Arrestin is required for agonist-induced trafficking of voltage-dependent calcium channels (Q56747585)

Dataset for "Continued use of retracted papers: Temporal trends in citations and (lack of) awareness of retractions shown in citation contexts in biomedicine"

Continued use of retracted papers: Temporal trends in citations and (lack of) awareness of retractions shown in citation contexts in biomedicine

title

Arrestin is required for agonist-induced trafficking of voltage-dependent calcium channels (English)

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Akil Puckerin

1

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Lanying Liu

2

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Natasha Permaul

3

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Paul Carman

4

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Jessica Lee

5

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María A Diversé-Pierluissi

Journal of Biological Chemistry

6

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language of work or name

English

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publication date

13 October 2006

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published in

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volume

281

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issue

41

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page(s)

31131-41

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cites work

G protein modulation of voltage-gated calcium channels

1 reference

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Determinants of G protein inhibition of presynaptic calcium channels

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Modulation of Ca2+ channels by G-protein beta gamma subunits

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Voltage-dependent modulation of N-type calcium channels by G-protein beta gamma subunits

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Novel form of crosstalk between G protein and tyrosine kinase pathways

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Tyrosine-kinase-dependent recruitment of RGS12 to the N-type calcium channel

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beta-Arrestin: a protein that regulates beta-adrenergic receptor function

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Heterodimerization is required for the formation of a functional GABA(B) receptor

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Cloning and functional expression of novel N-type Ca(2+) channel variants

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Desensitization of G protein-coupled receptors and neuronal functions

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beta-Arrestins bind and decrease cell-surface abundance of the Na+/H+ exchanger NHE5 isoform

21 January 2018

1 reference

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G protein modulation of N-type calcium channels is facilitated by physical interactions between syntaxin 1A and Gbetagamma.

21 January 2018

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Interaction of the synprint site of N-type Ca2+ channels with the C2B domain of synaptotagmin I.

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Requirement for the synaptic protein interaction site for reconstitution of synaptic transmission by P/Q-type calcium channels

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ORL1 receptor-mediated internalization of N-type calcium channels

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Transduction of receptor signals by beta-arrestins

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N-type Ca2+ channels as scaffold proteins in the assembly of signaling molecules for GABAB receptor effects

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Reciprocal regulation of angiotensin receptor-activated extracellular signal-regulated kinases by beta-arrestins 1 and 2.

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The proliferative and antiapoptotic effects of substance P are facilitated by formation of a beta -arrestin-dependent scaffolding complex

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Differential desensitization, receptor phosphorylation, beta-arrestin recruitment, and ERK1/2 activation by the two endogenous ligands for the CC chemokine receptor 7.

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Arrestin2 and arrestin3 are differentially expressed in the rat brain during postnatal development

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beta-Arrestin2, interacting with phosphodiesterase 4, regulates synaptic release probability and presynaptic inhibition by opioids

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