Non-competitive nicotinic cholinergic antagonist that selectively inhibits nicotinic-stimulated catecholamine secretion from chromaffin cells and noradrenergic neurons (IC50 ~ 200 nM). It blocks nicotinic-induced cationic signaling (IC50 ~ 200 - 250 nM) and inhibits nicotinic-agonist induced desensitization of catecholamine release, and also stimulates mast cell release of histamine via a separate mechanism.
CAT No: R1008
CAS No:142211-96-9
Synonyms/Alias:Catestatin;142211-96-9;Chromogranin A344-364;EX-A6265;AKOS024457258;PD079356;G83769;
Catestatin is a biologically active peptide fragment derived from chromogranin A, a prohormone and granulogenic protein widely distributed in neuroendocrine tissues. As a regulatory peptide, catestatin is recognized for its ability to modulate catecholamine release, influence cardiovascular function, and participate in immune and metabolic pathways. Its multifaceted physiological roles have made it an important focus of research in neurobiology, endocrinology, and cardiovascular science, providing a valuable tool for elucidating peptide-mediated signaling mechanisms and cellular responses.
Neuroendocrine research: Catestatin serves as a critical reagent for investigating the regulation of catecholamine secretion from chromaffin cells and sympathetic neurons. By acting as a non-competitive nicotinic cholinergic antagonist, it enables researchers to dissect the molecular mechanisms underlying neurotransmitter release and synaptic modulation. Utilization of this peptide in in vitro and ex vivo systems allows for precise analysis of neuroendocrine feedback loops, supporting the study of stress responses and autonomic nervous system function.
Cardiovascular studies: The peptide is extensively used in experimental models to explore its influence on vascular tone, cardiac contractility, and blood pressure regulation. Through its interaction with G-protein coupled receptors and downstream signaling pathways, catestatin provides a foundation for understanding endogenous mechanisms of cardiovascular homeostasis. Researchers employ it to probe the interplay between neuropeptides and endothelial function, facilitating insight into the pathophysiology of hypertension and related vascular disorders.
Immunomodulation assays: Catestatin's capacity to modulate immune cell activity and inflammatory responses has positioned it as a valuable tool in immunological research. It is utilized to assess its effects on monocyte and macrophage activation, cytokine secretion, and chemotactic behavior. Such studies support the characterization of peptide-mediated crosstalk between the nervous and immune systems, enabling detailed analysis of innate immunity and inflammatory signaling cascades.
Metabolic regulation investigations: The peptide is applied in metabolic studies to evaluate its impact on glucose uptake, lipid metabolism, and energy homeostasis in various cell types. By modulating insulin sensitivity and influencing adipocyte function, catestatin aids in unraveling the complex interactions between neuropeptides and metabolic pathways. This application is particularly relevant for researchers examining the biochemical basis of obesity, insulin resistance, and metabolic syndrome.
Peptide receptor characterization: Catestatin is frequently used as a reference ligand in studies aimed at identifying and characterizing peptide receptors on target cells. Its well-defined sequence and established bioactivity make it suitable for receptor binding assays, signaling pathway elucidation, and structure-activity relationship analyses. These approaches contribute to a deeper understanding of peptide-receptor interactions, supporting the development of novel probes and research tools for neuropeptide signaling studies.
CST is a biologically highly active peptide. It was originally found to be a non-competitive nicotinic cholinergic antagonist which inhibits catecholamine release from noradrenergic neurons, PC12 and bovine chromaffin cells by an autocrine negative feedback loop and nicotine-induced desensitization of catecholamine release. Furthermore, CST causes release of histamine from peritoneal and pleural mast cells, vasodilation in rats and humans, induces chemotaxis of human monocytes and acts as an antibacterial peptide. CST also exerts effects on the cardiovascular system. In particular, it abolishes isoproterenol-induced positive inotropic and lusitropic effects in the rat heartand regulates blood pressure by acting as an inhibitor of peripheralas well as centralnicotinic-cholinergic receptors and β-adrenoceptors. The significance of CST in the regulation of blood pressure should be emphasized by the facts that lower plasma levels of CST are a risk factor for the development of hypertension in humans, that a naturally occurring human variant of CST alters autonomic function and blood pressure and that arterial hypertension of chga knockout mouse is rescued by exogenous injection of CST. Furthermore, CST acts as an insulin-sensitizing peptide, inhibits gluconeogenesis and lipogenesis and stimulates fatty acid oxidation. And finally, CST is a potent angiogenic cytokine which acts via a basic fibroblast growth factor-dependent mechanism.
Catestatin-like immunoreactivity in the rat eye
Catestatin is a peptide which is a potent inhibitor of catecholamine secretion and played essential functions in the cardiovascular system. Previous research found that dramatic changes of catestatin were associated with hemodynamics in acute myocardial infarction (AMI) during the first week after the AMI symptoms onset, but whether catestatin is also involved in the pathophysiological progression after AMI and then a predictor for outcomes is not clear.
Correlation of Plasma Catestatin Level and the Prognosis of Patients with Acute Myocardial Infarction
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