STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.
10.1007/s12264-024-01272-5
- Author:
Ksenia SKOBELEVA
1
;
Guanghui WANG
2
;
Elena KAZNACHEYEVA
1
,
3
Author Information
1. Laboratory of Ion Channels of Cell Membranes, Institute of Cytology, Russian Academy of Sciences, Saint Petersburg, Russia,
2. Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.
3. evkazn@incras.ru.
- Publication Type:Review
- Keywords:
Brain;
Calcium;
Calcium channels;
Calcium entry;
Neurons;
STIM1;
STIM2
- MeSH:
Neurons/metabolism*;
Animals;
Humans;
Calcium/metabolism*;
Stromal Interaction Molecules/metabolism*;
Calcium Signaling/physiology*;
Calcium Channels/metabolism*;
Brain/metabolism*
- From:
Neuroscience Bulletin
2025;41(2):305-325
- CountryChina
- Language:English
-
Abstract:
Stromal interaction molecules (STIM)s are Ca2+ sensors in internal Ca2+ stores of the endoplasmic reticulum. They activate the store-operated Ca2+ channels, which are the main source of Ca2+ entry in non-excitable cells. Moreover, STIM proteins interact with other Ca2+ channel subunits and active transporters, making STIMs an important intermediate molecule in orchestrating a wide variety of Ca2+ influxes into excitable cells. Nevertheless, little is known about the role of STIM proteins in brain functioning. Being involved in many signaling pathways, STIMs replenish internal Ca2+ stores in neurons and mediate synaptic transmission and neuronal excitability. Ca2+ dyshomeostasis is a signature of many pathological conditions of the brain, including neurodegenerative diseases, injuries, stroke, and epilepsy. STIMs play a role in these disturbances not only by supporting abnormal store-operated Ca2+ entry but also by regulating Ca2+ influx through other channels. Here, we review the present knowledge of STIMs in neurons and their involvement in brain pathology.
