A portable site: a binding element for 17beta-estradiol can be placed on any subunit of a nicotinic alpha4beta2 receptor.

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Jin X, Steinbach JH

A portable site: a binding element for 17beta-estradiol can be placed on any subunit of a nicotinic alpha4beta2 receptor.

J Neurosci. 2011 Mar 30;31(13):5045-54. doi: 10.1523/JNEUROSCI.4802-10.2011.

PubMed ID

21451042 [ View in PubMed

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Abstract

Endogenous steroids can modulate the activity of transmitter-gated channels by directly interacting with the receptor. 17beta-Estradiol potentiates activation of neuronal nicotinic alpha4beta2 receptors by interacting with a 4 aa sequence at the extreme C terminus of the alpha4 subunit, but it is not known whether potentiation requires that the sequence be placed on a specific subunit (e.g., an alpha4 subunit that is involved in forming an acetylcholine-binding site). By using concatemers of subunits and chimeric subunits, we have found that the C-terminal domain can be moved from the alpha4 to the beta2 subunit and still result in potentiation. In addition, the sequence can be placed on a subunit that contributes to an acetylcholine-binding site or on the structural subunit. The data indicate that this estradiol-binding element is a discrete sequence and suggest that the effect of 17beta-estradiol is mediated by actions on single subunits and that the overall consequences for gating occur because of the summation of independent energetic contributions to overall gating of this receptor.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Estradiol	Neuronal acetylcholine receptor subunit alpha-4	Protein	Humans	Unknown	Binder	Details