Tunicamycin
Chemical Name: Tunicamycin from Streptomyces sp.
Purity: ≥98%
Biological Activity
Tunicamycin is an antibiotic; inhibits GlcNAc phosphotransferase (GPT). Blocks the formation of N-glycosidic linkages by inhibiting the first step in glycoprotein synthesis. Activity induces ER stress and causes G1 arrest; can be used to induce autophagy. Tunicamycin contains four main components as follows:- Homolog A, n=8, C37H60N4O16, molecular weight = 816.90
- Homolog B, n=9, C38H62N4O16, molecular weight = 830.93
- Homolog C, n=10, C39H64N4O16, molecular weight = 844.95
- Homolog D, n=11, C40H66N4O16, molecular weight = 858.99
Technical Data
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.
Background References
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The hepatitis B virus precore protein is retrotransported from endoplasmic reticulum (ER) to cytosol through the ER-associated pathway.
Duriez et al.
J.Biol.Chem., 2008;283:32352 -
Primary murine airway smooth muscle cells exposed to poly(I:C) or tunicamycin synthesize a leukocyte-adhesive hyaluronan matrix.
Lauer et al.
J.Biol.Chem., 2009;284:5299 -
Differential effects of endoplasmic reticulum stress-induced autophagy on cell survival.
Ding et al.
J.Biol.Chem., 2007;282:4702
Product Datasheets
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Citations for Tunicamycin
The citations listed below are publications that use Tocris products. Selected citations for Tunicamycin include:
8 Citations: Showing 1 - 8
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Caspase-mediated cleavage of IRE1 controls apoptotic cell commitment during endoplasmic reticulum stress.
Authors: Shemorry Et al.
Elife 2019;8
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A CASPR1-ATP1B3 protein interaction modulates plasma membrane localization of Na+/K+-ATPase in brain microvascular endothelial cells.
Authors: Zhang Et al.
J Biol Chem 2019;
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ONC201 kills breast cancer cells in vitro by targeting mitochondria.
Authors: Greer Et al.
Oncotarget 2018;9:18454
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Hyperactivation of nuclear receptor coactivators induces PERK-dependent cell death.
Authors: Hossain Et al.
Oncotarget 2018;9:11707
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N-Glycosylation Regulates the Trafficking and Surface Mobility of GluN3A-Containing NMDA Receptors.
Authors: Skrenkova Et al.
Front Mol Neurosci 2018;11:188
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Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer.
Authors: Bajikar Et al.
Dev Cell 2017;43:418
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NCOA3 coactivator is a transcriptional target of XBP1 and regulates PERK-eIF2α-ATF4 signalling in breast cancer.
Authors: Gupta Et al.
Oncogene 2016;35:5860
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ER stress induces anabolic resistance in muscle cells through PKB-induced blockade of mTORC1.
Authors: Deldicque Et al.
PLoS One 2011;6:e20993
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