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

Uramoto, Hidetaka; Izumi, Hiroto; Nagatani, Gunji; Ohmori, Hisamitsu; Nagasue, Naofumi; Ise, Tomoko; Yoshida, Takeshi; Yasumoto, Kosei; Kohno, Kimitoshi

doi:10.1042/bj20021646

Cited by 46 publications

(41 citation statements)

References 49 publications

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“…The plasmid construction of pGEX-p53 expressing GST-p53, TH-HA-p53 expressing N-terminal tagged HA-p53, pcDNA3-HA-p53, ThioHis-p53 and its deletion mutants (N376, N362, N322, N223, 60C, N160, 224C, 161/223; see Figure 2a) has been described previously Uramoto et al, 2002Uramoto et al, , 2003. The ThioHis-p53 deletion mutant D138-159 was constructed from the ThioHis-p53 full-length plasmid by deletion of the MlsI fragment.…”

Section: Plasmid Constructionmentioning

confidence: 99%

Twist and p53 reciprocally regulate target genes via direct interaction

et al. 2008

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Section: Plasmid Constructionmentioning

confidence: 99%

Twist and p53 reciprocally regulate target genes via direct interaction

et al. 2008

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“…Plasmid construction of pGEX-p53, pGEX-p73 and pGEX-ZNF143 that express GST-p53, GST-p73 and GST-ZNF143 proteins in bacteria, respectively, and pcDNA3-HA-p53 that expresses HA-p53 protein in mammalian cells were described previously (Imamura et al, 2001;Uramoto et al, 2002Uramoto et al, , 2003. pcDNA3-HA-p73 expression plasmid in mammalian cells was kindly provided by Dr G Melino (University of Rome, Rome, Italy) (De Laurenzi et al, 1998).…”

Section: Plasmid Constructionmentioning

confidence: 99%

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

et al. 2007

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Zinc-finger protein 143 (ZNF143) is a human homolog of Xenopus transcriptional activator staf that is involved in selenocystyl tRNA transcription. We previously showed that ZNF143 expression is induced by treatment with DNA-damaging agents and that it preferentially binds to cisplatin-modified DNA. In this study, the potential function of ZNF143 was investigated. ZNF143 was overexpressed in cisplatin-resistant cells. ZNF143 knockdown in prostate cancer caused increased sensitivity for cisplatin, but not for oxaliplatin, etoposide and vincristine. We also showed that ZNF143 is associated with tumor suppressor gene product p73 but not with p53. p73 could stimulate the binding of ZNF143 to both ZNF143 binding site and cisplatin-modified DNA, and modulate the function of ZNF143. We provide a direct evidence that both Rad51 and flap endonuclease-1 are target genes of ZNF143 and overexpressed in cisplatin-resistant cells. Taken together, these experiments demonstrate that an interplay of ZNF143, p73 and ZNF143 target genes is involved in DNA repair gene expression and cisplatin resistance.

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“…5). It has been shown that the p73 protein is regulated by diverse factors, including MDM2, MDMX, p300/ CBP, Amphiphysin IIb-1, ASPP (apoptosis-stimulated proteins of p53) 1 and 2, c-Abl (cellular Abelson oncogene), c-Myc, CTF2 (CCAATbinding transcription factor 2), Cyclin G, HCV (hepatitis C virus protein), MM1, PMS2 (mismatch-repair protein s2), WT1 (Wilms tumor protein), and YAP (Yes-associated protein) (15,16,(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). Among these regulators, MDM2 is a well known repressor of p73 and p53, but its inhibitory effect on p73 does not involve degradation.…”

Section: P19mentioning

confidence: 99%

p19 Interacts with and Activates p73 by Involving the MDM2 Protein

Jeong

Bae

Kim

et al. 2006

Journal of Biological Chemistry

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p73␤ is a structural and functional homologue of p53, a tumor suppressor gene. In this study, we identified a novel p73␤-binding protein, p19ras , by the yeast two-hybrid screening method. Alternative splicing of the proto-oncogene H-ras pre-mRNA has led to two distinct transcripts, p19 ras and p21 ras . In both endogenous and overexpressed systems, we confirmed that p19 ras binds to full-length p73␤ in vivo and in vitro. Coexpression of p19 ras with p73␤ stimulated the transcriptional activity of p73␤. Ras proteins are known to be small membrane-localized guanine nucleotide-binding proteins. However, unlike other Ras proteins, p19 ras is localized in the nucleus and the cytosol and its interaction with p73␤ occurred exclusively in the nucleus. Oncogenic MDM2 (mouse double minutes 2) is a known repressor of p73 transcriptional activity. In this study, when p19 ras was bound to MDM2, it further inhibited the association of MDM2 to the p73␤ protein. In addition, p19 ras abolished MDM2-mediated transcriptional repression of p73␤. Therefore, this study presents a novel pathway of Ras signaling that occurs in the nucleus, involving p19 ras and p73␤. Furthermore, a p19 rasmediated novel regulatory mechanism of p73 involving the MDM2 protein is described.More than a decade after the recognition of p53 as a major tumor suppressor, two p53 homologues, p73 and p63, were identified (1). The significant sequence homology between p73 and p53 suggests that the two proteins have similar functions as transcriptional factors. p73 not only activates the transcription of p53 target genes, but it also induces apoptosis and cell cycle arrest, like p53 (2, 3). However, a number of differences between p73 and p53 have been reported. p73 transactivates only certain p53-responsive genes (4, 5). Viral oncoproteins that bind to p53 and inhibit its activity do not interact with p73 (6, 7). Furthermore, the expression level of p73 is not affected by exposure to DNA-damaging agents that increase p53 levels, indicating that the two proteins have distinct cellular functions (8).MDM2 (mouse double minutes 2) is an oncoprotein that is overexpressed in many human cancers (9). It is well established that MDM2 inactivates p53 activity through monomeric ubiquitination of lysine residues of p53 (10 -12). In contrast, although p73 binds to MDM2 as well, their interaction does not lead to the proteosomal degradation of p73 (13). Nevertheless, the binding of p73 to MDM2 results in a dramatic inhibition of p73 transactivating activity (14). It has been shown that the binding to a cofactor, p300/CREB-binding protein (CBP), 3 is required for the transcriptional activity of p73 and that MDM2 competes with p73 for the p300/CBP (15). In a previous report, we demonstrated that Amphiphysin IIb-1 sequesters nascent p73 proteins in the cytoplasm and thus inhibits its transcriptional activity (16).Using the yeast two-hybrid screening method, we identified a novel p73␤-binding protein, p19ras , which is an alternative splicing variant of c-H-ras (17). Proto-oncogen...

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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

Cited by 46 publications

References 49 publications

Twist and p53 reciprocally regulate target genes via direct interaction

Twist and p53 reciprocally regulate target genes via direct interaction

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

p19 Interacts with and Activates p73 by Involving the MDM2 Protein

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