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UCLA GP130 2
Biological Activity for UCLA GP130 2
UCLA GP130 2 is a gp130 agonist. Protects against NMDA-induced toxicity in primary hippocampal neurons in vitro. Increases STAT3 phosphorylation in SH-SY5Y cells. Brain penetrant.
Compound Libraries for UCLA GP130 2
Technical Data for UCLA GP130 2
|Storage||Store at +4°C|
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.
Solubility Data for UCLA GP130 2
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for UCLA GP130 2
The following data is based on the product molecular weight 270.32. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.7 mL||18.5 mL||36.99 mL|
|5 mM||0.74 mL||3.7 mL||7.4 mL|
|10 mM||0.37 mL||1.85 mL||3.7 mL|
|50 mM||0.07 mL||0.37 mL||0.74 mL|
References for UCLA GP130 2
References are publications that support the biological activity of the product.
Alam et al (2018) A small molecule mimetic of the humanin peptide as a candidate for modulating NMDA-induced neurotoxicity. ACS Chem.Neurosci. 9 462 PMID: 29161500
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Citations for UCLA GP130 2
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Literature in this Area
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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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.