PMID- 9030555
OWN - NLM
STAT- MEDLINE
DCOM- 19970403
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 272
IP  - 8
DP  - 1997 Feb 21
TI  - Interaction of human T-cell lymphotropic virus type I Tax, Ets1, and Sp1 in 
      transactivation of the PTHrP P2 promoter.
PG  - 4953-8
AB  - We have previously shown that the parathyroid hormone-related protein (PTHrP) 
      promoter contains binding sites for transcription factors Ets1 and Sp1 and that 
      human T-cell lymphotropic virus type I (HTLV-I) Tax cooperates with Ets1 to 
      transactivate the PTHrP P2 promoter. Using the yeast two-hybrid interaction 
      system, we now provide evidence that Tax interacts with Ets1. Moreover, a double 
      mutation (D22A,C23S) in the Tax protein that abrogated the Tax/Ets1 interaction 
      also inhibited the Tax/Ets1 cooperative effect, suggesting that the interaction 
      between Tax and Ets1 is important for transactivation of the PTHrP promoter. In 
      coimmunoprecipitation assays, we find that Tax facilitates the interaction 
      between Ets1 and Sp1, forming a ternary complex. When the Sp1 site in the PTHrP 
      promoter was mutated, the Tax/Ets1 cooperative effect was dramatically decreased. 
      This suggests that Sp1 plays an important role in the Ets1-dependent Tax 
      transactivation of the PTHrP P2 promoter. Finally, we demonstrate that Gal4-Tax 
      is a strong activator of the Gal PTHrP promoter, implying that Tax contributes 
      directly to the transcriptional activation of the promoter. We propose a model in 
      which the Tax/Ets1 cooperative effect on the PTHrP P2 promoter is based on the 
      ability of Tax, Ets1, and Sp1 to form a ternary complex on the template DNA. Tax 
      facilitates the interaction of Ets1/Sp1 and participates directly in the 
      transcription initiation process.
FAU - Dittmer, J
AU  - Dittmer J
AD  - Virus Tumor Biology Section, Laboratory of Molecular Virology, NCI, National 
      Institutes of Health, Bethesda, Maryland 20892-5005, USA.
FAU - Pise-Masison, C A
AU  - Pise-Masison CA
FAU - Clemens, K E
AU  - Clemens KE
FAU - Choi, K S
AU  - Choi KS
FAU - Brady, J N
AU  - Brady JN
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (ETS1 protein, human)
RN  - 0 (Gene Products, tax)
RN  - 0 (PTHLH protein, human)
RN  - 0 (Parathyroid Hormone-Related Protein)
RN  - 0 (Proteins)
RN  - 0 (Proto-Oncogene Protein c-ets-1)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-ets)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Amino Acid Sequence
MH  - Gene Products, tax/*genetics
MH  - *Human T-lymphotropic virus 1
MH  - Humans
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Parathyroid Hormone-Related Protein
MH  - Promoter Regions, Genetic/genetics
MH  - Proteins/*genetics
MH  - Proto-Oncogene Protein c-ets-1
MH  - Proto-Oncogene Proteins/*genetics
MH  - Proto-Oncogene Proteins c-ets
MH  - Sp1 Transcription Factor/*genetics
MH  - Transcription Factors/*genetics
MH  - Transcriptional Activation
EDAT- 1997/02/21 00:00
MHDA- 1997/02/21 00:01
CRDT- 1997/02/21 00:00
PHST- 1997/02/21 00:00 [pubmed]
PHST- 1997/02/21 00:01 [medline]
PHST- 1997/02/21 00:00 [entrez]
AID - S0021-9258(19)79326-0 [pii]
AID - 10.1074/jbc.272.8.4953 [doi]
PST - ppublish
SO  - J Biol Chem. 1997 Feb 21;272(8):4953-8. doi: 10.1074/jbc.272.8.4953.