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Succinate is a pivotal tricarboxylic acid cycle metabolite but also specifically activates the G- and G-coupled succinate receptor 1 (SUCNR1). Contradictory roles of succinate and succinate-SUCNR1 signaling include reports about its anti- or pro-inflammatory effects. The link between cellular metabolism and localization-dependent SUCNR1 signaling qualifies as a potential cause for the reported conflicts.

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Background: Chronic hepatitis B virus (HBV) infection is a major risk for development of hepatocellular carcinoma (HCC), a frequent malignancy with a poor survival rate. HBV infection results in significant endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) signaling, a contributing factor to carcinogenesis. As part of the UPR, the ER-associated degradation (ERAD) pathway is responsible for removing the burden of misfolded secretory proteins, to re-establish cellular homeostasis.

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Indoxyl Sulfate Induces Ventricular Arrhythmias Attenuated by Secretoneurin in Right Ventricular Outflow Tract Cardiomyocytes.

Cardiovasc Toxicol

January 2025

Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250, Wuxing St., Taipei, 11031, Taiwan.

Ventricular arrhythmias (VAs) are major causes of sudden cardiac death in chronic kidney disease (CKD) patients. Indoxyl sulfate (IS) is one common uremic toxin found in CKD patients. This study investigated whether IS could induce VAs via increasing right ventricular outflow tract (RVOT) arrhythmogenesis.

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The beneficial properties of probiotics have always been a point of interest. Probiotics play a major role in maintaining the health of Gastrointestinal Tract (GIT), a healthy digestive system is responsible for modulating all other functions of the body. The effectiveness of probiotics can be enhanced by formulating them with prebiotics the formulation thus formed is referred to as synbiotics.

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The trimeric intracellular cation channel B (TRIC-B), encoded by TMEM38B, is a potassium (K) channel present in the endoplasmic reticulum membrane, where it counterbalances calcium (Ca) exit. Lack of TRIC-B activity causes a recessive form of the skeletal disease osteogenesis imperfecta (OI), namely OI type XIV, characterized by impaired intracellular Ca flux and defects in osteoblast (OB) differentiation and activity. Taking advantage of the OB-specific Tmem38b knockout mouse (Runx2Cre;Tmem38b; cKO), we investigated how the ion imbalance affects the osteogenetic process.

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