ddTTP tetrasodium
ddTTP tetrasodium is a DNA polymerase γ inhibitor, with Ki values of 0.05 μM and 0.4 μM against bovine testicular DNA polymerase γ. ddTTP tetrasodium can be incorporated into DNA to cause termination of the extended DNA strand. ddTTP tetrasodium can be used in the research of HIV infection.
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- Formule: C10H13N2Na4O13P3
- Masse moléculaire:554.10
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
In Vitro
ddTTP tetrasodium (0-100 μM; 30 min) potently inhibits bovine testicular DNA polymerase γ in a competitive manner relative to dTTP, with a Ki value of 0.05 μM when poly (rA)-oligo (dT) serves as the template-primer[1].
Tetrasodium ddTTP (0-100 μM; 30 min) potently inhibits bovine testicular DNA polymerase γ in a competitive manner relative to dTTP, with a Ki value of 0.4 μM when activated calf thymus DNA is used as the template-primer[1].
Tetrasodium ddTTP (2.5-10 μM; 60 min) can be incorporated into DNA by bovine testicular DNA polymerase γ and induce chain termination, and this effect is independent of 3'-exonuclease proofreading activity (verified by treatment with 1 mM 5'-GMP)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Masse moléculaire 554.10
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Formule C10H13N2Na4O13P3
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SMILES
O=[P](O[P](O[P](O[Na])(O[Na])=O)(O[Na])=O)(O[Na])OC[C@@H](O1)CC[C@@H]1N(C(NC2=O)=O)C=C2C
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)