PMID- 10650958
OWN - NLM
STAT- MEDLINE
DCOM- 20000210
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 141
IP  - 2
DP  - 2000 Feb
TI  - Characterization of the murine pituitary tumor transforming gene (PTTG) and its
      promoter.
PG  - 763-71
AB  - We recently isolated rat pituitary tumor transforming gene (PTTG) complementary
      DNA and showed its potent in vitro and in vivo transforming activity. We now
      characterize the mouse PTTG gene and its promoter. The entire gene is composed of
      five exons and four introns and spans about 7 kb. Northern analysis showed that
      PTTG was expressed in several tumor cell lines examined, but not in all normal
      tissues, implying a correlation between PTTG and tumorigenesis. Using rapid
      amplification of 5'-cDNA ends, the transcription start site was localized at -303
      nucleotides upstream to the ATG codon in both F9 and AtT20 cells. An
      approximately 4.3-kb upstream region demonstrated promoter activity in AtT20
      cells as well as other cell lines tested, and in vivo, the cloned promoter
      driving an enhanced green fluorescent protein transgene exhibited transcriptional
      activation in testis and embryo. Serial deletions showed that -313 bp of the
      5'-flanking region was critical for promoter activity. Three elements contribute 
      to promoter activity. Both element A (-313/-293) and element C (-180/-160), in an
      electrophoretic mobility shift assay using NIH-3T3 nuclear extract, formed three 
      specific complexes, which were competed by a known Sp1 oligo; one complex was
      supershifted by Sp1 antibody, and the other two complexes were both supershifted 
      by an Sp3 antibody. Two mutants disrupting element A resulted in up to 70% loss
      of promoter activity and abrogated formation of specific DNA-protein binding
      complexes, implying a more important role for element A. Element B (-249/-229)
      shows more than 80% homology to a consensus c-myb element, but formed two
      specific complexes that differed from that of c-myb in the electrophoretic
      mobility shift assay. Thus, the integrity and possible cooperation among these
      elements contribute to the basal promoter activity of the mouse PTTG oncogene
      homolog.
FAU - Wang, Z
AU  - Wang Z
AD  - Cedars-Sinai Research Institute, University of California School of Medicine, Los
      Angeles 90048, USA.
FAU - Melmed, S
AU  - Melmed S
LA  - eng
GR  - CA-75979/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (DNA, Complementary)
RN  - 0 (Luminescent Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Oncogene Proteins)
RN  - 0 (Securin)
RN  - 0 (Transcription Factors)
RN  - 0 (pituitary tumor-transforming protein 1, human)
RN  - 147336-22-9 (Green Fluorescent Proteins)
SB  - AIM
SB  - IM
MH  - 3T3 Cells
MH  - Amino Acid Sequence
MH  - Animals
MH  - Binding Sites
MH  - DNA, Complementary
MH  - Embryo, Mammalian
MH  - Green Fluorescent Proteins
MH  - Humans
MH  - Luminescent Proteins/genetics
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Molecular Sequence Data
MH  - Neoplasm Proteins/chemistry/*genetics
MH  - Oncogene Proteins/chemistry/*genetics
MH  - *Oncogenes
MH  - Pituitary Neoplasms/*genetics
MH  - *Promoter Regions, Genetic
MH  - Rats
MH  - Restriction Mapping
MH  - Securin
MH  - Sequence Alignment
MH  - Sequence Homology, Amino Acid
MH  - Testis/metabolism
MH  - Transcription Factors/metabolism
MH  - Transcriptional Activation
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 2000/01/29 00:00
MHDA- 2000/01/29 00:01
CRDT- 2000/01/29 00:00
PHST- 2000/01/29 00:00 [pubmed]
PHST- 2000/01/29 00:01 [medline]
PHST- 2000/01/29 00:00 [entrez]
AID - 10.1210/endo.141.2.7294 [doi]
PST - ppublish
SO  - Endocrinology. 2000 Feb;141(2):763-71. doi: 10.1210/endo.141.2.7294.