PMID- 10636866
OWN - NLM
STAT- MEDLINE
DCOM- 20000224
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 275
IP  - 3
DP  - 2000 Jan 21
TI  - Sp1 binding is critical for promoter assembly and activation of the MCP-1 gene by 
      tumor necrosis factor.
PG  - 1708-14
AB  - The monocyte chemoattractant protein-1 gene (MCP-1) is induced by the 
      inflammatory cytokine tumor necrosis factor through the coordinate assembly of an 
      NF-kappaB-dependent distal regulatory region and a proximal region that has been 
      suggested to bind Sp1 as well as other factors. To provide a genetic correlation 
      for Sp1 activity in this system, a cell line homozygous for a targeted truncation 
      of the Sp1 gene was derived and examined. We found that the lack of Sp1 binding 
      activity resulted in the inability of both the distal and proximal regions to 
      assemble in vivo even though the binding of NF-kappaB to distal region DNA was 
      unaffected in vitro. We also found that Sp1 and NF-kappaB were the minimal 
      mammalian transcription factors required for efficient activity when transfected 
      into Drosophila Schneider cells. Additionally, Sp3 was able to compensate for Sp1 
      in the Drosophila tissue cell system but not in the Sp1(-/-) cell line suggesting 
      that Sp1 usage is site-specific and is likely to depend on the context of the 
      binding site. Together, these data provide genetic and biochemical proof for Sp1 
      in regulating the MCP-1 gene.
FAU - Ping, D
AU  - Ping D
AD  - Department of Microbiology and Immunology, Emory University School of Medicine, 
      Atlanta, Georgia 30322, USA.
FAU - Boekhoudt, G
AU  - Boekhoudt G
FAU - Zhang, F
AU  - Zhang F
FAU - Morris, A
AU  - Morris A
FAU - Philipsen, S
AU  - Philipsen S
FAU - Warren, S T
AU  - Warren ST
FAU - Boss, J M
AU  - Boss JM
LA  - eng
GR  - T32 GM008490/GM/NIGMS NIH HHS/United States
GR  - CA74271/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.- (Sp1 kinase)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Base Sequence
MH  - Blotting, Northern
MH  - Cell Line
MH  - Chemokine CCL2/*genetics
MH  - Chemokine CXCL10
MH  - Chemokines, CXC/metabolism
MH  - DNA Footprinting
MH  - DNA-Binding Proteins/*physiology
MH  - Drosophila/genetics
MH  - Gene Expression Regulation
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Sequence Data
MH  - Mutagenesis
MH  - NF-kappa B/metabolism
MH  - *Promoter Regions, Genetic
MH  - Protein Binding
MH  - Protein Kinases/*physiology
MH  - Recombinant Proteins/metabolism
MH  - Time Factors
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2000/01/15 09:00
MHDA- 2000/02/26 09:00
CRDT- 2000/01/15 09:00
PHST- 2000/01/15 09:00 [pubmed]
PHST- 2000/02/26 09:00 [medline]
PHST- 2000/01/15 09:00 [entrez]
AID - S0021-9258(18)31099-8 [pii]
AID - 10.1074/jbc.275.3.1708 [doi]
PST - ppublish
SO  - J Biol Chem. 2000 Jan 21;275(3):1708-14. doi: 10.1074/jbc.275.3.1708.