Nucleotide deficiency promotes genomic instability in early stages of cancer development - Wikidata - wikimedia - TriplyDB

Nucleotide deficiency promotes genomic instability in early stages of cancer development

Nucleotide deficiency promotes genomic instability in early stages of cancer development

http://www.wikidata.org/entity/Q37087191

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FBH1 co-operates with MUS81 in inducing DNA double-strand breaks and cell death following replication stress Cyclin F-mediated degradation of ribonucleotide reductase M2 controls genome integrity and DNA repair Unbalanced replication as a major source of genetic instability in cancer cells Targeting DNA Replication Stress for Cancer Therapy One-Carbon Metabolism in Prostate Cancer: The Role of Androgen Signaling Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies Ribosomopathies: how a common root can cause a tree of pathologies Regulation of deoxynucleotide metabolism in cancer: novel mechanisms and therapeutic implications Network calisthenics: control of E2F dynamics in cell cycle entry Twists in views on RB functions in cellular signaling, metabolism and stem cells Serine, glycine and one-carbon units: cancer metabolism in full circle Ataxia-telangiectasia: future prospects RB1: a prototype tumor suppressor and an enigma The multiple connections between pRB and cell metabolism Molecular mechanisms underlying RB protein function Genetically-defined metabolic reprogramming in cancer Autophagy-mediated tumor promotion Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response The Role of the DNA Damage Response throughout the Papillomavirus Life Cycle Replication stress in Mammalian cells and its consequences for mitosis Polymerase δ replicates both strands after homologous recombination-dependent fork restart Initiation of genome instability and preneoplastic processes through loss of Fhit expression SIRT4 has tumor-suppressive activity and regulates the cellular metabolic response to DNA damage by inhibiting mitochondrial glutamine metabolism Loss of RBF1 changes glutamine catabolism DNA replication stress mediates APOBEC3 family mutagenesis in breast cancer Spontaneous slow replication fork progression elicits mitosis alterations in homologous recombination-deficient mammalian cells.Immortalised breast epithelia survive prolonged DNA replication stress and return to cycle from a senescent-like state.N-Aroyl indole thiobarbituric acids as inhibitors of DNA repair and replication stress response polymerases.Papillomavirus genomes associate with BRD4 to replicate at fragile sites in the host genome.Yeast DNA polymerase ζ maintains consistent activity and mutagenicity across a wide range of physiological dNTP concentrations Ribonucleotide Reductase Requires Subunit Switching in Hypoxia to Maintain DNA Replication Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control.Ssb1 and Ssb2 cooperate to regulate mouse hematopoietic stem and progenitor cells by resolving replicative stress.MYC and the control of DNA replication.Break-induced replication repair of damaged forks induces genomic duplications in human cells.Human papilloma virus E7 oncoprotein abrogates the p53-p21-DREAM pathway.Induction of homologous recombination following in utero exposure to DNA-damaging agents.PP2A-B55β antagonizes cyclin E1 proteolysis and promotes its dysregulation in cancer.Expression of the HPV18/E6 oncoprotein induces DNA damage.The role of the DNA damage response in zebrafish and cellular models of Diamond Blackfan anemia.

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Nucleotide deficiency promotes genomic instability in early stages of cancer development

http://www.wikidata.org/entity/Q37087191

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on April 2011

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Nucleotide deficiency promotes genomic instability in early stages of cancer development

@en

Nucleotide deficiency promotes genomic instability in early stages of cancer development.

@nl

type

label

Nucleotide deficiency promotes genomic instability in early stages of cancer development

@en

Nucleotide deficiency promotes genomic instability in early stages of cancer development.

@nl

prefLabel

Nucleotide deficiency promotes genomic instability in early stages of cancer development

@en

Nucleotide deficiency promotes genomic instability in early stages of cancer development.

@nl

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J.CELL.2011.03.044

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P1476

Nucleotide deficiency promotes genomic instability in early stages of cancer development

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Aaron Bensimon

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Assaf C Bester

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Batsheva Kerem

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Dan Sarni

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Donna S Shewach

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Gideon Zamir

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Maayan Roniger

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Malka Chaoat

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Michael M Im

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Yifat S Oren

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P2860

Replication fork velocities at adjacent replication origins are coordinately modified during DNA replication in human cells

DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139

A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage

The Myc/Max/Mad network and the transcriptional control of cell behavior

Characterization of homologous recombination induced by replication inhibition in mammalian cells

Impaired function of p53R2 in Rrm2b-null mice causes severe renal failure through attenuation of dNTP pools

Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions

DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis

Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

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435-446

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scholarly article

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10.1016/J.CELL.2011.03.044

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3

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145

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2011-04-01T00:00:00Z

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51086040

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21529715

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3740329

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