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PMID |
Sentence |
1 |
17434294
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Evidence suggests that dysregulation of TRPC4 and -C1 results in vascular endothelial barrier dysfunction; malfunction of TRPP1 and -P2 impairs endothelial NO synthase; the reduced expression or activity of TRPC4 and -V1 impairs agonist-induced vascular relaxation; the decreased activity of TRPV4 reduces flow-induced vascular responses; and the activity of TRPC3 and -C4 is associated with oxidative stress-induced endothelial damage.
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2 |
21290315
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The TRPC members TRPC3 and TRPC4 can serve as subunits of a redox-sensitive ion channel in native aortic endothelial cells.
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3 |
21290315
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The TRPM family member TRPM2 has a number of physiologic isoforms expressed in many cell types and responds to stimuli including oxidative stress, TNFα, and β-amyloid peptide.
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4 |
21290315
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The important role of TRPM2 isoforms in cell proliferation and oxidant-induced cell death has been well established using divergent cell systems and techniques including overexpression, channel depletion or inhibition, and calcium chelation.
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5 |
23858470
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Leptin promotes K(ATP) channel trafficking by AMPK signaling in pancreatic β-cells.
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6 |
23858470
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In this study, we provide evidence that leptin modulates pancreatic β-cell functions by promoting K(ATP) channel translocation to the plasma membrane via AMP-activated protein kinase (AMPK) signaling.
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7 |
23858470
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We discovered that the molecular mechanism of leptin-induced AMPK activation involves canonical transient receptor potential 4 and calcium/calmodulin-dependent protein kinase kinase β.
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8 |
23858470
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AMPK activation was dependent on both leptin and glucose concentrations, so at optimal concentrations of leptin, AMPK was activated sufficiently to induce K(ATP) channel trafficking and hyperpolarization of pancreatic β-cells in a physiological range of fasting glucose levels.
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