Tunicamycin is a mixture of homologous nucleoside antibiotic that inhibits N-linked glycosylation and blocks GlcNAc phosphotransferase (GPT). Tunicamycin causes accumulation of unfolded proteins in cell endoplasmic reticulum (ER) and induces ER stress, and causes blocking of DNA synthesis and cell cycle arrest in G1 phase. Tunicamycin inhibits gram-positive bacteria, yeasts, fungi, and viruses and has anti-cancer activity.Tunicamycin increases exosome release in cervical cancer cells.
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Tunicamycin Chemische Struktur
CAS. Nr. : 11089-65-9
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Based on 88 publication(s) in Google Scholar
Tunicamycin purchased from MedChemExpress. Usage Cited in:
PLoS Biol. 2018 Oct 18;16(10):e2006483.
[Abstract]
SK-Hep1 cells stably expressing EV or Flag-PGM1 are treated with or without 0.1 ug/mL Tunicamycin, and cell proliferation is measured.
Tunicamycin purchased from MedChemExpress. Usage Cited in:
Cell Death Dis. 2018 May 22;9(6):604.
[Abstract]
Western blot analysis of ER stress-related proteins after PPI treatment for 48 h in both pH 7.4 and pH 6.5 conditions. Cells treated with Thapsigargin (TG, 0.5 and 1 μM) or Tunicamycin (Tu, 2.5, 5 and 10 μg/mL) for 24 h served as positive controls.
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Beschreibung
Tunicamycin is a mixture of homologous nucleoside antibiotic that inhibits N-linked glycosylation and blocks GlcNAc phosphotransferase (GPT). Tunicamycin causes accumulation of unfolded proteins in cell endoplasmic reticulum (ER) and induces ER stress, and causes blocking of DNA synthesis and cell cycle arrest in G1 phase. Tunicamycin inhibits gram-positive bacteria, yeasts, fungi, and viruses and has anti-cancer activity[1][2][3].Tunicamycin increases exosome release in cervical cancer cells[4].
In Vitro
Tunicamycin (2 μg/mL; 24 hours; CD44+/CD24- and original MCF7 cells) treatment increases the spliced XBP-1, ATF6 nuclear translocation level and CHOP protein expression in CD44+/CD24- and original MCF7 cells[1].
Tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation. Under effect of Tunicamycin, the results show that inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Tunicamycin Related Antibodies
Western Blot Analysis
Cell Line:
CD44+/CD24- and original MCF7 cells[1]
Concentration:
2 µg/mL
Incubation Time:
24 hours
Result:
Increased level of spliced XBP-1, ATF6 nuclear translocation and CHOP protein expression are detected in CD44+/CD24- and original MCF7 cells.
In Vivo
Tunicamycin (0.1 mg/kg or 0.5 mg/kg) treatment dramatically suppresses tumor growth in the CD133+/- MHCC97L cells xenograft model (BALB/c (nu/nu) mice)[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
This protocol yields a clear solution of ≥ 2 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (20.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
This protocol yields a clear solution of ≥ 2 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (20.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
[1]. Hsu JL, et al. Tunicamycin induces resistance to camptothecin and etoposide in human hepatocellular carcinoma cells: role of cell-cycle arrest and GRP78. Naunyn Schmiedebergs Arch Pharmacol. 2009 Nov;380(5):373-82.
[Content Brief]
[2]. Hou H, et al. DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma. Mol Cancer Ther. 2013 Dec;12(12):2874-84.
[Content Brief]
[3]. Han C, et al. Endoplasmic reticulum stress inhibits cell cycle progression via induction of p27 in melanoma cells. Cell Signal. 2013 Jan;25(1):144-9.
[Content Brief]
[4]. Kathleen M McAndrews, et al. Mechanisms associated with biogenesis of exosomes in cancer. Mol Cancer. 2019 Mar 30;18(1):52.
[Content Brief]
[1]. Hsu JL, et al. Tunicamycin induces resistance to camptothecin and etoposide in human hepatocellular carcinoma cells: role of cell-cycle arrest and GRP78. Naunyn Schmiedebergs Arch Pharmacol. 2009 Nov;380(5):373-82.
[2]. Hou H, et al. DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma. Mol Cancer Ther. 2013 Dec;12(12):2874-84.
[3]. Han C, et al. Endoplasmic reticulum stress inhibits cell cycle progression via induction of p27 in melanoma cells. Cell Signal. 2013 Jan;25(1):144-9.
[4]. Kathleen M McAndrews, et al. Mechanisms associated with biogenesis of exosomes in cancer. Mol Cancer. 2019 Mar 30;18(1):52.
Tunicamycin Related Classifications
Anti-infection
BacterialFungalInfluenza VirusAntibiotic
Help & FAQs
Do most proteins show cross-species activity?
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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