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1. Ca ²⁺ release or Ca ²⁺ entry, that is the question: what governs Ca ²⁺ oscillations in pancreatic β cells?

   https://doi.org/10.1152/ajpendo.00030.2023  

   Fletcher, Patrick A.; Thompson, Ben; Liu, Chanté; Bertram, Richard; Satin, Leslie S.; Sherman, Arthur S. (June 2023, American Journal of Physiology-Endocrinology and Metabolism)

   The standard model for Ca 2+ oscillations in insulin-secreting pancreatic β cells centers on Ca 2+ entry through voltage-activated Ca 2+ channels. These work in combination with ATP-dependent K + channels, which are the bridge between the metabolic state of the cells and plasma membrane potential. This partnership underlies the ability of the β cells to secrete insulin appropriately on a minute-to-minute time scale to control whole body plasma glucose. Though this model, developed over more than 40 years through many cycles of experimentation and mathematical modeling, has been very successful, it has been challenged by a hypothesis that calcium-induced calcium release from the endoplasmic reticulum through ryanodine or inositol trisphosphate (IP3) receptors is instead the key driver of islet oscillations. We show here that the alternative model is in fact incompatible with a large body of established experimental data and that the new observations offered in support of it can be better explained by the standard model. 

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2. Phosphatidylinositol 3, 5‐bisphosphate regulates Ca ²⁺ transport during yeast vacuolar fusion through the Ca ²⁺ ATPase Pmc1

   https://doi.org/10.1111/tra.12736  

   Miner, Gregory E.; Sullivan, Katherine D.; Zhang, Chi; Rivera‐Kohr, David; Guo, Annie; Hurst, Logan R.; Ellis, Ez C.; Starr, Matthew L.; Jones, Brandon C.; Fratti, Rutilio A. (July 2020, Traffic)

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3. Phosphatidylserine affinity for and flip-flop dependence on Ca ²⁺ and Mg ²⁺ ions

   https://doi.org/10.1039/d4fd00206g  

   Hymas, Preston P; Conboy, John C (January 2025, Faraday Discussions)

   Ca²⁺ions are believed to play a crucial role in enzymatic regulation of lipid membrane asymmetry, yet direct effects of Ca²⁺on lipid flip-flop are unknown. Present work examines the influence of Ca–lipid interactions on lipid translocation. 

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4. Essential requirement for JPT2 in NAADP-evoked Ca ²⁺ signaling

   https://doi.org/10.1126/scisignal.abd5605  

   Gunaratne, Gihan S.; Brailoiu, Eugen; He, Shijun; Unterwald, Ellen M.; Patel, Sandip; Slama, James T.; Walseth, Timothy F.; Marchant, Jonathan S. (March 2021, Science Signaling)

   null (Ed.)

   Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that releases Ca 2+ from acidic organelles through the activation of two-pore channels (TPCs) to regulate endolysosomal trafficking events. NAADP action is mediated by NAADP-binding protein(s) of unknown identity that confer NAADP sensitivity to TPCs. Here, we used a “clickable” NAADP-based photoprobe to isolate human NAADP-binding proteins and identified Jupiter microtubule-associated homolog 2 (JPT2) as a TPC accessory protein required for endogenous NAADP-evoked Ca 2+ signaling. JPT2 was also required for the translocation of a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pseudovirus through the endolysosomal system. Thus, JPT2 is a component of the NAADP receptor complex that is essential for TPC-dependent Ca 2+ signaling and control of coronaviral entry. 

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5. Marine and Anthropogenic Bromopyrroles Alter Cellular Ca ²⁺ Dynamics of Murine Cortical Neuronal Networks by Targeting the Ryanodine Receptor and Sarco/Endoplasmic Reticulum Ca ²⁺ -ATPase

   https://doi.org/10.1021/acs.est.1c05214  

   Zheng, Jing; Antrobus, Shane; Feng, Wei; Purdy, Trevor N.; Moore, Bradley S.; Pessah, Isaac N. (December 2021, Environmental Science & Technology)