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Mutations in Cytoplasmic Loops of the KCNQ1 Channel and the Risk of Life-Threatening Events: Implications for Mutation-Specific Response to &bgr;-Blocker Therapy in Type 1 Long-QT Syndrome

Reduced channel activation after sympathetic activation can explain the increased clinical risk and response to therapy in patients with C-loop mutations and derive a pronounced benefit from treatment with &bgr;-blockers.
Wolters Kluwer (opens in a new tab)

Prognostic significance of epidermal growth factor receptor phosphorylation and mutation in head and neck squamous cell carcinoma.

Phosphorylated EGFR without mutations may be a marker of poor prognosis in patients with HNSCC, and associations between EGFR molecular status and patient characteristics and disease-free survival are elucidated.
PubMed (opens in a new tab)

Interaction of &agr;1-Adrenoceptor Subtypes With Different G Proteins Induces Opposite Effects on Cardiac L-type Ca2+ Channel

These findings demonstrated that the interactions of &agr;1-adrenoceptor subtypes with different G proteins elicit the formation of separate signaling cascades, which produce the opposite effects on ICa.
Wolters Kluwer (opens in a new tab)

Activation of Anoctamin‐1 Limits Pulmonary Endothelial Cell Proliferation via p38‐Mitogen‐activated Protein Kinase‐Dependent Apoptosis

Activation of Ano1 promotes apoptosis of pulmonary ECs and human IPAH‐pulmonary artery ECs, likely via increased mtROS and p38 phosphorylation, leading to apoptosis.
Wolters Kluwer (opens in a new tab)

Molecular identities of mitochondrial Ca2+ influx mechanism: Updated passwords for accessing mitochondrial Ca2+-linked health and disease

This paper aims to demonstrate the intracellular integrity of the Ca2+–Ca2+ exchanger system through the use of a simple, straightforward, and scalable “spatially-dense” approach.
PDF (opens in a new tab)

Molecular basis of decreased Kir4.1 function in SeSAME/EAST syndrome.

P perturbed pH gating may underlie the loss of channel function for the disease-associated mutant Kir4.1 channels and may have important physiologic consequences.
PubMed (opens in a new tab)

Pharmacological Modulation of Mitochondrial Ca2+ Content Regulates Sarcoplasmic Reticulum Ca2+ Release via Oxidation of the Ryanodine Receptor by Mitochondria-Derived Reactive Oxygen Species

Treatment with kaempferol or CGP-37157 increased the levels of reactive oxygen species (ROS) in mitochondria and the sarcoplasmic reticulum (SR), respectively, and redox-sensitive OMM-HyPer and ERroGFP_iE biosensors found this suggested facilitation of mitochondrial Ca2+ uptake in cardiac disease can exacerbate proarrhythmic disturbances in Ca2+.
PubMed (opens in a new tab)

Overexpression of ryanodine receptor type 1 enhances mitochondrial fragmentation and Ca2+-induced ATP production in cardiac H9c2 myoblasts.

RyR1 possesses a mitochondrial targeting/retention signal and modulates mitochondrial morphology and Ca(2+)-induced ATP production in cardiac H9c2 myoblasts, which indicates that the role of mitochondrial RyR1 in the regulation of mitochondrial morphology/function in cardiac cells is investigated.
PubMed (opens in a new tab)

Trigger-specific ion-channel mechanisms, risk factors, and response to therapy in type 1 long QT syndrome.

In patients with LQT1, cardiac events triggered by exercise, arousal, or rest/sleep are associated with distinctive risk factors and response to medical therapy, and can be used for improved recommendations for lifestyle modifications and therapeutic management in this population.
PubMed (opens in a new tab)

Mitochondrial Ion Channels/Transporters as Sensors and Regulators of Cellular Redox Signaling

Identification of detailed molecular mechanisms for redox-mediated regulation of mitochondrial ion channels will enable us to find novel therapeutic targets for many diseases that are associated with cellular redox signaling and mitochondrial ion channels/transporters.
SAGE (opens in a new tab)
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