate it from swelling-activated chloride channels in Chinese hamster ovary-K1 cells

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Antibodies and a cysteine-modifying reagent show correspondence of M current in neurons to KCNQ2 and KCNQ3 K+ channels

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Voltage-controlled gating at the intracellular entrance to a hyperpolarization-activated cation channel

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KCNQ5, a novel potassium channel broadly expressed in brain, mediates M-type currents

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Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy

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Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors

7 January 2021

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Closure of potassium M-channels by muscarinic acetylcholine-receptor stimulants requires a diffusible messenger

7 January 2021

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Dominant-negative KvLQT1 mutations underlie the LQT1 form of long QT syndrome.

7 January 2021

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Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current

7 January 2021

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A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns

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Recovery from muscarinic modulation of M current channels requires phosphatidylinositol 4,5-bisphosphate synthesis

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Calmodulin modulates the delay period between release of calcium from internal stores and activation of calcium influx via endogenous TRP1 channels

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Activation of a muscarinic receptor selectively inhibits a rapidly inactivated Ca2+ current in rat sympathetic neurons

7 January 2021

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Transformation of mammalian cells with genes from procaryotes and eucaryotes

7 January 2021

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Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy

7 January 2021

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PIP(2) activates KCNQ channels, and its hydrolysis underlies receptor-mediated inhibition of M currents

7 January 2021

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10.1016/J.VASCN.2004.08.008

7 January 2021

Identifiers

DOI

1 reference

22 December 2017

release_pd6f3rlyundzdpmfuoenx63jmu

Fatcat ID

1 reference

Fatcat

https://api.fatcat.wiki/v0/release/pd6f3rlyundzdpmfuoenx63jmu

mapped directly with Wikidata item

24 November 2022

based on heuristic

PubMed ID

15862463

1 reference

22 December 2017