ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53. - Wikidata - awgldk - TriplyDB

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

http://www.wikidata.org/entity/Q39337933

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Tumor-Derived Cell Lines as Molecular Models of Cancer Pharmacogenomics Models incorporating chromatin modification data identify functionally important p53 binding sites Global analysis of p53-regulated transcription identifies its direct targets and unexpected regulatory mechanisms.A Kinase-Independent Role for Cyclin-Dependent Kinase 19 in p53 Response.Pathological unfoldomics of uncontrolled chaos: intrinsically disordered proteins and human diseases Integrated high-throughput analysis identifies Sp1 as a crucial determinant of p53-mediated apoptosis.Bioinformatics-driven discovery of rational combination for overcoming EGFR-mutant lung cancer resistance to EGFR therapy.MDM2, MDMX and p53 in oncogenesis and cancer therapy ATM signalling and cancer.Development of synthetic lethality anticancer therapeutics.Computational methods and opportunities for phosphorylation network medicine Identification of potential synthetic lethal genes to p53 using a computational biology approach K-Map: connecting kinases with therapeutics for drug repurposing and development Wild type p53 reactivation: from lab bench to clinic.edgeR: a versatile tool for the analysis of shRNA-seq and CRISPR-Cas9 genetic screens.ATM regulates cell fate choice upon p53 activation by modulating mitochondrial turnover and ROS levels.Human ACAP2 is a homolog of C. elegans CNT-1 that promotes apoptosis in cancer cells The impact of post-transcriptional regulation in the p53 network.Tetraploidization or autophagy: The ultimate fate of senescent human endometrial stem cells under ATM or p53 inhibition Trisomy 21 consistently activates the interferon response.Tumor protein D52 (TPD52) and cancer-oncogene understudy or understudied oncogene?The kinome 'at large' in cancer.Regulation of the MET oncogene: molecular mechanisms.The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression.p53 induces formation of NEAT1 lncRNA-containing paraspeckles that modulate replication stress response and chemosensitivity.Chemical Inhibition of Wild-Type p53-Induced Phosphatase 1 (WIP1/PPM1D) by GSK2830371 Potentiates the Sensitivity to MDM2 Inhibitors in a p53-Dependent Manner.ZFX knockdown inhibits growth and migration of non-small cell lung carcinoma cell line H1299.Rational combination of a MEK inhibitor, selumetinib, and the Wnt/calcium pathway modulator, cyclosporin A, in preclinical models of colorectal cancer A genetic screen identifies TCF3/E2A and TRIAP1 as pathway-specific regulators of the cellular response to p53 activation.CRISPR-Barcoding for Intratumor Genetic Heterogeneity Modeling and Functional Analysis of Oncogenic Driver Mutations.Identification of a core TP53 transcriptional program with highly distributed tumor suppressive activity SMYD2 lysine methyltransferase regulates leukemia cell growth and regeneration after genotoxic stress Identification of synthetic lethal pairs in biological systems through network information centrality.Activation of the p53 Transcriptional Program Sensitizes Cancer Cells to Cdk7 Inhibitors.A Genome-Wide Loss-of-Function Screen Identifies SLC26A2 as a Novel Mediator of TRAIL Resistance.

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P2860

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

http://www.wikidata.org/entity/Q39337933

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

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2012年學術文章

@zh

2012年學術文章

@zh-hant

name

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@en

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@nl

type

label

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@en

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@nl

prefLabel

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@en

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@nl

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Nature Chemical Biology

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ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.

@en

P2093

Aik Choon Tan

http://www.w3.org/2001/XMLSchema#string

Christopher C Porter

http://www.w3.org/2001/XMLSchema#string

James DeGregori

http://www.w3.org/2001/XMLSchema#string

Jihye Kim

http://www.w3.org/2001/XMLSchema#string

Joaquín M Espinosa

http://www.w3.org/2001/XMLSchema#string

John J Tentler

http://www.w3.org/2001/XMLSchema#string

Kelly D Sullivan

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Nuria Padilla-Just

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Ryan E Henry

http://www.w3.org/2001/XMLSchema#string

S Gail Eckhardt

http://www.w3.org/2001/XMLSchema#string

P2860

PUMA induces the rapid apoptosis of colorectal cancer cells

PUMA, a novel proapoptotic gene, is induced by p53

NEMO and RIP1 control cell fate in response to extensive DNA damage via TNF-α feedforward signaling

The combined status of ATM and p53 link tumor development with therapeutic response

In vivo activation of the p53 pathway by small-molecule antagonists of MDM2

The p53 pathway as a target in cancer therapeutics: obstacles and promise

Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.

Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.

WAF1, a potential mediator of p53 tumor suppression

KILLER/DR5 is a DNA damage-inducible p53-regulated death receptor gene

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646-654

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10.1038/NCHEMBIO.965

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7

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8

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2012-06-03T00:00:00Z

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225097862

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22660439

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3430605

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