Filamin A (FLNA) is an actin-binding protein that has been reported to interact with STIM1 modulating the activation of Orai1 channels. Cleaving of FLNA by calpain leads to a C-terminal fragment that is involved in a variety of functional and pathological events, including pro-oncogenic activity in different types of cancer. Here we show that full-length FLNA is downregulated in samples from colon cancer patients as well as in the adenocarcinoma cell line HT-29.
View Article and Find Full Text PDFStore-operated Ca entry is a mechanism controlled by the filling state of the intracellular Ca stores, predominantly the endoplasmic reticulum (ER), where ER-resident proteins STIM1 and STIM2 orchestrate the activation of Orai channels in the plasma membrane, and Orai1 playing a predominant role. Two forms of Orai1, Orai1α and Orai1β, have been identified, which arises the question whether they are equally regulated by STIM proteins. We demonstrate that STIM1 preferentially activates Orai1α over STIM2, yet both STIM proteins similarly activate Orai1β.
View Article and Find Full Text PDFIndian J Thorac Cardiovasc Surg
May 2024
Introduction: Infections in cardiac implantable electronic devices (CIED) are increasing over time and associated with substantially mortality and healthcare costs. The best approach is the complete removal of the system by transvenous lead extraction (TLE). However, when leads are more than 10 years old, this technique requires considerable expertise and failures with the result of abandoned leads or serious complications may occur.
View Article and Find Full Text PDFIntroduction And Objectives: The current evaluation of acute heart failure (HF) does not allow an adequate prediction of its evolution. The electrical bioimpedance (BI) allows knowing the state of blood volume, until now only with fixed equipment. We have developed and validated a portable and wireless device to measure BI at the ankle (IVOL).
View Article and Find Full Text PDFThe upregulation of Orai1 and subsequent store-operated Ca entry (SOCE) has been associated with adverse cardiac remodeling and heart failure (HF). However, the mechanism underlying Orai1 upregulation and its role in myocardial infarction remains unclear. Our study investigated the role of Orai1 in activating adenylyl cyclase 8 (AC8) and cyclic AMP (cAMP) response element-binding protein (CREB), as well as its contribution to cardiac dysfunction induced by ischemia and reperfusion (I/R).
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