Overexpression of STIM1 and its impact on mitochondrial metabolism

Primárne karty

ISBN: 978-80-974608-0-8
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Overexpression of STIM1 and its impact on mitochondrial metabolism

Katarina Leskova Majdova1 , Maria Bencurova , Peter Kaplan , Peter Racay , Zuzana Tatarkova , Cecilia Song Jaekyung2 , Cheol Choi Won
1 Department of Medical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia
2 Luterion R&D Center, Seoul, South Korea

Calcium (Ca2+) is ubiquitously the second messenger involved in the regulation of many cell functions such as proliferation, differentiation, apoptosis, exocytosis, muscle contraction, and so on. The main organelle linked to calcium metabolism is the mitochondria. The influx of Ca2+ into the cells is mediated by store-operated calcium entry (SOCE), which is activated by the lack of intracellular storage of Ca2+. The sensor protein-stromal interaction molecule 1 (STIM1) and the ion channel ORAI1 are key players in the physiological function of SOCE. Mutation of the luminal EF-hand motif of STIM1 generates a constitutively active STIM1 and activates Ca2+ entry independently from the endoplasmic reticulum (ER) stores of Ca2+. In our project, we create the functional STIM1 cell model that will be used for the detection of changes related to continuous SOCE activation caused by STIM1 overexpression in the Tet-on inducible expression system in human embryonic kidney cells (HEK293). We assume, that this model creates a suitable environment for monitoring the impact as well as communication between cellular Ca2+ entry mediated by STIM1 and intracellular organelles such as mitochondria. Moreover, communication between these organelles has a direct impact on mitochondrial metabolism, shape, bioenergetics, or stress response, all involved in the development of disease-related pathological changes.


This work is supported by Luterion Co, Ltd., and project No.: Z/2022/2685/XIV/JLF/KD.