首页> 外文OA文献 >Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer.

【2h】

Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer.

机译：细胞命运因子腊肠犬的乙酰化决定了乳腺癌中的p53结合和信号传导模块。

代理获取

本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。

页面导航

摘要
著录项
相似文献
相关主题

摘要

Breast cancer is a leading form of cancer in the world. The Drosophila Dac gene was cloned as an inhibitor of the hyperactive epidermal growth factor (EGFR), ellipse. Herein, endogenous DACH1 co-localized with p53 in a nuclear, extranucleolar compartment and bound to p53 in human breast cancer cell lines, p53 and DACH1 bound common genes in Chip-Seq. Full inhibition of breast cancer contact-independent growth by DACH1 required p53. The p53 breast cancer mutants R248Q and R273H, evaded DACH1 binding. DACH1 phosphorylation at serine residue (S439) inhibited p53 binding and phosphorylation at p53 amino-terminal sites (S15, S20) enhanced DACH1 binding. DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628. DACH1 repressed p21CIP1 and induced RAD51, an association found in basal breast cancer. DACH1 inhibits breast cancer cellular growth in an NAD and p53-dependent manner through direct protein-protein association.

机译：乳腺癌是世界上癌症的主要形式。果蝇Dac基因被克隆为过度活跃的表皮生长因子（EGFR），椭圆形的抑制剂。在本文中，内源性DACH1与p53共定位于核外核区，并与人乳腺癌细胞系中的p53结合，p53和DACH1结合了Chip-Seq中的共同基因。 DACH1完全抑制乳腺癌接触非依赖性生长需要p53。 p53乳腺癌突变体R248Q和R273H逃避了DACH1的结合。丝氨酸残基处的DACH1磷酸化（S439）抑制了p53结合，而p53氨基末端位点（S15，S20）的磷酸化增强了DACH1的结合。通过DACH1 K628，NAD依赖性脱乙酰基作用抑制DACH1与p53的结合。 DACH1抑制p21CIP1并诱导RAD51，这是在基础乳腺癌中发现的一种关联。 DACH1通过直接的蛋白质-蛋白质结合以NAD和p53依赖性的方式抑制乳腺癌细胞的生长。

著录项

作者
Chen, Ke; Wu, Kongming; Gormley, Michael; Ertel, Adam; Wang, Jing; Zhang, Wei; Zhou, Jie; Disante, Gabriele; Li, Zhiping; Rui, Hallgeir; Quong, Andrew A; McMahon, Steven B; Deng, Haiteng; Lisanti, Michael P; Wang, Chenguang; Pestell, Richard G;
展开▼
作者单位

展开▼
年度 2013
总页数
原文格式 PDF
正文语种 eng
中图分类

相似文献

外文文献
中文文献
专利

1. The Endogenous Cell-Fate Factor Dachshund Restrains Prostate Epithelial Cell Migration via Repression of Cytokine Secretion via a CXCL Signaling Module [J] . Chen Ke, Wu Kongming, Jiao Xuanmao, Cancer research: The official organ of the American Association for Cancer Research, Inc . 2015,第10期

机译：内源性细胞命运因子腊肠犬通过CXCL信号传导模块抑制细胞因子的分泌，抑制前列腺上皮细胞的迁移
2. Cytosolic p53 protein and serum p53 autoantibody evaluation in breast cancer. Comparison with prognostic factors. [J] . Dalifard I, Daver A, Larra F Anticancer Research: International Journal of Cancer Research and Treatment . 1999,第6B期

机译：乳腺癌中的胞浆p53蛋白和血清p53自身抗体评估。与预后因素的比较。
3. Surface loops adjacent to the cation-binding site of the complement factor B von Willebrand factor type A module determine C3b binding specificity. [J] . Tuckwell DS, Xu Y, Newham P, Biochemistry . 1997,第22期

机译：与补体因子B von Willebrand因子A型模块的阳离子结合位点相邻的表面环确定C3b结合特异性。
4. Utilizing Targeted Proteomics to Determine the Factors that influence the Specificity of Rtt109 Histone Acetylation [C] . Yin-Ming Kuo, Ryan A. Henry, Andrew J. Andrews ASMS Conference on Mass Spectrometry and Allied Topics . 2014

机译：利用靶向蛋白质组学来确定影响RTT109组蛋白乙酰化特异性的因素
5. p53 expression and risk factors for breast cancer. [D] . Furberg, Anna Helena. 2001

机译：p53表达和乳腺癌的危险因素。
6. Acetylation of the Cell-Fate Factor Dachshund Determines p53 Binding and Signaling Modules in Breast Cancer [O] . Ke Chen, Kongming Wu, Michael Gormley, 2013

机译：细胞命运因子腊肠犬的乙酰化确定乳腺癌中的p53结合和信号传导模块。
7. Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer. [O] . Chen Ke, Wu Kongming, Gormley Michael, 2013

机译：细胞命运因子腊肠犬的乙酰化决定了乳腺癌中的p53结合和信号传导模块。
8. Role of NF-Kappa B Signaling in X-Box Binding Protein 1 (XBP1)-Mediated Antiestrogen Resistance in Breast Cancer. [R] . R. Hu 2013

机译：NF-κB信号在X-Box结合蛋白1（XBp1）介导的乳腺癌抗雌激素抗性中的作用。

代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

客服微信
服务号