Aphidicolin
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| Category | Antibiotics |
| Catalog number | BBF-00556 |
| CAS | 38966-21-1 |
| Molecular Weight | 338.48 |
| Molecular Formula | C20H34O4 |
| Purity | >98% |
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Description
Aphidicolin is an antibiotic produced by Cephalosporium aphidicola and Nigrospora sphaerica, which has the effect of inhibiting mitosis and anti-DNA virus. Aphidicolin potentiates apoptosis induced by arabinosyl nucleosides in a human promyelocytic leukemia cell line.
Specification
| Synonyms | (+)-Aphidicolin; (3R,4R,4aR,6aS,8R,9R,11aS,11bS)-4,9-bis(hydroxymethyl)-4,11b-dimethyltetradecahydro-8,11a-methanocyclohepta[a]naphthalene-3,9-diol |
| Shelf Life | As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly. |
| Storage | Store at -20°C |
| IUPAC Name | (1S,2S,5R,6R,7R,10S,12R,13R)-6,13-bis(hydroxymethyl)-2,6-dimethyltetracyclo[10.3.1.01,10.02,7]hexadecane-5,13-diol |
| Canonical SMILES | CC12CCC(C(C1CCC3C24CCC(C(C3)C4)(CO)O)(C)CO)O |
| InChI | InChI=1S/C20H34O4/c1-17(11-21)15-4-3-13-9-14-10-19(13,7-8-20(14,24)12-22)18(15,2)6-5-16(17)23/h13-16,21-24H,3-12H2,1-2H3/t13-,14+,15-,16+,17-,18-,19-,20-/m0/s1 |
| InChI Key | NOFOAYPPHIUXJR-APNQCZIXSA-N |
| Source | Nigrospora oryzae |
Properties
| Appearance | White to Off-white Powder |
| Application | A reversible inhibitor of eukaryotic nuclear DNA replication |
| Antibiotic Activity Spectrum | viruses |
| Boiling Point | 507.8°C at 760 mmHg |
| Melting Point | 225-233°C |
| Flash Point | 230.4±24.7 °C |
| Density | 1.22 g/cm3 |
| Solubility | Soluble in DMSO |
Reference Reading
1.Dynamics of the Plant Nuclear Envelope During Cell Division.
Evans DE1, Graumann K2. Methods Mol Biol. 2016;1370:115-26. doi: 10.1007/978-1-4939-3142-2_9.
The use of suspension cultures synchronised by aphidicolin provides a method to study cell division in living plant cells. This chapter describes the use of this technique in tobacco suspension cultures expressing nuclear and nuclear envelope proteins that have been fused to fluorescent proteins. The protocol provides advice on optimizing synchrony and on real-time imaging by confocal microscopy.
2.Long Neural Genes Harbor Recurrent DNA Break Clusters in Neural Stem/Progenitor Cells.
Wei PC1, Chang AN1, Kao J1, Du Z1, Meyers RM1, Alt FW2, Schwer B3. Cell. 2016 Feb 11;164(4):644-55. doi: 10.1016/j.cell.2015.12.039.
Repair of DNA double-strand breaks (DSBs) by non-homologous end joining is critical for neural development, and brain cells frequently contain somatic genomic variations that might involve DSB intermediates. We now use an unbiased, high-throughput approach to identify genomic regions harboring recurrent DSBs in primary neural stem/progenitor cells (NSPCs). We identify 27 recurrent DSB clusters (RDCs), and remarkably, all occur within gene bodies. Most of these NSPC RDCs were detected only upon mild, aphidicolin-induced replication stress, providing a nucleotide-resolution view of replication-associated genomic fragile sites. The vast majority of RDCs occur in long, transcribed, and late-replicating genes. Moreover, almost 90% of identified RDC-containing genes are involved in synapse function and/or neural cell adhesion, with a substantial fraction also implicated in tumor suppression and/or mental disorders. Our characterization of NSPC RDCs reveals a basis of gene fragility and suggests potential impacts of DNA breaks on neurodevelopment and neural functions.
3.Excess Cdt1 inhibits nascent strand elongation by repressing the progression of replication forks in Xenopus egg extracts.
Nakazaki Y1, Tsuyama T2, Seki M3, Takahashi M1, Enomoto T4, Tada S5. Biochem Biophys Res Commun. 2016 Feb 5;470(2):405-10. doi: 10.1016/j.bbrc.2016.01.028. Epub 2016 Jan 8.
Cdt1 is a protein essential for initiation of DNA replication; it recruits MCM helicase, a core component of the replicative DNA helicase, onto replication origins. In our previous study, we showed that addition of excess Cdt1 inhibits nascent strand elongation during DNA replication in Xenopus egg extracts. In the present study, we investigated the mechanism behind the inhibitory effect of Cdt1. We found that addition of recombinant Cdt1 inhibited nascent DNA synthesis in a reinitiation-independent manner. To identify the mechanism by which Cdt1 inhibits nascent strand elongation, the effect of Cdt1 on loading of Mcm4 and Rpa70 onto chromatin was examined. The results showed that Cdt1 suppressed the excessive Rpa70 binding caused by extensive, aphidicolin-induced DNA unwinding; this unwinding occurs between stalled DNA polymerases and advancing replication forks. These findings suggested that excess Cdt1 suppressed the progression of replication forks.
4.5-Hydroxymethylcytosine Marks Sites of DNA Damage and Promotes Genome Stability.
Kafer GR1, Li X2, Horii T3, Suetake I4, Tajima S5, Hatada I3, Carlton PM6. Cell Rep. 2016 Feb 16;14(6):1283-92. doi: 10.1016/j.celrep.2016.01.035. Epub 2016 Feb 4.
5-hydroxymethylcytosine (5hmC) is a DNA base created during active DNA demethylation by the recently discovered TET enzymes. 5hmC has essential roles in gene expression and differentiation. Here, we demonstrate that 5hmC also localizes to sites of DNA damage and repair. 5hmC accumulates at damage foci induced by aphidicolin and microirradiation and colocalizes with major DNA damage response proteins 53BP1 and γH2AX, revealing 5hmC as an epigenetic marker of DNA damage. Deficiency for the TET enzymes eliminates damage-induced 5hmC accumulation and elicits chromosome segregation defects in response to replication stress. Our results indicate that the TET enzymes and 5hmC play essential roles in ensuring genome integrity.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
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g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
