|Cis-syn Thymine Dimer Phosphoramidite
Catalog Number: 11-1330-xx
Description: Cis-syn Thymine Dimer Phosphoramidite
Diluent: Anhydrous Acetonitrile
|Coupling: 10 minute coupling recommended.
|Deprotection: 1. Remove the methyl phosphate groups by treating the support with thiophenol/triethylamine/THF (1:2:2) v/v/v for 45 minutes at room temperature. Wash the support with THF 1X, methanol 5X, acetonitrile 3X and dry with air or argon.2. Cleave and deprotect the oligo in the dark with ammonium hydroxide at room temperature under conditions appropriate to remove the protecting groups on the nucleobases.
|Storage: Freezer storage, -10 to -30°C, dry
|Stability in Solution: 2-3 days
The following products are used to investigate the effect on the activity of an oligonucleotide when key structural elements are changed. The 7-deaza purine monomers lack groups critical for hydrogen bonding. 7-Deaza-8-aza-A and 7-deaza-8-aza-G (PPG) monomers are isomers of A and G and have similar electron density. Their presence in oligos is slightly stabilizing relative to A and G. Unlike G, PPG does not lead to aggregation and G-rich oligos can be easily prepared and isolated. 5’-Fluorescein oligos with PPG at the 5’-terminus are much less quenched than the equivalent G oligos. As a purine analogue of Thymidine, 7-deaza-2’-deoxyXanthosine (7-deaza-dX) promises to have interesting effects on DNA structure of triplexes. 7-Deaza-dX also forms a non-standard base pair with a 2,4-diaminopyrimidine nucleoside analogue. Standard nucleobases have an unshared pair of electrons that project into the minor groove of duplex DNA. Enzymes that interact with DNA, polymerases, reverse transcriptases, restriction enzymes, etc., may use a hydrogen bond donating group to contact the hydrogen bond acceptor in the minor groove. 3-Deaza-2’-deoxyadenosine is very interesting in that it maintains the ability for regular Watson-Crick hydrogen bonding to T but is lacking the electron pair at the 3-position normally provided by N3.
One of the major sources of DNA damage in all organisms is the UV component of sunlight. The predominant reaction induced by UV light on DNA is dimerization of adjacent pyrimidine bases leading to cyclobutane dimers (CPDs). The dimers formed in the most significant quantity are the cis-syn cyclobutane dimer of two thymine bases. Although formed routinely, these dimer products are efficiently excised and repaired enzymatically (nucleotide excision repair) or the dimerization is reversed by photolase enzymes. These lesions have been connected to the formation of squamous cell carcinomas. In addition, humans who lack ability to repair CPD lesions with high efficiency may be genetically predisposed to Xeroderma Pigmentosa (XP), a disease characterized by extreme sensitivity to sunlight and high frequency of skin cancer. Polymerases encountering unrepaired CPD lesions are quite error-prone, leading to incorrect base insertions and subsequent mutations.
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