PMID- 7989580
OWN - NLM
STAT- MEDLINE
DCOM- 19950106
LR  - 20181113
IS  - 0021-9738 (Print)
IS  - 0021-9738 (Linking)
VI  - 94
IP  - 6
DP  - 1994 Dec
TI  - cAMP responsive element-mediated regulation of the gene transcription of the 
      alpha 1B adrenergic receptor by thyrotropin.
PG  - 2245-54
AB  - To elucidate the molecular mechanism of the stimulatory effect of thyrotropin on 
      the gene regulation of alpha 1B adrenergic receptor in functioning rat thyroid 
      (FRTL-5) cells, we established a competitive reverse-transcriptase (RT) 
      polymerase chain reaction (PCR) and nuclear run-off assay to quantify changes in 
      mRNA levels and transcription rates. A binding assay showed that FRTL-5 cells 
      predominantly expressed alpha 1B adrenergic receptor and that thyrotropin 
      increased its expression sevenfold. By means of RT-PCR, we found that thyrotropin 
      induced an 11-fold increase in alpha 1B receptor mRNA abundance. The nuclear 
      run-off assay demonstrated that thyrotropin caused a ninefold increase at the 
      gene transcriptional level, which occurred in the presence of the protein 
      synthesis inhibitor cycloheximide. The half-life of the alpha 1B receptor mRNA in 
      cells incubated with thyrotropin for 1 h increased 1.5-fold but returned to the 
      original value after 12 h. Dibutyryl cAMP and forskolin mimicked the stimulatory 
      effects of thyrotropin on the gene transcriptional level. The 5'-flanking region 
      of the rat alpha 1B receptor gene contained a putative cAMP responsive element 
      (CRE) at nucleotide -438 relative to the translation start site. The promoter 
      analysis using the reporter gene indicated that the CRE motif confers the cAMP 
      sensitivity to the transcription of the rat alpha 1B receptor gene. These results 
      demonstrated that a CRE-mediated mechanism is involved in the transcriptional 
      regulation of the alpha 1B receptor gene by thyrotropin without requiring new 
      protein synthesis.
FAU - Kanasaki, M
AU  - Kanasaki M
AD  - Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
FAU - Matsubara, H
AU  - Matsubara H
FAU - Murasawa, S
AU  - Murasawa S
FAU - Masaki, H
AU  - Masaki H
FAU - Nio, Y
AU  - Nio Y
FAU - Inada, M
AU  - Inada M
LA  - eng
SI  - GENBANK/D32045
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Invest
JT  - The Journal of clinical investigation
JID - 7802877
RN  - 0 (Adra1b protein, rat)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Adrenergic, alpha-1)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 1F7A44V6OU (Colforsin)
RN  - 63X7MBT2LQ (Bucladesine)
RN  - 9002-71-5 (Thyrotropin)
RN  - E0399OZS9N (Cyclic AMP)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites
MH  - Bucladesine/pharmacology
MH  - Cells, Cultured
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/pharmacology
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - DNA Mutational Analysis
MH  - Gene Expression Regulation/*drug effects
MH  - Molecular Sequence Data
MH  - Polymerase Chain Reaction
MH  - Promoter Regions, Genetic/*genetics
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptors, Adrenergic, alpha-1/biosynthesis/*genetics
MH  - Recombinant Fusion Proteins/biosynthesis
MH  - Sequence Deletion
MH  - Thyroid Gland/cytology/drug effects/*metabolism
MH  - Thyrotropin/*pharmacology
MH  - Transcription, Genetic/drug effects
PMC - PMC330051
EDAT- 1994/12/01 00:00
MHDA- 1994/12/01 00:01
PMCR- 1994/12/01
CRDT- 1994/12/01 00:00
PHST- 1994/12/01 00:00 [pubmed]
PHST- 1994/12/01 00:01 [medline]
PHST- 1994/12/01 00:00 [entrez]
PHST- 1994/12/01 00:00 [pmc-release]
AID - 10.1172/JCI117587 [doi]
PST - ppublish
SO  - J Clin Invest. 1994 Dec;94(6):2245-54. doi: 10.1172/JCI117587.