Dataset Information

Na⁺/Ca²⁺ exchanger isoform 1 takes part to the Ca²⁺-related prosurvival pathway of SOD1 in primary motor neurons exposed to beta-methylamino-L-alanine.

ABSTRACT:

Background

The cycad neurotoxin beta-methylamino-L-alanine (L-BMAA), one of the environmental trigger factor for amyotrophic lateral sclerosis/Parkinson-dementia complex (ALS/PDC), may cause neurodegeneration by disrupting organellar Ca²⁺ homeostasis. Through the activation of Akt/ERK1/2 pathway, the Cu,Zn-superoxide dismutase (SOD1) and its non-metallated form, ApoSOD1, prevent endoplasmic reticulum (ER) stress-induced cell death in motor neurons exposed to L-BMAA. This occurs through the rapid increase of intracellular Ca²⁺ concentration ([Ca²⁺]_i) in part flowing from the extracellular compartment and in part released from ER. However, the molecular components of this mechanism remain uncharacterized.

Methods

By an integrated app

SUBMITTER: Petrozziello T

PROVIDER: S-EPMC8756626 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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Dataset Information

Na⁺/Ca²⁺ exchanger isoform 1 takes part to the Ca²⁺-related prosurvival pathway of SOD1 in primary motor neurons exposed to beta-methylamino-L-alanine.

Background

Methods

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Na+/Ca2+ exchanger isoform 1 takes part to the Ca2+-related prosurvival pathway of SOD1 in primary motor neurons exposed to beta-methylamino-L-alanine.

Background

Methods

OmicsDI is part of the ELIXIR infrastructure

Tweets

Na⁺/Ca²⁺ exchanger isoform 1 takes part to the Ca²⁺-related prosurvival pathway of SOD1 in primary motor neurons exposed to beta-methylamino-L-alanine.