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:
26 Citations: Showing 1 - 10
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Staufen Impairs Autophagy in Neurodegeneration.
Authors: Daniel R Et al.
Ann Neurol 2023;93:398-416
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Soluble Klotho protects against glomerular injury through regulation of ER stress response.
Authors: Mikhail Et al.
Commun Biol 2023;6:208
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Maximizing protein production by keeping cells at optimal secretory stress levels using real-time control approaches.
Authors: François Et al.
Nat Commun 2023;14:3028
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Mannose metabolism inhibition sensitizes acute myeloid leukaemia cells to therapy by driving ferroptotic cell death.
Authors: Jochen H M Et al.
Nat Commun 2023;14:2132
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Hepatic SEL1L-HRD1 ER-associated degradation regulates systemic iron homeostasis via ceruloplasmin.
Authors: Yatrik M Et al.
Proc Natl Acad Sci U S A 2023;120:e2212644120
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Integrated stress response restricts macrophage necroptosis.
Authors: Parimal Et al.
Life Sci Alliance 2022;5
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The Sec61 translocon is a therapeutic vulnerability in multiple myeloma.
Authors: Jean-Christophe Et al.
EMBO Mol Med 2022;14:e14740
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Systemic lipolysis promotes physiological fitness in Drosophila melanogaster.
Authors: Lu Et al.
Aging (Albany NY) 2022;14:6481-6506
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Targeting the IRE1α/XBP1 Endoplasmic Reticulum Stress Response Pathway in ARID1A-Mutant Ovarian Cancers.
Authors: Andrew V Et al.
Cancer Res 2021;81:5325-5335
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A genome-wide CRISPR/Cas9 screen in acute myeloid leukemia cells identifies regulators of TAK-243 sensitivity.
Authors: Troy Et al.
JCI Insight 2021;6
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Colchicine acts selectively in the liver to induce hepatokines that inhibit myeloid cell activation.
Authors: Ho-Chou Et al.
Nat Metab 2021;3:513-522
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Endoplasmic Reticulum Stress in Subepithelial Myofibroblasts Increases the TGF-β1 Activity That Regulates Fibrosis in Crohn's Disease.
Authors: Chao Et al.
Inflamm Bowel Dis 2020;26:809-819
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Antagonistic relationship between the unfolded protein response and myocardin-driven transcription in smooth muscle.
Authors: Catarina Et al.
J Cell Physiol 2020;235:7370-7382
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MINPP1 prevents intracellular accumulation of the chelator inositol hexakisphosphate and is mutated in Pontocerebellar Hypoplasia.
Authors: Nathalie Et al.
Nat Commun 2020;11:6087
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Probing natural variation of IRE1 expression and endoplasmic reticulum stress responses in Arabidopsis accessions.
Authors: Karolina M Et al.
Sci Rep 2020;10:19154
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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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Coordination between Two Branches of the Unfolded Protein Response Determines Apoptotic Cell Fate.
Authors: Peter Et al.
Mol Cell 2018;71:629-636.e5
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High N-glycan multiplicity is critical for neuronal adhesion and sensitizes the developing cerebellum to N-glycosylation defect.
Authors: Nathalie Et al.
Elife 2018;7
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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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CHOP and caspase 3 induction underlie glioblastoma cell death in response to endoplasmic reticulum stress.
Authors: Quincy A Et al.
Exp Ther Med 2012;3:487-492
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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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