一类新型基因组DNA结合位点的鉴定揭示了肿瘤抑制蛋白p53激活靶基因时的选择性机制。
Identification of a novel class of genomic DNA-binding sites suggests a mechanism for selectivity in target gene activation by the tumor suppressor protein p53.
作者信息
Resnick-Silverman L, St Clair S, Maurer M, Zhao K, Manfredi J J
机构信息
Derald H. Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, New York 10029 USA.
出版信息
Genes Dev. 1998 Jul 15;12(14):2102-7. doi: 10.1101/gad.12.14.2102.
Abstract
There are two response elements for p53 in the promoter of the gene for the cyclin-dependent kinase inhibitor p21. The binding of p53 to the 5' site was enhanced by incubation with monoclonal antibody 421, whereas the binding of p53 to the 3' site was inhibited. Mutational analysis showed that a single-base change caused one element to behave like the other. A response element in the human cdc25C promoter is bound by p53 with properties similar to the 3' site. These results identify two classes of p53-binding sites and suggest a mechanism for target gene selectivity by p53.
摘要
细胞周期蛋白依赖性激酶抑制剂p21基因的启动子中有两个p53反应元件。用单克隆抗体421孵育可增强p53与5'位点的结合，而p53与3'位点的结合则受到抑制。突变分析表明，单个碱基的变化会使一个元件表现得与另一个元件相似。人cdc25C启动子中的一个反应元件被p53结合，其特性类似于3'位点。这些结果确定了两类p53结合位点，并提出了p53对靶基因选择性的机制。
相似文献
1
Identification of a novel class of genomic DNA-binding sites suggests a mechanism for selectivity in target gene activation by the tumor suppressor protein p53.一类新型基因组DNA结合位点的鉴定揭示了肿瘤抑制蛋白p53激活靶基因时的选择性机制。
Genes Dev. 1998 Jul 15;12(14):2102-7. doi: 10.1101/gad.12.14.2102.
2
Indirect p53-dependent transcriptional repression of Survivin, CDC25C, and PLK1 genes requires the cyclin-dependent kinase inhibitor p21/CDKN1A and CDE/CHR promoter sites binding the DREAM complex.Survivin、CDC25C和PLK1基因的间接p53依赖性转录抑制需要细胞周期蛋白依赖性激酶抑制剂p21/CDKN1A以及与DREAM复合物结合的CDE/CHR启动子位点。
Oncotarget. 2015 Dec 8;6(39):41402-17. doi: 10.18632/oncotarget.6356.
3
DNA damage-induced downregulation of Cdc25C is mediated by p53 via two independent mechanisms: one involves direct binding to the cdc25C promoter.DNA损伤诱导的Cdc25C下调由p53通过两种独立机制介导：一种涉及与cdc25C启动子的直接结合。
Mol Cell. 2004 Dec 3;16(5):725-36. doi: 10.1016/j.molcel.2004.11.002.
4
In vitro transcriptional activation of p21 promoter by p53.p53对p21启动子的体外转录激活作用。
Biochem Biophys Res Commun. 1997 May 19;234(2):300-2. doi: 10.1006/bbrc.1997.6637.
5
Myc suppression of the p21(Cip1) Cdk inhibitor influences the outcome of the p53 response to DNA damage.Myc对p21（Cip1）细胞周期蛋白依赖性激酶抑制剂的抑制作用影响p53对DNA损伤反应的结果。
Nature. 2002 Oct 17;419(6908):729-34. doi: 10.1038/nature01119. Epub 2002 Oct 2.
6
Binding to the naturally occurring double p53 binding site of the Mdm2 promoter alleviates the requirement for p53 C-terminal activation.与Mdm2启动子天然存在的双p53结合位点结合可减轻对p53 C末端激活的需求。
Nucleic Acids Res. 2001 May 1;29(9):1989-93. doi: 10.1093/nar/29.9.1989.
7
Tumor-derived mutations within the DNA-binding domain of p53 that phenotypically resemble the deletion of the proline-rich domain.p53 蛋白 DNA 结合结构域内源自肿瘤的突变，其表型类似于富含脯氨酸结构域的缺失。
Oncogene. 2000 Mar 30;19(14):1834-42. doi: 10.1038/sj.onc.1203500.
8
Hepatitis B virus-X protein upregulates the expression of p21waf1/cip1 and prolongs G1-->S transition via a p53-independent pathway in human hepatoma cells.乙型肝炎病毒X蛋白通过一条不依赖p53的途径上调p21waf1/cip1的表达并延长人肝癌细胞中G1期向S期的转变。
Oncogene. 2000 Jul 13;19(30):3384-94. doi: 10.1038/sj.onc.1203674.
9
A novel p53 transcriptional repressor element (p53TRE) and the asymmetrical contribution of two p53 binding sites modulate the response of the placental transforming growth factor-beta promoter to p53.一种新型p53转录抑制元件（p53TRE）以及两个p53结合位点的不对称作用调节胎盘转化生长因子-β启动子对p53的反应。
J Biol Chem. 2002 Jul 19;277(29):26699-707. doi: 10.1074/jbc.M203020200. Epub 2002 May 14.
10
Human RAD9 checkpoint control/proapoptotic protein can activate transcription of p21.人类RAD9检查点控制/促凋亡蛋白可激活p21的转录。
Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):8864-9. doi: 10.1073/pnas.0403130101. Epub 2004 Jun 7.
引用本文的文献
1
A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.RBM42 在 DNA 损伤反应中调节 CDKN1A/p21 的剪接和翻译的双重作用。
Nat Commun. 2023 Nov 22;14(1):7628. doi: 10.1038/s41467-023-43495-6.
2
Optimisation of TP53 reporters by systematic dissection of synthetic TP53 response elements.通过系统剖析合成 TP53 反应元件优化 TP53 报告基因。
Nucleic Acids Res. 2023 Oct 13;51(18):9690-9702. doi: 10.1093/nar/gkad718.
3
Apoptosis-inducing factor: a mitochondrial protein associated with metabolic diseases-a narrative review.凋亡诱导因子：一种与代谢性疾病相关的线粒体蛋白——综述
Cardiovasc Diagn Ther. 2023 Jun 30;13(3):609-622. doi: 10.21037/cdt-23-123. Epub 2023 Jun 19.
4
Influence of chain length and branching on poly(ADP-ribose)-protein interactions.长链和支化对聚（ADP-核糖）-蛋白相互作用的影响。
Nucleic Acids Res. 2023 Jan 25;51(2):536-552. doi: 10.1093/nar/gkac1235.
5
Unraveling the Structural Changes in the DNA-Binding Region of Tumor Protein p53 () upon Hotspot Mutation p53 Arg248 by Comparative Computational Approach.利用比较计算方法阐明肿瘤蛋白 p53()热点突变 p53 Arg248 时 DNA 结合区域的结构变化。
Int J Mol Sci. 2022 Dec 7;23(24):15499. doi: 10.3390/ijms232415499.
6
At a Crossroads to Cancer: How p53-Induced Cell Fate Decisions Secure Genome Integrity.处于癌症的十字路口：p53 诱导的细胞命运决定如何确保基因组完整性。
Int J Mol Sci. 2021 Oct 8;22(19):10883. doi: 10.3390/ijms221910883.
7
DNA repair pathways and their roles in drug resistance for lung adenocarcinoma.DNA 修复途径及其在肺腺癌耐药中的作用。
Mol Biol Rep. 2021 Apr;48(4):3813-3825. doi: 10.1007/s11033-021-06314-z. Epub 2021 Apr 15.
8
Pilot Study to Detect Genes Involved in DNA Damage and Cancer in Humans: Potential Biomarkers of Exposure to E-Cigarette Aerosols.人类 DNA 损伤和癌症相关基因的初步研究：电子烟气溶胶暴露的潜在生物标志物。
Genes (Basel). 2021 Mar 22;12(3):448. doi: 10.3390/genes12030448.
9
Distinct mechanisms control genome recognition by p53 at its target genes linked to different cell fates.不同的机制控制着 p53 在与其靶基因的基因组识别，这些靶基因与不同的细胞命运有关。
Nat Commun. 2021 Jan 20;12(1):484. doi: 10.1038/s41467-020-20783-z.
10
at the interface between intermediary metabolism and oncogenesis.在中间代谢与肿瘤发生的界面处。
World J Biol Chem. 2017 Nov 26;8(4):175-186. doi: 10.4331/wjbc.v8.i4.175.
本文引用的文献
1
Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.通过p53 C末端结构域的乙酰化激活p53序列特异性DNA结合。
Cell. 1997 Aug 22;90(4):595-606. doi: 10.1016/s0092-8674(00)80521-8.
2
Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53.野生型p53在缺乏功能性p53的人类肿瘤细胞中触发快速衰老程序。
Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9648-53. doi: 10.1073/pnas.94.18.9648.
3
Protein interactions at the carboxyl terminus of p53 result in the induction of its in vitro transactivation potential.p53羧基末端的蛋白质相互作用导致其体外反式激活潜能的诱导。
Oncogene. 1997 Jul 10;15(2):237-44. doi: 10.1038/sj.onc.1201174.
4
DNA bending is essential for the site-specific recognition of DNA response elements by the DNA binding domain of the tumor suppressor protein p53.DNA弯曲对于肿瘤抑制蛋白p53的DNA结合结构域对DNA反应元件的位点特异性识别至关重要。
J Biol Chem. 1997 Jun 6;272(23):14842-9. doi: 10.1074/jbc.272.23.14842.
5
Architectural accommodation in the complex of four p53 DNA binding domain peptides with the p21/waf1/cip1 DNA response element.四个p53 DNA结合域肽与p21/waf1/cip1 DNA反应元件复合物中的结构适应性
J Biol Chem. 1997 Jun 6;272(23):14830-41. doi: 10.1074/jbc.272.23.14830.
6
p53, the cellular gatekeeper for growth and division.p53，细胞生长和分裂的守门人。
Cell. 1997 Feb 7;88(3):323-31. doi: 10.1016/s0092-8674(00)81871-1.
7
A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis.一种能区分p53反应基因的突变型p53无法诱导细胞凋亡。
Mol Cell Biol. 1996 Sep;16(9):4961-71. doi: 10.1128/MCB.16.9.4961.
8
Differential activation of target cellular promoters by p53 mutants with impaired apoptotic function.具有受损凋亡功能的p53突变体对靶细胞启动子的差异性激活。
Mol Cell Biol. 1996 Sep;16(9):4952-60. doi: 10.1128/MCB.16.9.4952.
9
p53 in growth control and neoplasia.生长控制与肿瘤形成中的p53
Biochim Biophys Acta. 1996 Jun 7;1287(2-3):77-102. doi: 10.1016/0304-419x(95)00019-c.
10
p53: puzzle and paradigm.p53：谜题与范式
Genes Dev. 1996 May 1;10(9):1054-72. doi: 10.1101/gad.10.9.1054.
Zotero 插件