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The point mutation was generated using PCR overlap extension technology with the mutated PCR primers (5′-GTGTTGCGCCTGCGAGGTGGCAgaAgaGAGCCTTCTCTC-3′ for I77,78R; 5′-GTGTTGCGCCTGCGAGGTGcaAgaATTGAGCCTTCTCTC-3′ for G76A/I77R; 5′-GTGTTGCGCCTGCGAGcaGcaATTATTGAGCCTTCTCTC-3′ for G75,76A; 5′-GTGTTGCGCCTGCGAGGTGGCAgaATTGAGCCTTCTCTC-3′ for I77R; and 5′-GTGTTGCGCCTGCGAGGTGcaATTATTGAGCCTTCTCTC-3′ for G78A).
The hha(C18E) mutation was generated in a pET15b expression plasmid35 that produces a His6-tagged form of Hha.
The pAH79 derivative containing the gtsB(A10T) mutation was generated by amplifying the 2-kb gtsB locus using primers 22F-5324097 and 22R-5324097 from DNA isolated from an evolved clone carrying the mutation.
A mutation was generated in the site complementary to the miR-139-5p miR-139-5p miR-139-5pUTR of AMFR or NOTCH1, aseeddicated.
The RasK104R point mutation was generated by PCR-based site-directed mutagenesis of pDNR-Dual-Ras1.
The original Fmr1 knock-out mutation was generated using 129P2 stem cells [12].
Similar(14)
iPSC lines harboring the m.3243A>G mtDNA mutation were generated from patient fibroblasts with various levels of heteroplasmy.
Mice with conditional Separase inhibitory phosphosite mutation were generated, genotyped and sex determined as described [30].
A nonsense (NS) and a frameshift (FS) mutation were generated introducing the alterations with two different forward primers.
The mutation is generated by an insertion of the ROSA β-gal gene trap vector (Friedrich and Soriano 1991).
The pWSKDE-KR mutant (K13R K19R K23R K37R K41R K541R mutations) was generated by site-directed mutagenesis with the Quikchange kit (Stratagene).
More suggestions(15)
mutant was generated
transfer was generated
rotation was generated
mutagenesis was generated
variation was generated
mutation was described
mutation was detected
mutation was repeated
mutation was confirmed
mutation was genotyped
mutation was introduced
mutation were generated
mutation was named
mutation was identified
mutation was labeled
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