(Ala13)-Apelin-13 corresponds to Apelin-13 with a Phe-to-Ala substitution at the C-terminus (F13A) and functions as an antagonist against apelin-dependent APJ functions both in cultures and in animal studies in vivo.
Apelin-13 with a Phe-to-Ala substitution at the C-terminus (F13A) and functions as an antagonist against apelin-dependent APJ functions.
American journal of physiology. Gastrointestinal and liver physiology, 310(4), G249-G261 (2015-12-19)
Apelin, an endogenous ligand for APJ receptor, has been reported to be upregulated in paraventricular nucleus (PVN) following stress. Central apelin is known to stimulate release of corticotropin-releasing factor (CRF) via APJ receptor. We tested the hypothesis that stress-induced gastrointestinal
Apelin peptide and its receptor APJ are directly implicated in various physiological processes ranging from cardiovascular homeostasis to immune signaling. Here, we show that apelin is a key player in hemostasis with an ability to inhibit thrombin- and collagen-mediated platelet
The apelin peptide is the endogenous ligand for the apelin G protein-coupled receptor. The distribution of the apelin peptides and receptor are widespread in the central nervous system and periphery, with reported roles in the hypothalamic-pituitary-adrenal axis, blood pressure regulation
The journal of physiological sciences : JPS, 67(3), 373-385 (2016-07-03)
The objective of this study was to explore the role of apelin in the healing of gastric lesions induced by stress. Male Wistar rats were exposed to water immersion and restraint stress (WIRS) for 6 h with or without the apelin
Vascular calcification (VC) is closely related to cardiovascular events in chronic kidney disease (CKD). Apelin has emerged as a potent regulator of cardiovascular function, but its role in VC during CKD remains unknown. We determined whether apelin plays a role
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