a p chk2 thr 68 Search Results


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Artemis is not involved in established G2/M checkpoint pathways. Where not indicated, the IR dose was 20 Gy and the UV dose was 50 J/m2. All experiments were performed 2 h after irradiation. (A) Phosphorylation of Chk1 (phospho-Ser345) and <t>Chk2</t> <t>(phospho-Thr68)</t> are unaffected in Artemis-depleted cells after IR or UV irradiation. UT, untreated cells; LC, loading control. (B) Phosphorylation of H2AX is unaffected in Artemis-depleted cells. Numbers shown after the indicated treatment specify the dosage in grays (IR) or joules per square meter (UV). (C) Phosphorylation of Artemis is unaffected in Rad17-depleted cells. Depletion of Rad17 in RAD17flox/− cells is shown after infection with adenovirus expressing Cre recombinase. (D) Phosphorylation of Artemis is unaffected in 53BP1-depleted cells.
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Artemis is not involved in established G2/M checkpoint pathways. Where not indicated, the IR dose was 20 Gy and the UV dose was 50 J/m2. All experiments were performed 2 h after irradiation. (A) Phosphorylation of Chk1 (phospho-Ser345) and <t>Chk2</t> <t>(phospho-Thr68)</t> are unaffected in Artemis-depleted cells after IR or UV irradiation. UT, untreated cells; LC, loading control. (B) Phosphorylation of H2AX is unaffected in Artemis-depleted cells. Numbers shown after the indicated treatment specify the dosage in grays (IR) or joules per square meter (UV). (C) Phosphorylation of Artemis is unaffected in Rad17-depleted cells. Depletion of Rad17 in RAD17flox/− cells is shown after infection with adenovirus expressing Cre recombinase. (D) Phosphorylation of Artemis is unaffected in 53BP1-depleted cells.
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List of primary antibodies, their sources, dilutions and molecular weights.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and <t>p-Chk2</t> in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.
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Image Search Results


Artemis is not involved in established G2/M checkpoint pathways. Where not indicated, the IR dose was 20 Gy and the UV dose was 50 J/m2. All experiments were performed 2 h after irradiation. (A) Phosphorylation of Chk1 (phospho-Ser345) and Chk2 (phospho-Thr68) are unaffected in Artemis-depleted cells after IR or UV irradiation. UT, untreated cells; LC, loading control. (B) Phosphorylation of H2AX is unaffected in Artemis-depleted cells. Numbers shown after the indicated treatment specify the dosage in grays (IR) or joules per square meter (UV). (C) Phosphorylation of Artemis is unaffected in Rad17-depleted cells. Depletion of Rad17 in RAD17flox/− cells is shown after infection with adenovirus expressing Cre recombinase. (D) Phosphorylation of Artemis is unaffected in 53BP1-depleted cells.

Journal:

Article Title: Artemis Is a Phosphorylation Target of ATM and ATR and Is Involved in the G 2 /M DNA Damage Checkpoint Response

doi: 10.1128/MCB.24.20.9207-9220.2004

Figure Lengend Snippet: Artemis is not involved in established G2/M checkpoint pathways. Where not indicated, the IR dose was 20 Gy and the UV dose was 50 J/m2. All experiments were performed 2 h after irradiation. (A) Phosphorylation of Chk1 (phospho-Ser345) and Chk2 (phospho-Thr68) are unaffected in Artemis-depleted cells after IR or UV irradiation. UT, untreated cells; LC, loading control. (B) Phosphorylation of H2AX is unaffected in Artemis-depleted cells. Numbers shown after the indicated treatment specify the dosage in grays (IR) or joules per square meter (UV). (C) Phosphorylation of Artemis is unaffected in Rad17-depleted cells. Depletion of Rad17 in RAD17flox/− cells is shown after infection with adenovirus expressing Cre recombinase. (D) Phosphorylation of Artemis is unaffected in 53BP1-depleted cells.

Article Snippet: Polyclonal antibodies for phosphorylated Chk1 (phospho-Chk1) (Ser345) and phospho-Chk2 (Thr68) and a monoclonal antibody for phospho-histone H3 (P-H3) (Ser10) were purchased from Cell Signaling.

Techniques: Irradiation, Infection, Expressing

List of primary antibodies, their sources, dilutions and molecular weights.

Journal: Leukemia & lymphoma

Article Title: Synergistic cytotoxicity of busulfan, melphalan, gemcitabine, panobinostat, and bortezomib in lymphoma cells

doi: 10.3109/10428194.2016.1157871

Figure Lengend Snippet: List of primary antibodies, their sources, dilutions and molecular weights.

Article Snippet: The primary antibodies, their sources, dilutions, and antigen molecular weights are listed in (Supplementary Materials). table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antibodies Source (Catalogue #) Clone type Dilutions Molecular weight (kDa) AcH3K9 Active Motif/39137 pAb 3500 17 AKT Cell Signaling/4691 pAb 2000 60 ATM Santa Cruz/23921 mAb 800 250 BCL-2 DAKO/124 mAb 1500 26 c-MYC Cell Signaling/9402 pAb 2500 57–70 Cleaved Caspase 3 Cell Signaling/9661 pAb 2000 17,19 Caspase 8 Cell Signaling/9746 mAb 2000 43 Caspase 9 Cell Signaling/9502 pAb 2000 35–47 CHK2 Cell Signaling/2662 pAb 1000 62 HDAC4 Cell Signaling/5392 mAb 3000 140 KAP1 Bethyl Lab A300-275A pAb 2500 100–117 MCL-1 Santa Cruz/819 pAb 700 40 mTOR Cell Signaling/2983 pAb 2500 289 NOXA Calbiochem/0180 mAb 1500 15 p-ATM (Ser1981) Rockland/200–301-400 mAb 2000 250 p-AKT (Ser 473) Cell Signaling/4060 pAb 2500 60 p-CHK2 (Thr68) Cell Signaling/2661 pAb 2000 62 p-KAP1 (Ser824) Cell Signaling/4127 pAb 2500 100 p-mTOR (Ser2448) Cell Signaling/5536 pAb 1500 289 p-P53 (Ser 15) Cell Signaling/9284 pAb 2000 53 p-PI3K (Tyr199/Tyr458) Cell Signaling /4228 pAb 2500 60, 85 p-SMC1 (Ser957) Novus Biologicals/100–205 pAb 1500 140 P53 Santa Cruz/126 pAb 2000 53 PARP1 Santa Cruz /8007 mAb 1000 116 PI3K Santa Cruz/423 pAb 500 85 SMC1 Cell Signaling/4802 pAb 2500 140 XIAP Cell Signaling/2045 pAb 2000 53 α-Tubulin Cell Signaling/2144 pAb 1000 57 β-ACTIN Sigma/A5316 mAb 10000 42 γ-H2AX Millipore/2554898 mAb 3000 15 3MeH3K27 Active Motif/39155 pAb 3500 17 Open in a separate window List of primary antibodies, their sources, dilutions and molecular weights.

Techniques: Molecular Weight

HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and p-Chk2 in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.

Journal: Biochemical pharmacology

Article Title: Mechanisms of tolvaptan-induced toxicity in HepG2 cells

doi: 10.1016/j.bcp.2015.03.015

Figure Lengend Snippet: HepG2 cells were treated with tolvaptan (0–100 μM) for 24 or 48 h. (A) Tail moment in alkaline comet assays with or without post-incubation with Fpg. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (B) Relative levels of 8-oxoguanine and (C) ROS in the HepG2 cells treated with tolvaptan. The results shown are the mean and standard deviation of three independent experiments. * Significantly (p < 0.05) different from 0 μM tolvaptan. (D) Representative Western blot images of γ-H2AX, p-Chk1, and p-Chk2 in the HepG2 cells treated with tolvaptan. β-Actin was used as a loading control.

Article Snippet: Mouse monoclonal antibodies against cyclin D1, cyclin D3, cyclin-dependent kinase (CDK) 4 (CDK4), and CDK6, rabbit monoclonal antibodies against CDK2, phosphorylated checkpoint kinase 1 at Ser345 (p-Chk1), Bcl-2, Bad, Bim, Bax, phosphorylated-ERK1/2 at Thr202/Tyr204 (p-ERK1/2), ERK1/2, phosphorylated-JNK at Thr183/Tyr185 (p-JNK), JNK, phosphorylated-p38 at Thr180/Tyr182 (p-p38), and p38, and rabbit polyclonal antibodies against phosphorylated checkpoint kinase 2 at Thr68 (p-Chk2), cytochrome C, and Bid were purchased from Cell Signaling Technology (Danvers, MA).

Techniques: Incubation, Standard Deviation, Western Blot