Department of Medicine and Clinical Science (Y.N., T.U., H.Mi.,
H.Mu., S.M., M.S., K.T., I.T., K.N.), and Department of Laboratory
Medicine (A.S.), Kyoto University Graduate School of Medicine, Kyoto
606-8397, Japan; and International Institute for Advanced Studies
(T.U.), Kizugawa-dai Kizu-cho Soraku-gun Kyoto 619-0225, Japan
Address all correspondence and requests for reprints to: Dr. Takeshi Usui, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: tusui{at}kuhp.kyoto-u.ac.jp
Prophet of Pit-1 (Prop-1), which is a paired-like
homeodomaintranscription factor, is capable of binding to sites in an
earlyenhancer of the Pit-1 gene and regulating its expression.
Accordingto a previous report, Prop-1 messenger RNA (mRNA) is
expressedin the developing pituitary gland before Pit-1 mRNA
expressionand maximum expression are observed at e 12.0. After e 14.5,
Prop-1mRNA expression rapidly decreases, and only trace amounts of
mRNAare detectable in adult mouse pituitary. Human Pit-1 is expressed
considerably,not only in normal adult pituitary but also in pituitary
adenomas,so we studied human Prop-1 gene expression in adult pituitary
andpituitary adenomas. We also cloned human Prop-1 complementaryDNA
(cDNA) and sequenced the Prop-1 cDNAs in pituitary adenomas.The amino
acid sequence of human Prop-1 cDNA that we clonedwas identical to that
of the previously reported sequence, exceptThr substituted at codon
142 instead of Ala. This amino acidsubstitution is considered to be a
polymorphism because it didnot alter transcriptional activity, and 7
of 28 alleles wereAla. Human Prop-1 transcript was detected in normal
adult pituitary,by Northern blot analysis, and in all pituitary
adenomas examinedby RT-PCR analysis. The expression of human Prop-1 in
pituitaryadenomas was confirmed by in situ
hybridization in one of thesomatotroph adenomas. The sequence analysis
of human Prop-1cDNAs in these pituitary adenomas revealed that there
were nomutations, except 5 silent nucleic acid substitutions,
suggestingthat mutations of Prop-1 gene do not represent a frequent
mechanismof human pituitary tumorigenesis.
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