| First Author | Otto C | Year | 1997 |
| Journal | J Biol Chem | Volume | 272 |
| Issue | 42 | Pages | 26665-8 |
| PubMed ID | 9334249 | Mgi Jnum | J:43621 |
| Mgi Id | MGI:1098108 | Doi | 10.1074/jbc.272.42.26665 |
| Citation | Otto C, et al. (1997) Absence of glucocorticoid receptor-beta in mice. J Biol Chem 272(42):26665-8 |
| abstractText | Two human glucocorticoid receptor (GR) isoforms, GR alpha and GR beta, are derived from the same gene by alternative splicing involving exon 9 of the GR locus, The non-ligand binding isoform GR beta was proposed to act as a transdominant negative inhibitor of GR alpha, thus modulating glucocorticoid responsiveness of target tissues, To study GR beta in mice we characterized the genomic region around exon 9 of the murine GR gene. Sequence analysis revealed that the presumed exon 9 beta contained an open reading frame of 59 amino acids, In contrast, human exon 9 beta encoded only 15 amino acids, Using reverse transcriptase polymerase chain reaction the ab absence of GR beta mRNA was demonstrated in all adult mouse tissues examined, To exclude the possibility that the polymerase chain reaction conditions employed were not suitable for the amplification of GR beta mRNA, we synthesized an artificial template corresponding to the presumed GRP mRNA spanning exons 7, 8, and 9 beta, Various amounts of this template were added to brain cDNA preparations and as little as 25 molecules were detectable under the polymerase chain reaction conditions chosen, Since GR beta is not conserved across species its physiological significance in humans appears questionable. |
