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Gregory Martin

As seen in: JACC (Journal of the American College of Cardiology), The Journal of Biological Chemistry, The Burlington Magazine
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Articles by Gregory Martin

July 2024, #1456 - Vol 166

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By Gregory Martin, Anna Orlando, Zuzana Macurová, Jolijn Schilder
| The Burlington Magazine Verified
Cuts, cuts, cuts: this seems to be the endless refrain that attends any discussion of the arts in the United Kingdom. On the one hand many recognise the profound benefits to a civilised society of a vibrant cultural sector; however, the reality is increasingly characterised in certain areas by a woeful lack of investment, a crumbling infrastructure and the loss of skills and expertise. Such issues are often explored in the press and have been aired in the past in the Editorials of this Magazine.
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Loss of Bone Morphogenetic Protein-9 Reduces Survival and Increases MMP Activity After Myocardial Infarction:

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By Shreyas Bhave, Michele L. Esposito Verified, Xiaoying Qiao, Gregory Martin
| JACC (Journal of the American College of Cardiology)
Introduction Myocardial infarction (MI) is a major cause of global morbidity and mortality that affects nearly 800,000 patients each year in the United States alone.1 Cardiac wound healing after MI is a complex and multiphase process that begins with necrosis and apoptosis of cardiomyocytes due to ischemic injury with or without reperfusion followed by the formation of a fibrotic scar.2 The acute phase of this process involves an inflammatory response and degradation of the extracellular...
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Pharmacological Correction of Trafficking Defects in ATP-sensitive Potassium Channels Caused by Sulfonylurea Receptor 1 Mutations

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By Gregory Martin, Emily A. Rex, Prasanna Devaraneni, Jerod S. Denton
| The Journal of Biological Chemistry Verified
ATP-sensitive potassium (K ) channels play a key role in mediating glucose-stimulated insulin secretion by coupling metabolic signals to ?-cell membrane potential. Loss of K channel function due to mutations in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifying potassium channel Kir6.2, respectively, results in congenital hyperinsulinism. Many SUR1 mutations prevent trafficking of channel proteins from the endoplasmic reticulum to the cell surface.
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Pharmacological Correction of Trafficking Defects in ATP-Sensitive Potassium Channels Caused by Sulfonylurea Receptor 1 Mutations

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By Gregory Martin, Emily A. Rex, Prasanna Devaraneni, Jerod S. Denton
| The Journal of Biological Chemistry Verified
ATP-sensitive potassium (K ) channels play a key role in mediating glucose-stimulated insulin secretion by coupling metabolic signals to β-cell membrane potential. Loss of K channel function due to mutations in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifying potassium channel Kir6.2, respectively, results in congenital hyperinsulinism. Many SUR1 mutations prevent trafficking of channel proteins from the endoplasmic reticulum to the cell surface.
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