dsb stress Search Results


hcs dna damage kit  (Thermo Fisher)
99
Thermo Fisher hcs dna damage kit
A. The absorption spectra at 300–600 nm of the normal cells (GM05757) with/without the 24 hr treatment of 30 and 50 μM EGCG; B. The yield of reductive <t>DNA</t> <t>damage</t> given by the integrated spectral intensity over 300–600 nm. The results show significant enhancements in reductive DNA damage in the cells treated by EGCG.
Hcs Dna Damage Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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inhibitors of dna-dependent protein kinase  (Dohmen GmbH)
90
Dohmen GmbH inhibitors of dna-dependent protein kinase
Coordination of multiple <t>DNA</t> repair pathways in a common DNA ICL repair pathway. (a,b) Stalled replication forks at DNA ICLs are recognized by FANCM-FAAP24-MHF1-MFH2 (FAAPs) or UHRF1. Eviction of the replicative CMG helicase by BRCA1 allows one replication fork to approach the ICLs. (c) FANCM promotes the ATR kinase–dependent checkpoint response. (d) The FA core complex monoubiquitinates the FANCI-FANCD2 (ID2) complex. (e,f) FANCD2-Ub and SLX4/FANCP recruit SSEs to execute the unhooking step, generating DNA DSBs in the strand opposite to the strand on which the cross-linked nucleotide tethers. (g) DNA replication resumes by the bypass step, passing the tethered ICL by TLS polymerases, such as REV1 or Polζ. The USP1-UAF1 complex deubiquitinates the ID2 complex to efficiently execute the FA pathway. (h) The <t>DSB</t> ends are processed to generate single-strand DNA by the initial DSB resection machinery. The processed DSB ends can be repaired by alt-NHEJ. Alternatively, inhibition of end resection leads to direct ligation of the DNA ends by C-NHEJ. (i) Extensive DSB resection by EXO1 and the BLM-DNA2 complex generate longer stretches of RPA-coated ssDNA. (j) RPA is displaced by recombination mediators to load RAD51 to promote HR. (k,l) Alternatively, the repair is diverted to RAD52-mediated SSA. The different consequences of these DSB repair pathways are deletions, insertions, and LOH. The key players of each pathway are shown in the insets. Abbreviations: alt-NHEJ, alternative nonhomologous end joining; C-NHEJ, classical nonhomologous end joining; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; DSB, double-strand break; FA, Fanconi anemia; FAAPs, Fanconi anemia–associated proteins; HR, homologous recombination; ICL, interstrand cross-link; LOH, loss of heterozygosity; SSA, single-strand annealing; ssDNA, single-stranded DNA; SSE, structure-specific endonuclease; TLS, translesion synthesis.
Inhibitors Of Dna Dependent Protein Kinase, supplied by Dohmen GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A. The absorption spectra at 300–600 nm of the normal cells (GM05757) with/without the 24 hr treatment of 30 and 50 μM EGCG; B. The yield of reductive DNA damage given by the integrated spectral intensity over 300–600 nm. The results show significant enhancements in reductive DNA damage in the cells treated by EGCG.

Journal: Scientific Reports

Article Title: Antioxidant Induces DNA Damage, Cell Death and Mutagenicity in Human Lung and Skin Normal Cells

doi: 10.1038/srep03169

Figure Lengend Snippet: A. The absorption spectra at 300–600 nm of the normal cells (GM05757) with/without the 24 hr treatment of 30 and 50 μM EGCG; B. The yield of reductive DNA damage given by the integrated spectral intensity over 300–600 nm. The results show significant enhancements in reductive DNA damage in the cells treated by EGCG.

Article Snippet: The Vybrant 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) Cell Proliferation/viability Assay Kit and the HCS DNA Damage Kit (for DNA DSB measurements) were purchased from Invitrogen.

Techniques:

Intrinsic or exogenous reductive sources, such as antioxidants, ionizing radiation and O 2 − produced in cellular processes, can give rise to weakly-bound electrons, leading to reductive DNA damage, genomic mutations and ultimately diseases (cancer). Thus, abnormal cells such as cancer cells may have a higher level of intrinsic antioxidants. Simultaneously, abnormal (cancer) cells may activate protective mechanisms to balance the detrimental effects of chronically high antioxidant levels and therefore have some resistance to exogenous antioxidants especially at low levels.

Journal: Scientific Reports

Article Title: Antioxidant Induces DNA Damage, Cell Death and Mutagenicity in Human Lung and Skin Normal Cells

doi: 10.1038/srep03169

Figure Lengend Snippet: Intrinsic or exogenous reductive sources, such as antioxidants, ionizing radiation and O 2 − produced in cellular processes, can give rise to weakly-bound electrons, leading to reductive DNA damage, genomic mutations and ultimately diseases (cancer). Thus, abnormal cells such as cancer cells may have a higher level of intrinsic antioxidants. Simultaneously, abnormal (cancer) cells may activate protective mechanisms to balance the detrimental effects of chronically high antioxidant levels and therefore have some resistance to exogenous antioxidants especially at low levels.

Article Snippet: The Vybrant 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) Cell Proliferation/viability Assay Kit and the HCS DNA Damage Kit (for DNA DSB measurements) were purchased from Invitrogen.

Techniques: Produced

Coordination of multiple DNA repair pathways in a common DNA ICL repair pathway. (a,b) Stalled replication forks at DNA ICLs are recognized by FANCM-FAAP24-MHF1-MFH2 (FAAPs) or UHRF1. Eviction of the replicative CMG helicase by BRCA1 allows one replication fork to approach the ICLs. (c) FANCM promotes the ATR kinase–dependent checkpoint response. (d) The FA core complex monoubiquitinates the FANCI-FANCD2 (ID2) complex. (e,f) FANCD2-Ub and SLX4/FANCP recruit SSEs to execute the unhooking step, generating DNA DSBs in the strand opposite to the strand on which the cross-linked nucleotide tethers. (g) DNA replication resumes by the bypass step, passing the tethered ICL by TLS polymerases, such as REV1 or Polζ. The USP1-UAF1 complex deubiquitinates the ID2 complex to efficiently execute the FA pathway. (h) The DSB ends are processed to generate single-strand DNA by the initial DSB resection machinery. The processed DSB ends can be repaired by alt-NHEJ. Alternatively, inhibition of end resection leads to direct ligation of the DNA ends by C-NHEJ. (i) Extensive DSB resection by EXO1 and the BLM-DNA2 complex generate longer stretches of RPA-coated ssDNA. (j) RPA is displaced by recombination mediators to load RAD51 to promote HR. (k,l) Alternatively, the repair is diverted to RAD52-mediated SSA. The different consequences of these DSB repair pathways are deletions, insertions, and LOH. The key players of each pathway are shown in the insets. Abbreviations: alt-NHEJ, alternative nonhomologous end joining; C-NHEJ, classical nonhomologous end joining; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; DSB, double-strand break; FA, Fanconi anemia; FAAPs, Fanconi anemia–associated proteins; HR, homologous recombination; ICL, interstrand cross-link; LOH, loss of heterozygosity; SSA, single-strand annealing; ssDNA, single-stranded DNA; SSE, structure-specific endonuclease; TLS, translesion synthesis.

Journal: Annual review of cancer biology

Article Title: The Fanconi Anemia Pathway in Cancer

doi: 10.1146/annurev-cancerbio-030617-050422

Figure Lengend Snippet: Coordination of multiple DNA repair pathways in a common DNA ICL repair pathway. (a,b) Stalled replication forks at DNA ICLs are recognized by FANCM-FAAP24-MHF1-MFH2 (FAAPs) or UHRF1. Eviction of the replicative CMG helicase by BRCA1 allows one replication fork to approach the ICLs. (c) FANCM promotes the ATR kinase–dependent checkpoint response. (d) The FA core complex monoubiquitinates the FANCI-FANCD2 (ID2) complex. (e,f) FANCD2-Ub and SLX4/FANCP recruit SSEs to execute the unhooking step, generating DNA DSBs in the strand opposite to the strand on which the cross-linked nucleotide tethers. (g) DNA replication resumes by the bypass step, passing the tethered ICL by TLS polymerases, such as REV1 or Polζ. The USP1-UAF1 complex deubiquitinates the ID2 complex to efficiently execute the FA pathway. (h) The DSB ends are processed to generate single-strand DNA by the initial DSB resection machinery. The processed DSB ends can be repaired by alt-NHEJ. Alternatively, inhibition of end resection leads to direct ligation of the DNA ends by C-NHEJ. (i) Extensive DSB resection by EXO1 and the BLM-DNA2 complex generate longer stretches of RPA-coated ssDNA. (j) RPA is displaced by recombination mediators to load RAD51 to promote HR. (k,l) Alternatively, the repair is diverted to RAD52-mediated SSA. The different consequences of these DSB repair pathways are deletions, insertions, and LOH. The key players of each pathway are shown in the insets. Abbreviations: alt-NHEJ, alternative nonhomologous end joining; C-NHEJ, classical nonhomologous end joining; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; DSB, double-strand break; FA, Fanconi anemia; FAAPs, Fanconi anemia–associated proteins; HR, homologous recombination; ICL, interstrand cross-link; LOH, loss of heterozygosity; SSA, single-strand annealing; ssDNA, single-stranded DNA; SSE, structure-specific endonuclease; TLS, translesion synthesis.

Article Snippet: Of the DSB DNA damage response proteins, inhibitors of DNA-dependent protein kinase, ATM, and ATR are in early-phase clinical trials ( Dohmen et al. 2017 , Dong et al. 2017 , Kondrashova et al. 2017 ).

Techniques: Inhibition, Ligation, Homologous Recombination, Translesion Synthesis