1: Exp Cell Res. 2005 Jan 1;302(1):129-42. 

Sp1/Sp3 and the myeloid zinc finger gene MZF1 regulate the human N-cadherin
promoter in osteoblasts.

Le Mee S, Fromigue O, Marie PJ.

Laboratory of Osteoblast Biology and Pathology, INSERM U606, Lariboisiere
Hospital, 75475 Cedex 10 Paris, France.

To determine the molecular mechanisms by which N-cadherin transcription is
regulated, we cloned and sequenced a 3681-bp of the 5'-flanking region of the
human N-cadherin gene. Deletion analysis of the proximal region identified a
minimal 318-bp region with strong promoter activity in human osteoblasts. The
cryptic promoter is characterized by high GC content and a GA-rich binding core
that may bind zing finger transcription factors. Electrophoretic mobility shift
assays (EMSA), competition and supershift EMSA revealed that an Sp1/Sp3 binding
site acts as a basal regulatory element of the promoter in osteoblasts.
Incubation of osteoblast nuclear extracts with -163/-131 wild-type probe
containing the GA-rich binding core revealed another specific complex, which was
not formed with a -163/-131 probe mutated in the GA repeat. EMSA identified the
nuclear factor involved as myeloid zinc finger-1 (MZF1). Mutation analysis
showed that Sp1/Sp3 and MZF1 binding sites contribute to basal promoter
activity. Cotransfection analyses showed that Sp1 and MZF1 overexpression
increases whereas Sp3 antagonizes Sp1-induced N-cadherin promoter activity in
osteoblasts. RT-PCR analysis showed that human osteoblastic cells express MZF1
and that Sp1/MZF1 overexpression increased N-cadherin expression. These results
indicate that Sp1/Sp3 and MZF1 are important transcription factors regulating
N-cadherin promoter activity and expression in osteoblasts.

PMID: 15541732 [PubMed - indexed for MEDLINE]


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2: Mol Cells. 2004 Oct 31;18(2):157-62. 

Regulatory elements involved in transcription of the human
NeuAcalpha2,3Galbeta1,3GalNAcalpha2,6-sialyltransferase (hST6GalNAc IV) gene.

Kang NY, Park YD, Choi HJ, Kim KS, Lee YC, Kim CH.

National Research Laboratory for Glycobiology, Department of Biochemistry and
Molecular Biology, College of Oriental Medicine, Dongguk University, Kyungju
780-714, Korea.

We previously cloned and characterized the promoter region of the human
NeuAcalpha2,3Galbeta1,3GalNAcalpha2,6-sialyltransferase (hST6GalNAc IV) gene
[Kim et al. (2003)]. In the present study, we identified a region of 294 bp
upstream of exon 1 of the gene that produced maximal transcriptional activity in
human Jurkat T cells. Site-directed mutagenesis and transient transfection
assays demonstrated that Sp1 and MZF1 elements in this region were required for
the promoter activity. Further analysis by electrophoretic mobility shift assays
using specific competitors and antibody revealed that Sp1 and MZF1 nuclear
proteins interacted with these elements. These results indicate that Sp1 and
MZF1 are involved in the transcriptional regulation of the hST6GalNAc IV gene in
Jurkat T cells.

PMID: 15528990 [PubMed - indexed for MEDLINE]


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3: Eur J Immunogenet. 2004 Feb;31(1):15-9. 

Allele-specific binding to the -308 single nucleotide polymorphism site in the
tumour necrosis factor-alpha promoter.

Baseggio L, Bartholin L, Chantome A, Charlot C, Rimokh R, Salles G.

Equipe d'Accueil 3737 Pathologie des Cellules Lymphoides, Claude Bernard
University, Lyon, France.

Single nucleotide polymorphisms in the tumour necrosis factor alpha (TNF-alpha)
promoter region may modulate TNF-alpha gene transcriptional activity by
modifying the binding of transcription factors. Here we confirm that a specific
DNA complex binds preferentially the variant TNF2 allele in various cell types
and demonstrate that activating protein (AP)-2, myeloid zinc finger gene 1
(MZF-1) and Sp1 are not involved in this complex.

PMID: 15009176 [PubMed - indexed for MEDLINE]


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