PMID- 10425445 OWN - NLM STAT- MEDLINE DCOM- 19990922 LR - 20191024 IS - 0952-5041 (Print) IS - 0952-5041 (Linking) VI - 23 IP - 1 DP - 1999 Aug TI - Structure and expression of the mouse growth hormone receptor/growth hormone binding protein gene. PG - 33-44 AB - The mouse growth hormone receptor/growth hormone-binding protein (GHR/BP) gene produces several distinct mRNA forms through alternative splicing, including mRNAs encoding the membrane-bound growth hormone receptor (GHR) and the soluble growth hormone-binding protein (GHBP). Transcripts are also heterogeneous in their 5' regions due to alternative selection of two major 5' untranslated region (5'UTR) sequences, designated L1 and L2. Here we report the cloning of all mouse GHR/BP coding exons as well as the exon encoding 5'UTR L2, the most widely expressed 5'UTR. The mouse GHR/GHBP gene contains 11 coding exons, 9 of which are homologous in size and sequence to human GHR exons 2-10. The two mouse exons that do not have homologs in the human gene are designated exons 4B and 8A. Exon 4B, located between exons 4 and 5, encodes an 8-amino acid segment of the ligand binding domain that is unique to mouse GHR and GHBP. Analysis by reverse transcriptase-polymerase chain reaction indicated that exon 4B is constitutively present in mouse GHR and GHBP mRNA. Exon 8A encodes the GHBP hydrophilic tail and 3'UTR sequence. 5'UTR L2 is encoded by a single exon located at least 27 kb upstream of exon 2 and at least 12 kb upstream of the exon encoding 5'UTR L1. The transcription start sites of UTR L2 were mapped and the 5' flanking region sequenced. The exon and proximal promoter region are GC rich, and share a high level of conservation with the equivalent exons in the sheep, bovine and human GHR genes. A CCAAT motif and several putative Sp1 motifs are present, and there is no TATA box. Homology between the mouse sequence and other species is limited to a region of 450 bp upstream of the exon due to the insertion of a fragment of a LINE-1 element upstream of the mouse L2 exon. Ribonuclease protection assays were used to confirm that 5'UTR L2 is widely expressed in multiple tissues and is the predominant form of transcript except in the liver during pregnancy, in which 5'UTR L1 is the major form. FAU - Moffat, J G AU - Moffat JG AD - Department of Biology, University of California, Santa Cruz, California 95060, USA. FAU - Edens, A AU - Edens A FAU - Talamantes, F AU - Talamantes F LA - eng SI - GENBANK/AF120480 SI - GENBANK/AF120481 SI - GENBANK/AF120482 SI - GENBANK/AF120483 SI - GENBANK/AF120484 SI - GENBANK/AF120485 SI - GENBANK/AF120486 SI - GENBANK/AF120487 SI - GENBANK/AF120488 SI - GENBANK/AF120489 SI - GENBANK/AH007734 GR - CA71590/CA/NCI NIH HHS/United States GR - GM08132/GM/NIGMS NIH HHS/United States GR - HD14966/HD/NICHD NIH HHS/United States GR - etc. PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - J Mol Endocrinol JT - Journal of molecular endocrinology JID - 8902617 RN - 0 (Carrier Proteins) RN - 0 (RNA, Messenger) RN - 0 (Receptors, Somatotropin) RN - 9007-49-2 (DNA) RN - W06KFL3RDT (somatotropin-binding protein) SB - IM MH - Amino Acid Sequence MH - Animals MH - Base Sequence MH - Carrier Proteins/*genetics MH - Cloning, Molecular MH - DNA/chemistry/genetics/isolation & purification MH - Exons MH - Female MH - Gene Expression MH - Genes/genetics MH - Introns MH - Male MH - Mice MH - Mice, Inbred DBA MH - Molecular Sequence Data MH - Pregnancy MH - Promoter Regions, Genetic MH - RNA, Messenger/genetics/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Somatotropin/*genetics MH - Sequence Alignment MH - Sequence Analysis, DNA MH - Sequence Homology, Amino Acid MH - Sequence Homology, Nucleic Acid MH - Tissue Distribution MH - Transcription, Genetic EDAT- 1999/07/30 00:00 MHDA- 1999/07/30 00:01 CRDT- 1999/07/30 00:00 PHST- 1999/07/30 00:00 [pubmed] PHST- 1999/07/30 00:01 [medline] PHST- 1999/07/30 00:00 [entrez] AID - JME00787 [pii] AID - 10.1677/jme.0.0230033 [doi] PST - ppublish SO - J Mol Endocrinol. 1999 Aug;23(1):33-44. doi: 10.1677/jme.0.0230033.