The repression of oncoprotein SET by the tumor suppressor p53 reveals a p53-SET-PP2A feedback loop for cancer therapy
出版年份 2022 全文链接
标题
The repression of oncoprotein SET by the tumor suppressor p53 reveals a p53-SET-PP2A feedback loop for cancer therapy
作者
关键词
-
出版物
Science China-Life Sciences
Volume -, Issue -, Pages -
出版商
Springer Science and Business Media LLC
发表日期
2022-07-26
DOI
10.1007/s11427-021-2123-8
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- The interaction of SET and protein phosphatase 2A as target for cancer therapy
- (2021) E.C. Dacol et al. BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
- Loss of SET reveals both the p53-dependent and the p53-independent functions in vivo
- (2019) Ning Kon et al. Cell Death & Disease
- The multiple mechanisms that regulate p53 activity and cell fate
- (2019) Antonina Hafner et al. NATURE REVIEWS MOLECULAR CELL BIOLOGY
- Inhibition of p53 and/or AKT as a new therapeutic approach specifically targeting ALT cancers
- (2019) Yuanlong Ge et al. Protein & Cell
- A comprehensive and perspective view of oncoprotein SET in cancer
- (2018) Buuvee Bayarkhangai et al. Cancer Medicine
- Targeting PP2A in cancer: Combination therapies
- (2018) Sahar Mazhar et al. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
- Overexpression of SET oncoprotein is associated with tumor progression and poor prognosis in human gastric cancer
- (2017) Xiaoning Yuan et al. ONCOLOGY REPORTS
- The “readers” of unacetylated p53 represent a new class of acidic domain proteins
- (2017) Donglai Wang et al. Nucleus
- The “readers” of unacetylated p53 represent a new class of acidic domain proteins
- (2017) Donglai Wang et al. Nucleus
- Acetylation-regulated interaction between p53 and SET reveals a widespread regulatory mode
- (2016) Donglai Wang et al. NATURE
- Upregulation of the oncoprotein SET determines poor clinical outcomes in hepatocellular carcinoma and shows therapeutic potential
- (2016) M-H Hung et al. ONCOGENE
- Overexpression of PP2A inhibitor SET oncoprotein is associated with tumor progression and poor prognosis in human non-small cell lung cancer
- (2015) Hao Liu et al. Oncotarget
- Stable SET knockdown in head and neck squamous cell carcinoma promotes cell invasion and the mesenchymal-like phenotype in vitro, as well as necrosis, cisplatin sensitivity and lymph node metastasis in xenograft tumor models
- (2014) Lays M Sobral et al. Molecular Cancer
- Targeting c-MYC by antagonizing PP2A inhibitors in breast cancer
- (2014) M. Janghorban et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Ser9 phosphorylation causes cytoplasmic detention of I2PP2A/SET in Alzheimer disease
- (2013) Guang Yu et al. NEUROBIOLOGY OF AGING
- Genome-wide profiling reveals stimulus-specific functions of p53 during differentiation and DNA damage of human embryonic stem cells
- (2013) Kadir C. Akdemir et al. NUCLEIC ACIDS RESEARCH
- Sphingosine analogue drug FTY720 targets I2PP2A/SET and mediates lung tumour suppression via activation of PP2A-RIPK1-dependent necroptosis
- (2012) Sahar A. Saddoughi et al. EMBO Molecular Medicine
- Fingolimod for Multiple Sclerosis
- (2012) Daniel Pelletier et al. NEW ENGLAND JOURNAL OF MEDICINE
- Overexpression of SET is a recurrent event associated with poor outcome and contributes to protein phosphatase 2A inhibition in acute myeloid leukemia
- (2011) I. Cristobal et al. HAEMATOLOGICA
- Inhibition of p53 acetylation by INHAT subunit SET/TAF-Iβ represses p53 activity
- (2011) Ji-Young Kim et al. NUCLEIC ACIDS RESEARCH
- Targeting SET/I2PP2A oncoprotein functions as a multi-pathway strategy for cancer therapy
- (2011) C H Switzer et al. ONCOGENE
- ATM-mediated phosphorylation activates the tumor-suppressive function of B56γ–PP2A
- (2011) G P Shouse et al. ONCOGENE
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExploreAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started