Sentence examples for mutations at template from inspiring English sources

Polymerases η and κ are responsible for the generation 90% of all mutations at template A/T around the initial mismatch [16], [17], [18], [19], [36], [37].

Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C transversions.

Consistently, PCNA knock-out mice reconstituted with a PCNAK164R transgene showed a reduction of A/T mutations in Ig genes [20], suggesting that during SHM PCNA-Ub recruits polymerase η and κ to introduce mutations at template A/T.

While mutations at template A/T by polymerase η are regulated at the level of PCNA ubiquitination, future studies will have to reveal the underlying molecular mechanism how TLS polymerases like Rev1, involved in the generation of G/C transversions become activated.

Interestingly, the combination of hRev1 and hPolκ produced a significant number of deletion mutations at template positions +1 and +2 (Tables S10 and S11, Supporting Information).

Let PSSM i, aa) denote the mutation potential for amino acid aa at template position i and PSFM j, aa) the observed frequency of amino acid aa at target position j.

Although hPolι produced a significant number of frameshift mutations while replicating the undamaged control template, the average hPolι base deletion rate at template positions downstream from the 8-oxodG site increased by an average of 3.0-fold (Tables S3, S8, and S9, Supporting Information).

The search used the Alu-sequence of Def {4} as template and tolerated up to 10 point mutations at arbitrary locations for successful matches.

A full-length human NEMO cDNA containing cysteine-to-alanine mutations at positions 11, 76, 95, 131, and 167 was used as a template.

The CREmut/SBE445mut construct with double mutations at –461CRE and –445SBE was generated using –795CREmut Csrp2-luc [ 13] as a template to mutate putative –445SBE site as above.

The resulting I-T mismatch in DNA is potentially mutagenic since a dI in the DNA template prefers to pair with dCTP during replication, yielding A T to G C transition mutations at sites of adenine deamination [ 5].