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Potent GPR171 agonist (EC50 = 1.6 nM). ProSAAS-derived peptide. Regulates body weight in mice and promotes the outgrowth of neurites in Neuro2A cells.
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The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Gomes et al (2013) GPR171 is a hypothalamic G protein-coupled receptor for BigLEN, a neuropeptide involved in feeding. Proc.Natl.Acad.Sci.USA. 110 16211 PMID: 24043826
Mack et al (2019) Neuropeptide PEN and its receptor GPR83: distribution, signaling, and regulation. ACS Chem.Neurosci. 10 1884 PMID: 30726666
Keywords: BigLEN (rat), BigLEN (rat) supplier, agonists, agonism, GPR171, body, weight, neurite, outgrowth, 6306, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Written by Sonia Tucci, Lynsay Kobelis and Tim Kirkham, this review provides a synopsis of the increasing number of peptides that have been implicated in appetite regulation and energy homeostasis; putative roles of the major peptides are outlined and compounds available from Tocris are listed.
Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. Compounds available from Tocris are listed.
This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.
This poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.