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Gibco™
Blasticidin S HCl (10 mg/mL)
Blasticidin S is a peptidyl nucleoside antibiotic isolated from Streptomyces griseochromogenes. It is a potent inhibitor of protein synthesis inRead more
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| Catalog Number | Quantity |
|---|---|
| A1113902 | 20 mL |
| A1113903 | 10 x 1 mL |
Catalog number A1113902
Price (USD)
1,042.00
Each
In stock
Quantity:
20 mL
Price (USD)
1,042.00
Each
Blasticidin S is a peptidyl nucleoside antibiotic isolated from Streptomyces griseochromogenes. It is a potent inhibitor of protein synthesis in in bacteria and eukaryotes, while also active against fungi, nematodes, and tumor cells. Blasticidin S acts by blocking hydrolysis of peptidyl-tRNA induced by release factors and inhibits peptide bond formation. It is used as a selection agent in both mammalian cells and bacterial cells. The recommended working concentration ranges from 1 to 30 μg/mL depending on the cell line and 25–100 μg/mL for bacterial selection. Cell death occurs rapidly, and blasticidin-resistant stable mammalian cell lines can be generated in less than one week.
Resistance to blasticidin S is conferred by BSR and BSD, isolated from Bacillus cereus K55-S and Aspergillus terreus respectively. The BSR resistance gene encodes blasticidin S deaminase, which catalyzes the conversion of blasticidin S to deaminohydroxyblasticidin S. Deaminohydroxyblasticidin S is a biologically inactive derivative of blasticidin S and does not interact with or inhibit prokaryotic or eukaryotic ribosomes. The BSD resistance gene also encodes a blasticidin S deaminase, which catalyzes a similar reaction to the BSR deaminase. For bacterial selection purposes, the salt content of the LB medium must remain low (less than 90 mM) and the pH should not exceed 7.0 to maintain the activity of basticidin S. A kill curve is recommended in order to determine the minimum effective blasticidin S concentration to kill non-resistant cells.
Applications
View detailed protocols on blasticidin selection in mammalian cells, E. coli, and yeast.
Resistance to blasticidin S is conferred by BSR and BSD, isolated from Bacillus cereus K55-S and Aspergillus terreus respectively. The BSR resistance gene encodes blasticidin S deaminase, which catalyzes the conversion of blasticidin S to deaminohydroxyblasticidin S. Deaminohydroxyblasticidin S is a biologically inactive derivative of blasticidin S and does not interact with or inhibit prokaryotic or eukaryotic ribosomes. The BSD resistance gene also encodes a blasticidin S deaminase, which catalyzes a similar reaction to the BSR deaminase. For bacterial selection purposes, the salt content of the LB medium must remain low (less than 90 mM) and the pH should not exceed 7.0 to maintain the activity of basticidin S. A kill curve is recommended in order to determine the minimum effective blasticidin S concentration to kill non-resistant cells.
Applications
View detailed protocols on blasticidin selection in mammalian cells, E. coli, and yeast.
For Research Use Only. Not for use in diagnostic procedures.
Specifications
Cell TypeEukaryotic Cells, Prokaryotic Cells
Concentration10 mg/mL
Culture TypeMammalian Cell Culture, Insect Cell Culture
Product LineGibco™
Quantity20 mL
Shelf Life9 Months
FormLiquid
Product TypeAntibiotic
SterilitySterile-filtered
With AdditivesHEPES
Unit SizeEach
Contents & Storage
Storage conditions: -5°C to -20°C (protect from light)
Shipping conditions: Dry ice
Shelf life: 9 months from date of manufacture
Shipping conditions: Dry ice
Shelf life: 9 months from date of manufacture
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Lot #Certificate TypeDateCatalog Number(s)
1023500Certificate of AnalysisJun 07, 2025A1113903, A1113902
1023498Certificate of AnalysisMay 04, 2025A1113903, A1113902
1023494Certificate of AnalysisApr 25, 2025A1113903, A1113902
1016808Certificate of AnalysisMar 28, 2025A1113903, A1113902
1016807Certificate of AnalysisFeb 19, 2025A1113903, A1113902
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Citations & References (12)
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Citations & References
Abstract
A Scalable, Multiplexed Assay for Decoding GPCR-Ligand Interactions with RNA Sequencing.
Journal:Cell Syst
PubMed ID:30904378
'G protein-coupled receptors (GPCRs) are central to how mammalian cells sense and respond to chemicals. Mammalian olfactory receptors (ORs), the largest family of GPCRs, mediate the sense of smell through activation by small molecules, though for most bonafide ligands, they have not been identified. Here, we introduce a platform to
Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens.
Journal:Nature
PubMed ID:30971826
'Functional genomics approaches can overcome limitations-such as the lack of identification of robust targets and poor clinical efficacy-that hamper cancer drug development. Here we performed genome-scale CRISPR-Cas9 screens in 324 human cancer cell lines from 30 cancer types and developed a data-driven framework to prioritize candidates for cancer therapeutics. We integrated cell
ZFP30 promotes adipogenesis through the KAP1-mediated activation of a retrotransposon-derived Pparg2 enhancer.
Journal:Nat Commun
PubMed ID:31000713
'Krüppel-associated box zinc finger proteins (KZFPs) constitute the largest family of mammalian transcription factors, but most remain completely uncharacterized. While initially proposed to primarily repress transposable elements, recent reports have revealed that KFZPs contribute to a wide variety of other biological processes. Using murine and human in vitro and in
A Brain Penetrant Mutant IDH1 Inhibitor Provides In Vivo Survival Benefit.
Journal:Sci Rep
PubMed ID:29062039
'Mutations in IDH1 are highly prevalent in human glioma. First line treatment is radiotherapy, which many patients often forego to avoid treatment-associated morbidities. The high prevalence of IDH1 mutations in glioma highlights the need for brain-penetrant IDH1 mutant-selective inhibitors as an alternative therapeutic option. Here, we have explored the utility
Genome-wide mapping reveals that deoxyuridine is enriched in the human centromeric DNA.
Journal:Nat Chem Biol
PubMed ID:29785056
'Uracil in DNA can be generated by cytosine deamination or dUMP misincorporation; however, its distribution in the human genome is poorly understood. Here we present a selective labeling and pull-down technology for genome-wide uracil profiling and identify thousands of uracil peaks in three different human cell lines. Surprisingly, uracil is
12 total citations