TRPV1 channels: Not so inactive on the ER

Elliot Imler; Konrad E. Zinsmaier

doi:10.1016/j.neuron.2014.10.052

TRPV1 channels: Not so inactive on the ER

Elliot Imler
, Konrad E. Zinsmaier

Research output: Contribution to journal › Short survey › peer-review

8 Scopus citations

Abstract

In this issue of Neuron, Wong etal. (2014) report a remarkable evolutionarily conserved role for the Drosophila TRPV1 homolog Inactive controlling synaptic growth at larval neuromuscular junctions by facilitating Ca²⁺ release from the endoplasmic reticulum. In this issue of Neuron, Wong etal. (2014) report a remarkable evolutionarily conserved role for the Drosophila TRPV1 homolog Inactive controlling synaptic growth at larval neuromuscular junctions by facilitating Ca²⁺ release from the endoplasmic reticulum.

Original language	English (US)
Pages (from-to)	659-661
Number of pages	3
Journal	Neuron
Volume	84
Issue number	4
DOIs	https://doi.org/10.1016/j.neuron.2014.10.052
State	Published - Nov 19 2014

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neuron.2014.10.052

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abstract = "In this issue of Neuron, Wong etal. (2014) report a remarkable evolutionarily conserved role for the Drosophila TRPV1 homolog Inactive controlling synaptic growth at larval neuromuscular junctions by facilitating Ca2+ release from the endoplasmic reticulum. In this issue of Neuron, Wong etal. (2014) report a remarkable evolutionarily conserved role for the Drosophila TRPV1 homolog Inactive controlling synaptic growth at larval neuromuscular junctions by facilitating Ca2+ release from the endoplasmic reticulum.",

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TRPV1 channels: Not so inactive on the ER

Abstract

ASJC Scopus subject areas

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