DMT-dU(Crotonic hexanediamine 3-(benzoylthio)propanoic)-CE phosphoramidite
DMT-dU (Crotonic hexanediamine 3-(benzoylthio) propanoic)-CE phosphoramidite is a phosphoramidite reagent used to synthesize chemically modified guide RNAs for forming CRISPR-Cas RNP conjugates with Cas proteins. DMT-dU (Crotonic hexanediamine 3-(benzoylthio) propanoic)-CE phosphoramidite can be applied in research on antiviral agents, cancer, neurodegenerative diseases and genetic diseases.
For research use only. We do not sell to patients.
- CAS No.: 3069451-89-1
- Formula: C58H71N6O11PS
- Molecular Weight:1091.26
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 3069451-89-1
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Molecular Weight 1091.26
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Formula C58H71N6O11PS
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SMILES
O=C1N([C@H]2C[C@H](OP(N(C(C)C)C(C)C)OCCC#N)[C@@H](COC(C3=CC=C(OC)C=C3)(C4=CC=CC=C4)C5=CC=C(OC)C=C5)O2)C=C(/C=C/C(NCCCCCCNC(CCSC(C6=CC=CC=C6)=O)=O)=O)C(N1)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Gene Editing
Gene editing modify specific sites within the genome through gene deletions, insertions or conversions to study functionally unknown genes or conduct gene therapy. It is also used to change the biological traits of organisms to establish new varieties. Gene editing techniques include zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas 9) (CRISPR/Cas9).
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)