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. Author manuscript; available in PMC: 2012 Feb 2.
Published in final edited form as: Birth Defects Res A Clin Mol Teratol. 2011 Feb 2;91(2):77–84. doi: 10.1002/bdra.20763

Figure 1.

Figure 1

Vector structure of the cloned NAT1 fragments containing the 873-bp NAT1 open reading frame (ORF) and 302 bp of the NAT1 3′-UTR. NAT1 mRNA transcription was driven by cytomegalovirus (CMV) promoter, whereas RNA processing at the 3-end was facilitated by the NAT1 putative polyA signals since the BGH polyA signal in the vector was deleted.