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The completion of BER occurs by short-patch (single nucleotide) or long-patch (2 13 nucleotides) repair pathways involving DNA polymerase gap filling and DNA ligation.
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Incision and removal of the first UV-induced dimer leaves to the refilling polymerase a gap containing a lesion in the template strand.
The lyase domain recognizes the 5′-phosphate in DNA gaps thereby targeting the polymerase for gap-filling DNA synthesis.
The LD recognizes the 5′-phosphate in DNA gaps, thereby targeting the polymerase for gap-filling DNA synthesis.
End processing proceeds as required, via XRF-ERCC1 flap cleavage and polymerase-mediated gap-filling.
A similar sized footprint was obtained with human Polβ, a monomeric polymerase involved in gap filling, suggesting that a single PolDom binds to gapped substrates.
The polymerase fills the gap.
All patients were also screened for − α3.7, − α4.2, and the −−MED−1 α-thal deletions as well as the alpha triplication ααα by gap polymerase chain reaction, as described by Oron-Karni and coworkers [ 9].
Mutation analysis was performed by multiplex amplification refractory mutation system (M-ARMS), direct DNA sequencing of beta-globin gene, and gap polymerase chain reaction for 3.4 kb deletion detection, respectively.
All of the beta-thalassemia alleles have been characterized by a combination of techniques including M-ARMS, DNA sequencing, and gap polymerase chain reaction for 3.4 kb deletion detection.
After hybridization of the oligonucleotides to the DNA templates to be analyzed a polymerase fills the gap between one of the allele- and the locus-specific oligonucleotide and a ligase seals the nick so that a contiguous template is formed.
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