TATA-binding Protein (TBP)-like Protein Is Required for p53-dependent Transcriptional Activation of Upstream Promoter of p21 Gene

Suzuki, Haruo; Itô, Ryo; Ikeda, Kaori; Tamura, Tomohiro

doi:10.1074/jbc.m112.369629

Cited by 20 publications

(53 citation statements)

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“…We have demonstrated that TLP activates several TATA-less promoters but not TATA-containing promoters [19]. Other research groups have reported the same phenomenon [37].…”

Section: Introductionsupporting

confidence: 74%

“…A reporter plasmid (p21up/GL4) containing an upstream region of the human p21 gene encompassing from −2266 to −1875 was described previously [19].…”

Section: Methodsmentioning

confidence: 99%

“…The recombinant proteins were induced by isopropyl 1-thio-β-D-galactoside and purified as described previously [19].…”

Section: Methodsmentioning

confidence: 99%

“…TLP has 38% identity to the C-terminal conserved region of TBP and binds to transcription factor IIA (TFIIA) more strongly than TBP does [29], [30]. Previously, we demonstrated that TLP inhibits cell growth and induces apoptosis of chicken [31] and mammalian cells [19]. Although TLP has no obvious sequence-specific DNA-binding activity, accumulating evidence indicates that TLP has transcription activation capacity [32], [33].…”

Section: Introductionmentioning

confidence: 99%

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Interaction between Transactivation Domain of p53 and Middle Part of TBP-Like Protein (TLP) Is Involved in TLP-Stimulated and p53-Activated Transcription from the p21 Upstream Promoter

et al. 2014

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TBP-like protein (TLP) is involved in transcriptional activation of an upstream promoter of the human p21 gene. TLP binds to p53 and facilitates p53-activated transcription from the upstream promoter. In this study, we clarified that in vitro affinity between TLP and p53 is about one-third of that between TBP and p53. Extensive mutation analyses revealed that the TLP-stimulated function resides in transcription activating domain 1 (TAD1) in the N-terminus of p53. Among the mutants, #22.23, which has two amino acid substitutions in TAD1, exhibited a typical mutant phenotype. Moreover, #22.23 exhibited the strongest mutant phenotype for TLP-binding ability. It is thus thought that TLP-stimulated and p53-dependent transcriptional activation is involved in TAD1 binding of TLP. #22.23 had a decreased transcriptional activation function, especially for the upstream promoter of the endogenous p21 gene, compared with wild-type p53. This mutant did not facilitate p53-dependent growth repression and etoposide-mediated cell-death as wild-type p53 does. Moreover, mutation analysis revealed that middle part of TLP, which is requited for p53 binding, is involved in TLP-stimulated and p53-dependent promoter activation and cell growth repression. These results suggest that activation of the p21 upstream promoter is mediated by interaction between specific regions of TLP and p53.

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“…We have demonstrated that TLP activates several TATA-less promoters but not TATA-containing promoters [19]. Other research groups have reported the same phenomenon [37].…”

Section: Introductionsupporting

confidence: 74%

“…A reporter plasmid (p21up/GL4) containing an upstream region of the human p21 gene encompassing from −2266 to −1875 was described previously [19].…”

Section: Methodsmentioning

confidence: 99%

“…The recombinant proteins were induced by isopropyl 1-thio-β-D-galactoside and purified as described previously [19].…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interaction between Transactivation Domain of p53 and Middle Part of TBP-Like Protein (TLP) Is Involved in TLP-Stimulated and p53-Activated Transcription from the p21 Upstream Promoter

et al. 2014

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“…A key target gene executing the role of p53 in cell cycle arrest is p21, which is induced by p53 through direct binding to the p21 promoter (9)(10)(11). The p21 gene is localized on chromosome 6p21.2, comprising 3 exons and 2 introns, and encodes the p21 protein.…”

Section: Introductionmentioning

confidence: 99%

Association of p53 and p21 polymorphisms with prostate cancer

Sivoňová¹,

Vilčková²,

Kliment³

et al. 2015

Biomedical Reports

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Abstract. Cell cycle deregulation is common in human cancer. Alterations of the tumor-suppressor gene p53 and its downstream effector p21 have been indicated in the development of numerous human malignancies. Therefore, we hypothesize that the p53 codon 72 polymorphism, either on its own or in combination with p21 (C98A and C70T) polymorphisms, modifies the risk of prostate cancer within the Slovak population, and no previous studies have investigated these gene-gene interactions in the pathogenesis of prostate cancer in the Slovak population. Polymerase chain reaction-restriction fragment length polymorphism was used to determine the p53 and p21 genotypes in subjects comprising 300 prostate cancer patients and 446 healthy individuals. These 3 polymorphisms individually did not correlate with the prostate cancer risk. Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Neither the p53 genotypes nor the p21 genotypes showed statistically significant differences in Gleason score or serum prostate-specific antigen levels (P>0.05). A decreased risk of prostate cancer association with the p21 C98A CA genotype (OR=0.58; 95% CI, 0.36-0.93; P<0.05) in non-smokers compared to the non-smokers with the p21 C98A CC genotype was observed. Smokers carrying the p53 codon 72 Pro/Pro genotype were not at any significant risk of prostate cancer (OR=2.97; 95% CI, 0.51-17.15) compared to the non-smokers with the Arg/Arg genotype. Taken together, to the best of our knowledge this is the first study to show that a combination of the variant genotypes of p53 codon 72 and p21 C98A may modify the prostate cancer risk within the Slovak population.

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Effect of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in pancreatic cancer

Zhang

et al. 2018

Journal Cellular Physiology

159

125

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Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase-9, caspase-3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β-Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase-9, caspase-3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase-9, caspase-3, p53, and p21. The shCCNB1 group had decreased proliferation and S-phase cell proportion and increased apoptosis, senescence, and G0/G1-phase cell proportion. The PFT-α group showed higher expressions of MDM2 and lower expressions of Bax, caspase-9, caspase-3, p53, and p21. The PFT-α group had increased proliferation and S-phase cell proportion and declined apoptosis, senescence, and G0/G1-phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC.

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TATA-binding Protein (TBP)-like Protein Is Required for p53-dependent Transcriptional Activation of Upstream Promoter of p21 Gene

Cited by 20 publications

References 50 publications

Interaction between Transactivation Domain of p53 and Middle Part of TBP-Like Protein (TLP) Is Involved in TLP-Stimulated and p53-Activated Transcription from the p21 Upstream Promoter

Interaction between Transactivation Domain of p53 and Middle Part of TBP-Like Protein (TLP) Is Involved in TLP-Stimulated and p53-Activated Transcription from the p21 Upstream Promoter

Association of p53 and p21 polymorphisms with prostate cancer

Effect of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in pancreatic cancer

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