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A PCR product containing the epe1H297A point mutation was obtained by amplification of the mutated epe1 gateway entry plasmid.
The major structural changes in the subunit structure caused by the S228P mutation was obtained by tracing the structural fluctuations during the 20 ns simulations (Fig. S11A).
Approval for analysis of these samples for the FOXL2 mutation was obtained through the British Columbia Cancer Agency's research ethics board.
A fragment of LHP1 containing the RNP1.2 mutation was obtained by digestion of pRNP1.2-GFP with EcoRI and transformed into LHP1 CORE-PrAA.
T451 to Ala mutation was introduced using the attB2ABF3TA_R primer and S126A mutation was obtained as described in the previous section.
The hypomorphic gene mutation was obtained by introducing a 141-bp long wild-type (wt) cDNA fragment of the β1 integrin gene coding for the entire β1 integrin cytoplasmic tail, including the stop codon from exon 16 (called Cyto-cDNA), in frame into exon 15 (see Figure S1A in Supporting Information).
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Primary skin fibroblasts with T122K mutation were obtained from a skin biopsy of two US American siblings.
Transgenic mice expressing the murine G86R SOD1 mutation were obtained in our animal facility and genotyped as described [9].
Leaner heterozygous mice without the Os mutation were obtained by crossing Os +/+ Cacna1atg−la mice with C57BL/6 mice, and C57BL/6 mice were used as controls.
The pedigrees of the 14 families with the germline mutation were obtained together with the history of cancer reported by both sides of the families; ipsilateral and contralateral to the parental side segregating the R337H mutation (Table 1).
NPC1I1061T homozygous fibroblasts GM18453, GM17909 and the heterozygous GM03123 fibroblast cell line containing the I1061T mutation were obtained from Coriell cell repositories (Camden, NJ). and NPC1I1061T homozygous fibroblasts 83.16 and 59413 were obtained from Dr. John O'Brien (Mayo Clinic, Rochester, MN).
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