In conclusion, TRPM2 channels were constitutively activated by intracellular ADPR currents in mice native megakaryocyte.
📌 3 Key Takeaways
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Objective & Hypothesis:Since the mechanisms that lead to melastatin-like transient receptor potential 2 (TRPM2) channel activation in response to ADP-Ribose (ADPR) are not understood, I tested the effects of ADP-Ribose on TRPM2 cation channel currents in native bone marrow megakaryocyte of mice.
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Key Findings & Data:Kv1.3-deficient mice megakaryocyte cells were freshly isolated from bone marrow and the cells studied with the conventional whole-cell patch clamp technique.
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Conclusion & Impact:In conclusion, TRPM2 channels were constitutively activated by intracellular ADPR currents in mice native megakaryocyte.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:TRPM2 channels · ADP-Ribose · bone marrow
Abstract
Since the mechanisms that lead to melastatin-like transient receptor potential 2 (TRPM2) channel activation in response to ADP-Ribose (ADPR) are not understood, I tested the effects of ADP-Ribose on TRPM2 cation channel currents in native bone marrow megakaryocyte of mice. Kv1.3-deficient mice megakaryocyte cells were freshly isolated from bone marrow and the cells studied with the conventional whole-cell patch clamp technique. ADPR (1mM) was applied intracellularly through the pipette. Non-selective cation currents in the mice were consistently induced by ADPR. Current density of ADPR in the cells were significantly (p<0.001) higher than in control. The time courses of ADPR effects in the mice were characterized by a delay of 3.66 ± 0.69. In conclusion, TRPM2 channels were constitutively activated by intracellular ADPR currents in mice native megakaryocyte.
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