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Molecular Genetic Diagnosis of Human Malignant Hyperthermia
Published in S. Tsuyoshi Ohnishi, Tomoko Ohnishi, Malignant Hyperthermia, 1994
Other skeletal muscle proteins promising as candidate genes include triadin,55 inositol trisphosphatases,56 the inositol trisphosphate receptor,57 the sodium channel α-subunit,58 and enzymes integral to fatty acid metabolism.59,60 While ongoing investigations of muscle calcium regulation and excitation-contraction coupling will undoubtedly suggest additional candidates, genetic investigations of human MH may correspondingly yield new genes encoding hitherto unknown proteins.
Effects of nano-titanium dioxide on calcium homeostasis in vivo and in vitro: a systematic review and meta-analysis
Published in Toxicology Mechanisms and Methods, 2023
Yaqian Yang, Yiman Zhao, Qianqian Wang, Mi Liu, Hongmei Chang, Li Li, Xiaojia Meng, Yaxin Deng, Chunmei Ling, Kui Wang, Guanling Song, Xin Sui
Cellular Ca2+ levels are mainly regulated by plasma membrane calcium transport and intracellular calcium pools, both of which work together to maintain intracellular calcium homeostasis. The regulation process of Ca2+ levels involves the carrier protein Ca2+-ATPase and multiple channel proteins, including L-type voltage-gated Ca2+ channels (L-VGCC), Na+/Ca2+ exchanger (NCX), inositol triphosphate receptor (IP3R) and ryanodine receptor (RyR) (Kaplan et al. 2003; Brini 2009; Chen et al. 2012). TiO2 NPs are known to induce the production of ROS, and ROS, as an important intermediate factor, can indirectly lead to disturbance of calcium homeostasis (Delamere et al. 1991; Zaidi and Michaelis 1999; Zaidi et al. 2009). Meanwhile, Ca2+ concentration is also affected by other factors, such as the interaction of TiO2 NPs with biological macromolecules.
Emerging pharmacological strategies for the management of chemotherapy-induced peripheral neurotoxicity (CIPN), based on novel CIPN mechanisms
Published in Expert Review of Neurotherapeutics, 2020
Andreas A. Argyriou, Jordi Bruna, Susanna B. Park, Guido Cavaletti
In addition, evidence from preclinical studies using paclitaxel points toward another axon degenerative cascade dependent on inositol triphosphate receptor type 3 (IP3R1) that can lead to the activation of axon calpain proteases. IP3R1 receptors located in the mitochondrial-associated endoplasmic reticulum membranes, ensure proper Ca2+ signaling from the reticulum to the mitochondria. Bclw, a Bcl2 peptide family member, modulates IP3R1 activity. Paclitaxel administration has been demonstrated to reduce RNA-granules containing Bclw mRNA and its axonal synthesis, resulting in mitochondrial dysfunction and activation of calcium-dependent proteases [24]. Improving Bclw levels/activity or IP3R1 function might represent a novel therapeutic target for prevention of CIPN. In this respect, sigma-1 receptor ligand contributes to sustain the correct conformation of IP3R1, ensuring maintenance of proper Ca2+ signaling [25], and it has already been tested in a CIPN proof of concept clinical trial [26].
Assessment of sigma-1 receptor occupancy in mice with non-radiolabelled FTC-146 as a tracer
Published in Journal of Receptors and Signal Transduction, 2018
Gopinadh Bhyrapuneni, Jagadeesh Babu Thentu, Abdul Rasheed Mohammed, Raghupathi Reddy Aleti, Nagasurya Prakash Padala, Devender Reddy Ajjala, Ramakrishna Nirogi
The role of sigma-1 receptors in causing neurological and psychiatric conditions is imparting the need of high therapeutic actions through these receptors [1,2]. Sigma-1 regulates the function of the inositol trisphosphate receptor, thus stabilizing calcium signaling between mitochondria and the endoplasmic reticulum and renders its protective role [3]. The calcium hypothesis supports that the disruption of calcium signaling plays a key role in the emergence and development of neurodegenerative diseases.