Abstract
Only two isoforms of the adenine nucleotide translocase (Ant) protein have been identified in mouse, as opposed to the three in humans. To determine whether the homologous mouse and human proteins share similar patterns of expression, Northern and Western analyses were performed on several mouse tissues. Mouse Ant1 is expressed at high levels in skeletal muscle and heart, similar to human ANT1. Mouse Ant2 is strongly expressed in all tissues but muscle, in marked contrast to human ANT2. To investigate the molecular basis of these differences, we cloned and sequenced the genomic loci of mouse Ant1 and Ant2, and compared them to the three human ANT loci. The mouse and human ANT1 and ANT2 genes showed substantial homology starting about 300 base pairs (bp) 5′ to the coding region and continuing through the 3′ untranslated region (UTR). Repeats constituted 32% of 15 kb of Ant1 sequence and 36% of the 27 kb of Ant2 sequence and included SINEs, LINEs and LTR elements. The core promoters of the mouse and human ANT1 and ANT2 genes are very similar. However, the mouse Ant1 gene lacks the upstream OXBOX and REBOX elements found in human ANT1 genes, thought to be important for muscle-specific expression. The mouse Ant2 gene, like human ANT2, has an upstream GRBOX, yet this element is not associated with suppression of transcription, as hypothesized for human ANT2. These discrepancies indicate that additional studies will be required to fully understand the transcriptional regulation of both Ant1 and Ant2.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.