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PMID: 12534345 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Physical interaction of tumour suppressor p53/p73 with CCAAT-binding transcription factor 2 (CTF2) and differential regulation of human high-mobility group 1 (HMG1) gene expression.

The Biochemical journal ·Vol. 371 ·No. Pt 2 ·2003-04-15 ·Pages 301-10

Uramoto H, Izumi H, Nagatani G, Ohmori H, Nagasue N, Ise T, Yoshida T, Yasumoto K, Kohno K

Abstract

The CCAAT-binding transcription factor (CTF)/nuclear factor I (NF-I) group of cellular DNA-binding proteins recognizes the sequence GCCAAT and is implicated in eukaryotic transcription, as well as DNA replication. Molecular analysis of human CTF/NF-I cDNA clones revealed multiple mRNA species that contain alternative coding regions, apparently as a result of differential splicing. Expression and functional analysis established that individual gene products can bind to GCCAAT recognition sites and serve as both promoter-selective transcriptional activators and initiation factors for DNA replication. The interaction between CTF2 and p53/p73 was shown to modulate their ability to regulate transcription of their respective target genes. In the present paper, we report that p53 down-regulates the activity of the high mobility group 1 (HMG1) gene promoter, whereas p73alpha up-regulates the activity of this promoter. Furthermore, CTF2 transactivates p53-induced p21 promoter activity, but inhibits p73alpha-induced p21 promoter activity. Using deletion mutants, we found that the DNA-binding domains of both p53 and p73alpha are required for physical interaction with CTF2 via the regions between amino acid residues 161 and 223, and 228 and 312 respectively. CTF2 enhances the DNA-binding activity of p53 and inhibits the DNA-binding activity of p73alpha. These results provide novel information on the functional interplay between CTF2 and p53/p73 as important determinants of their function in cell proliferation, apoptosis, DNA repair and cisplatin resistance.

MeSH Terms
Base Sequence CCAAT-Binding Factor/metabolism Cloning, Molecular DNA Primers DNA-Binding Proteins/metabolism Escherichia coli/genetics,metabolism Gene Expression Regulation Genes, Tumor Suppressor HMGB1 Protein/genetics,metabolism Humans Kinetics Nuclear Proteins/metabolism Promoter Regions, Genetic Transcription Factors/metabolism Transfection Tumor Cells, Cultured Tumor Protein p73 Tumor Suppressor Protein p53/metabolism Tumor Suppressor Proteins
Chemicals
CCAAT-Binding Factor DNA Primers DNA-Binding Proteins HMGB1 Protein Nuclear Proteins TP73 protein, human Transcription Factors Tumor Protein p73 Tumor Suppressor Protein p53 Tumor Suppressor Proteins
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Uramoto Hidetaka
Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Izumi Hiroto
Nagatani Gunji
Ohmori Haruki
Nagasue Naofumi
Ise Tomoko
Yoshida Takeshi
Yasumoto Kosei
Kohno Kimitoshi
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Article Info
Journal
The Biochemical journal
Abbr.
Biochem J
ISSN
0264-6021
DOI
10.1042/BJ20021646
Published
2003-04-15
Pages
301-10
Language
English
Region
England
NLM ID
2984726R
PMCID
PMC1223307
Subset
IM
External Links
PubMed source DOI: 10.1042/BJ20021646 PMC Full Text View journal details
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