dna damage repair markers Search Results


92
TargetMol dna damage
Chemical screen of <t>DNA</t> <t>damage</t> response inhibitors in KRAS mutant lung cancer cell. (A) Representative Western blot results. VE822 is a known ATR inhibitor. (B) Screening results. Each dot represents one compound. The value represents pCHK1/CHK1 ratio normalized to that of CPT only and are presented in log2 scale. Zero represents that of CPT. (C) A549 cells were pre-, co- or 1 h post-treated with 500 nM AT2, AT3 or TP4 with 500 nM CPT for 4 h, and protein levels of pCHK1 and CHK1 were analyzed. Ponceau S staining indicates equal protein loading. (D) A549 cells were pre-treated with 500 nM AT2 for 2 h, added 500 nM CPT for 1, 2 and 8 h, and levels of pCHK1 and CHK1 were examined. (E) A549 cells were pre-treated with different concentrations of AT2 for 2 h, added 500 nM CPT for another 4 h, and protein expression was examined using indicated antibodies. Lower: levels of pCHK1 normalized to total CHK1 from 5 independent experiments were used to determine the IC50 of AT2. (F) A549 cells were transfected with siRNA control or targeting the α1 subunit of Na/K-ATPase for 48 h, treated with 500 nM AT2 for 2 h, added 200 nM CPT for another 4 h, and protein expression was examined. Relative pCHK1 levels are shown above.
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Selleck Chemicals dna damage repair
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Dna Damage Repair, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SuperArray Bioscience Corporation ge array q series human dna damage and repair signaling pathway cdna expression array membranes
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Ge Array Q Series Human Dna Damage And Repair Signaling Pathway Cdna Expression Array Membranes, supplied by SuperArray Bioscience Corporation, 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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Verlag GmbH free-radical-induced dna damage and its repair
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Free Radical Induced Dna Damage And Its Repair, supplied by Verlag 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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Immunome Inc dna damage repair (ddr) score
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
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Abbott Laboratories transcription-coupled repair of oxidative dna damage
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
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Verlag GmbH free-radical induced dna damage and its repair: a chemical perspective
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Free Radical Induced Dna Damage And Its Repair: A Chemical Perspective, supplied by Verlag 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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Myriad Genetics mutational status and loh determination for genes involved in dna damage and repair
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Mutational Status And Loh Determination For Genes Involved In Dna Damage And Repair, supplied by Myriad Genetics, 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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MyBiosource Biotechnology p53 dna-damage markers
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
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Invitae Inc dna damage repair panel
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Dna Damage Repair Panel, supplied by Invitae Inc, 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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Hao Wen Holdings dna damage repair (ddr) network
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
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Bydgoszcz dna damage markers
Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to <t>DNA</t> <t>damage</t> reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-
Dna Damage Markers, supplied by Bydgoszcz, 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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Image Search Results


Chemical screen of DNA damage response inhibitors in KRAS mutant lung cancer cell. (A) Representative Western blot results. VE822 is a known ATR inhibitor. (B) Screening results. Each dot represents one compound. The value represents pCHK1/CHK1 ratio normalized to that of CPT only and are presented in log2 scale. Zero represents that of CPT. (C) A549 cells were pre-, co- or 1 h post-treated with 500 nM AT2, AT3 or TP4 with 500 nM CPT for 4 h, and protein levels of pCHK1 and CHK1 were analyzed. Ponceau S staining indicates equal protein loading. (D) A549 cells were pre-treated with 500 nM AT2 for 2 h, added 500 nM CPT for 1, 2 and 8 h, and levels of pCHK1 and CHK1 were examined. (E) A549 cells were pre-treated with different concentrations of AT2 for 2 h, added 500 nM CPT for another 4 h, and protein expression was examined using indicated antibodies. Lower: levels of pCHK1 normalized to total CHK1 from 5 independent experiments were used to determine the IC50 of AT2. (F) A549 cells were transfected with siRNA control or targeting the α1 subunit of Na/K-ATPase for 48 h, treated with 500 nM AT2 for 2 h, added 200 nM CPT for another 4 h, and protein expression was examined. Relative pCHK1 levels are shown above.

Journal: Cancer letters

Article Title: Targeting UHRF1-dependent DNA repair selectively sensitizes KRAS mutant lung cancer to chemotherapy

doi: 10.1016/j.canlet.2020.08.008

Figure Lengend Snippet: Chemical screen of DNA damage response inhibitors in KRAS mutant lung cancer cell. (A) Representative Western blot results. VE822 is a known ATR inhibitor. (B) Screening results. Each dot represents one compound. The value represents pCHK1/CHK1 ratio normalized to that of CPT only and are presented in log2 scale. Zero represents that of CPT. (C) A549 cells were pre-, co- or 1 h post-treated with 500 nM AT2, AT3 or TP4 with 500 nM CPT for 4 h, and protein levels of pCHK1 and CHK1 were analyzed. Ponceau S staining indicates equal protein loading. (D) A549 cells were pre-treated with 500 nM AT2 for 2 h, added 500 nM CPT for 1, 2 and 8 h, and levels of pCHK1 and CHK1 were examined. (E) A549 cells were pre-treated with different concentrations of AT2 for 2 h, added 500 nM CPT for another 4 h, and protein expression was examined using indicated antibodies. Lower: levels of pCHK1 normalized to total CHK1 from 5 independent experiments were used to determine the IC50 of AT2. (F) A549 cells were transfected with siRNA control or targeting the α1 subunit of Na/K-ATPase for 48 h, treated with 500 nM AT2 for 2 h, added 200 nM CPT for another 4 h, and protein expression was examined. Relative pCHK1 levels are shown above.

Article Snippet: Chemical library screen The chemical library contains 874 compounds from both the Institute of Traditional Chinese Medicine and the DNA damage and repair library from TargetMol (#L3900) ( Supplementary Table S1 ).

Techniques: Mutagenesis, Western Blot, Staining, Expressing, Transfection

Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to DNA damage reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-

Journal: Molecular oncology

Article Title: PTEN-mediated dephosphorylation of 53BP1 confers cellular resistance to DNA damage in cancer cells.

doi: 10.1002/1878-0261.13563

Figure Lengend Snippet: Fig. 7. Blocking PTEN SUMOylation pathway sensitizes tumor cells to DNA damage reagents. (A–C) DU145-PTEN/ and PTENWT cells were treated with or without different doses of Cisplatin for 3 days, Zeocin for 2 days or CPT for 2 days and then cultured for another 7– 10 days. Colony number was counted and presented as bar graph. (D) DU145-PTEN/, PTENWT, PTENK254R and PTENK266R cells were trea- ted with or without TAK981 (100 nM) for 3 days and cultured for another 7–10 days. Total intensity of stained colony was measured by IMA-

Article Snippet: Ni2+-NTA pull down for SUMOylation assay For the detection of PTEN SUMOylation during DNA damage repair, 293T cells were transfected with His-SUMO1 and indicated plasmids for 48 h. CPT (#S1288, Selleck, Houston, TX, USA) and Zeocin (#60216ES80, Yeasen) were used to induce DNA damage for 1 h. cells were harvested at indicated time, 10% cells were used as input.

Techniques: Blocking Assay, Cell Culture, Staining