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Stefan Amisten

Researcher at King's College London

Publications -  47
Citations -  2311

Stefan Amisten is an academic researcher from King's College London. The author has contributed to research in topics: Islet & Receptor. The author has an hindex of 25, co-authored 47 publications receiving 2033 citations. Previous affiliations of Stefan Amisten include Lund University & University of Oxford.

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GLP-1 inhibits and adrenaline stimulates glucagon release by differential modulation of N- and L-type Ca2+ channel-dependent exocytosis.

TL;DR: It is proposed that GLP-1 inhibits glucagon secretion by PKA-dependent inhibition of the N-type Ca(2+) channels via a small increase in intracellular cAMP ([cAMP](i) and Adrenaline stimulates L- type Ca( 2+) channel-dependent exocytosis by activation of the low-affinity cAMP sensor Epac2 via a large increase in [cAMP]-i.
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Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease

TL;DR: It is suggested that interferogenic immune complexes stimulate production of IFNα that up-regulates the megakaryocytic type I IFN-regulated genes and proteins and could affect platelet activation and contribute to development of vascular disease in SLE.
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An atlas and functional analysis of G-protein coupled receptors in human islets of Langerhans

TL;DR: This atlas of all GPCRs expressed by human islets is constructed and identifies GPCR/ligand/drug interactions that might affect insulin secretion, which are important for understanding the metabolic side effects of drugs.
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Gene expression profiling for the identification of G-protein coupled receptors in human platelets.

TL;DR: Several GPCRs not previously known to be expressed in platelets are detected, including a functional adenosine A(2B) receptor, which could improve the understanding of platelet aggregation and provide new targets for drug development.
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Chronic Palmitate Exposure Inhibits Insulin Secretion by Dissociation of Ca2+ Channels from Secretory Granules

TL;DR: In both mouse and human islets, thePalmitate-induced secretion defect was reversed when the β cell action potential was pharmacologically prolonged, and the release competence of the granules was not affected by palmitate.