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(Received for publication, May 19, 1995; and in revised form, October 24, 1995) Tissue transglutaminase (transglutaminase type II) is an
intracellular protein cross-linking enzyme that accumulates in
connective tissue and in cells undergoing apoptosis. Retinoids regulate
the transcription of the mouse tissue transglutaminase gene via
activation of regulatory elements contained within 4 kilobases of the
5`-end of the gene. Co-transfection studies with retinoid receptor
expression vectors in CV-1 cells demonstrated that the mouse tissue
transglutaminase promoter is activated by ligand activation of either
retinoic acid receptor-retinoid X receptor (RAR
Volume 271,
Number 8,
Issue of February 23, 1996 pp. 4355-4365
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
RXR) heterodimers
or RXR homodimers. Optimal induction is achieved with retinoid receptor
panagonists; partial activation can also be achieved with either
RAR-specific or RXR-specific retinoids. Retinoid-dependent activation
of the tissue transglutaminase promoter depends on both a proximal
regulatory region containing sequences highly conserved between the
human and the mouse tissue transglutaminase promoters and a distal
region that includes a 30-base pair retinoid response element
(mTGRRE1). mTGRRE1 contains three hexanucleotide half-sites (two
canonical and one non-canonical) in a DR7/DR5 motif that bind both
RARRXR heterodimers and RXR homodimers. These studies suggest
that retinoid-dependent expression of the mouse tissue transglutaminase
gene is mediated by a versatile tripartite retinoid response element
located 1.7 kilobases upstream of the transcription start site.
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