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Rotein expression in Nav1.7 embryonic null mice – mechanisms of compensation

ABSTRACT: Mice and humans who have lost the expression of functional sodium channel Nav1.7 are pain-free, but otherwise normal. This is the result of a loss of neurotransmitter release such as glutamate and Substance P from primary sensory neurons. The sensory neurons are otherwise normal apart from loss of neurotransmitter release. Adult gene deletion results in a loss of neuronal excitability with some analgesia that is not linked to opioid activity. Drugs that block Nav1.7 have lethal effects through action on the autonomic nervous system and the heart. But the embryonic null humans and mice are fine. Therefore there must be compensation for the embryonic loss of Nav1.7. This experiment compares the protein components of wild type normal mice and Nav1.7 embryonic deletion mice in order to identify compensatory mechanisms.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Ganglion Cell Layer

SUBMITTER: riccardo zenezini chiozzi

LAB HEAD: Konstantinos Thalassinos

PROVIDER: PXD052513 | Pride | 2024-10-17

REPOSITORIES: Pride

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			Action	DRS
	08032024_P12_STP0093_MouseTissue_A1_L.htrms	Other
	08032024_P12_STP0093_MouseTissue_A1_L.raw	Raw
	08032024_P12_STP0093_MouseTissue_A1_R.htrms	Other
	08032024_P12_STP0093_MouseTissue_A1_R.raw	Raw
	08032024_P12_STP0093_MouseTissue_DD1_L.htrms	Other

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