Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence. - Wikidata - awgldk - TriplyDB

Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence.

Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence.

http://www.wikidata.org/entity/Q39631945

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MTH1 inhibition eradicates cancer by preventing sanitation of the dNTP pool Crystal structure of human MTH1 and the 8-oxo-dGMP product complex Stereospecific targeting of MTH1 by (S)-crizotinib as an anticancer strategy Crystal structure, biochemical and cellular activities demonstrate separate functions of MTH1 and MTH2 Proteomic profiling of small-molecule inhibitors reveals dispensability of MTH1 for cancer cell survival (1)H NMR studies distinguish the water soluble metabolomic profiles of untransformed and RAS-transformed cells Oxidative stress-induced apoptosis in granulosa cells involves JNK, p53 and Puma A Chimeric ATP-Linked Nucleotide Enables Luminescence Signaling of Damage Surveillance by MTH1, a Cancer Target.Cancer therapy. Targeting the poison within.Creation and validation of a ligation-independent cloning (LIC) retroviral vector for stable gene transduction in mammalian cells MTH1 as a Chemotherapeutic Target: The Elephant in the Room.MutT Homolog 1 (MTH1) maintains multiple KRAS-driven pro-malignant pathways.RAS transformation requires CUX1-dependent repair of oxidative DNA damage.Human dCTP pyrophosphatase 1 promotes breast cancer cell growth and stemness through the modulation on 5-methyl-dCTP metabolism and global hypomethylation.Lamin B1 loss is a senescence-associated biomarker.Human Mut T Homolog 1 (MTH1): a roadblock for the tumor-suppressive effects of oncogenic RAS-induced ROS.Echinacoside induces apoptotic cancer cell death by inhibiting the nucleotide pool sanitizing enzyme MTH1.Physiological and pathological consequences of cellular senescence.The druggability of intracellular nucleotide-degrading enzymes.Human MutT homologue 1 mRNA overexpression correlates to poor response of multiple myeloma.MTH1 expression is required for effective transformation by oncogenic HRAS.Myc and Ras oncogenes engage different energy metabolism programs and evoke distinct patterns of oxidative and DNA replication stress.Src homology domain-containing phosphatase 2 suppresses cellular senescence in glioblastoma.Progression of genotype-specific oral cancer leads to senescence of cancer-associated fibroblasts and is mediated by oxidative stress and TGF-β.Ras-induced ROS upregulation affecting cell proliferation is connected with cell type-specific alterations of HSF1/SESN3/p21Cip1/WAF1 pathways.Parallel pathways in RAF-induced senescence and conditions for its reversion.Chenodeoxycholic Acid Derivative HS-1200 Inhibits Hepatocarcinogenesis and Improves Liver Function in Diethylnitrosamine-Exposed Rats by Downregulating MTH1.MTH1 counteracts oncogenic oxidative stress.Substrate ambiguity among the nudix hydrolases: biologically significant, evolutionary remnant, or both?Thioredoxin-1 protects against androgen receptor-induced redox vulnerability in castration-resistant prostate cancer.Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence.Anticancer effect of (S)-crizotinib on osteosarcoma cells by targeting MTH1 and activating reactive oxygen species.Identification and structure-activity relationship of purine derivatives as novel MTH1 inhibitors.Cancer: Damage prevention targeted.Cystathionase mediates senescence evasion in melanocytes and melanoma cells.MTH1 deficiency selectively increases non-cytotoxic oxidative DNA damage in lung cancer cells: more bad news than good?A patient-derived xenograft pre-clinical trial reveals treatment responses and a resistance mechanism to karonudib in metastatic melanoma In-vitro evaluation of apoptotic effect of OEO and thymol in 2D and 3D cell cultures and the study of their interaction mode with DNA

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Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence.

http://www.wikidata.org/entity/Q39631945

description

2010 nî lūn-bûn

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name

Enhanced elimination of oxidiz ...... mage and premature senescence.

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Enhanced elimination of oxidiz ...... mage and premature senescence.

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Enhanced elimination of oxidiz ...... mage and premature senescence.

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Enhanced elimination of oxidiz ...... mage and premature senescence.

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Enhanced elimination of oxidiz ...... mage and premature senescence.

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D G A Burton

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J J Young

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M G Giribaldi

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P Rai

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R A Weinberg

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P2860

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Hydroxylation of deoxyguanosine at the C-8 position by ascorbic acid and other reducing agents

Diversity of gene expression in adenocarcinoma of the lung

Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?

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

Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability

Mechanism of guanine-specific DNA damage by oxidative stress and its role in carcinogenesis and aging.

Synthetic lethal screening identifies compounds activating iron-dependent, nonapoptotic cell death in oncogenic-RAS-harboring cancer cells.

Carcinogen-specific mutation and amplification of Ha-ras during mouse skin carcinogenesis.

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