PMID- 9224612
OWN - NLM
STAT- MEDLINE
DCOM- 19970925
LR  - 20190501
IS  - 0305-1048 (Print)
IS  - 1362-4962 (Electronic)
IS  - 0305-1048 (Linking)
VI  - 25
IP  - 15
DP  - 1997 Aug 1
TI  - Sp3 encodes multiple proteins that differ in their capacity to stimulate or 
      repress transcription.
PG  - 3110-7
AB  - The product of the retinoblastoma (Rb) susceptibility gene ( RB-1 ) regulates 
      expression of a variety of growth control genes via discrete promoter elements 
      termed retinoblastoma control elements (RCEs). We have previously shown that RCEs 
      are bound and regulated by a common set of ubiquitously expressed nuclear 
      proteins of 115, 95 and 80 kDa, termed retinoblastoma control proteins (RCPs). We 
      have also previously determined that Sp3 and Sp1, two members of the Sp family of 
      transcription factors, encode the 115 and 95 kDa RCPs respectively and that Rb 
      stimulates Sp1/Sp3-mediated transcription in vivo. In this report we have 
      extended these results by determining that the 80 kDa RCP arises from Sp3 mRNA 
      via translational initiation at two internal sites located within the Sp3 trans 
      -activation domain. Internally initiated Sp3 proteins readily bind to Sp1 binding 
      sites in vitro yet have little or no capacity to stimulate transcription of 
      Sp-regulated genes in vivo. Instead, these Sp3-derived proteins function as 
      potent inhibitors of Sp1/Sp3- mediated transcription. Since cell cycle- or 
      signal- induced expression of a variety of genes, including p21 waf1/cip1, p15 
      INK4B, CYP11A, mdr1 and acetyl-CoA carboxylase, have been mapped to GC-rich 
      promoter elements that bind Sp family members, we speculate that alterations of 
      the protein and/or DNA binding activities of internally initiated Sp3 isoforms 
      may account in part for the regulation of such differentially expressed genes.
FAU - Kennett, S B
AU  - Kennett SB
AD  - Departments of Molecular Cancer Biology and Microbiology, Box 3686, Duke 
      University Medical Center, Durham, NC 27710, USA.
FAU - Udvadia, A J
AU  - Udvadia AJ
FAU - Horowitz, J M
AU  - Horowitz JM
LA  - eng
GR  - CA53248/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  - England
TA  - Nucleic Acids Res
JT  - Nucleic acids research
JID - 0411011
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Repressor Proteins)
RN  - 0 (SP3 protein, human)
RN  - 0 (Transcription Factors)
RN  - 148710-94-5 (Sp3 Transcription Factor)
SB  - IM
MH  - Cell Line
MH  - DNA-Binding Proteins/genetics/metabolism/*physiology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Promoter Regions, Genetic
MH  - Protein Biosynthesis
MH  - Repressor Proteins/genetics/metabolism/*physiology
MH  - Retinoblastoma/genetics
MH  - Sp3 Transcription Factor
MH  - Transcription Factors/genetics/metabolism/*physiology
MH  - *Transcription, Genetic
MH  - Tumor Cells, Cultured
PMC - PMC146854
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
PMCR- 1997/08/01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
PHST- 1997/08/01 00:00 [pmc-release]
AID - gka489 [pii]
AID - 10.1093/nar/25.15.3110 [doi]
PST - ppublish
SO  - Nucleic Acids Res. 1997 Aug 1;25(15):3110-7. doi: 10.1093/nar/25.15.3110.