crispr associated protein 9 cas9 expression cassette Search Results


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Addgene inc protein 9 cas9 based chd1 knockout crispr cas9 based chd1 knockout
Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
Protein 9 Cas9 Based Chd1 Knockout Crispr Cas9 Based Chd1 Knockout, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
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Addgene inc cas9 endonuclease dead dcas9
Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
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Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
Streptococcus Pyogenes Cas9 Protein, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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CEM Corporation ccrf-cem cells
Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
Ccrf Cem Cells, supplied by CEM 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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New England Biolabs cas9 protein
Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
Cas9 Protein, supplied by New England Biolabs, 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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Hamamatsu cas9 protein
Figure 3: <t>CHD1</t> deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.
Cas9 Protein, supplied by Hamamatsu, 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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ToolGen Incorporated cas9 protein cas9 wild type nuclease protein with nls

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Santa Cruz Biotechnology protein 9 nuclease crispr cas9 knockout plasmid

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Image Search Results


Figure 3: CHD1 deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.

Journal: Asian journal of andrology

Article Title: CHD1 deletion stabilizes HIF1α to promote angiogenesis and glycolysis in prostate cancer.

doi: 10.4103/aja202287

Figure Lengend Snippet: Figure 3: CHD1 deletion stabilizes HIF1α via PHD2. (a) Expression of key proteins involved in HIF1α degradation in ARCaPE and DU145 cells after CHD1 knockout. (b) PHD2 mRNA levels in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (c) Hydroxylation of HIF1α in ARCaPE and DU145 cells after CHD1 knockout. (d) Luciferase reporter assay of ODD domain degradation in ARCaPE and DU145 cells after CHD1 knockout. *P < 0.05. (e) Diagram of the CRISPR-resistant CHD1 overexpression system. The CRISPR-targeted CHD1 sequence was mutated to escape recognition by the gRNA, but the amino acid sequence was not changed. The mutated CHD1 cDNA was cloned into a lentiviral expression vector. (f) Expression of PHD2 and HIF1α after overexpression of CRISPR-resistant CHD1 in ARCaPE and DU145 cells with CHD1 knockout. HIF1α: hypoxia-inducible factor 1α; CHD1: chromodomain-helicase-DNA-binding protein 1; PHD2: prolyl hydroxylase domain protein 2; ODD: oxygen-dependent degradation; CRISPR: clustered regularly interspaced palindromic repeat; Cas9: CRISPR-associated protein 9; gRNA: guide RNA; cDNA: complementary DNA; KO: knockout; p-eIF2α: phosphorylated eukaryotic translation initiation factor 2 subunit alpha; VHL: von Hippel–Lindau tumor suppressor; IB: immunoblotting; IP: immunoprecipitation.

Article Snippet: Clustered regularly interspaced palindromic repeat (CRISPR)/ CRISPR-associated protein 9 (Cas9)-based CHD1 knockout CRISPR/Cas9-based CHD1 knockout was conducted with a Cas9 lentiviral vector (#71489, Addgene, Watertown, MA, USA) and a guide RNA (gRNA) vector (#84752, Addgene).

Techniques: Expressing, Knock-Out, Luciferase, Reporter Assay, CRISPR, Over Expression, Sequencing, Clone Assay, Plasmid Preparation, Binding Assay, Western Blot, Immunoprecipitation

Journal: eLife

Article Title: Natural variation in C. elegans arsenic toxicity is explained by differences in branched chain amino acid metabolism

doi: 10.7554/eLife.40260

Figure Lengend Snippet:

Article Snippet: Cas9 protein (IDT, 1074182) was injected at 23 µM.

Techniques: Sequencing, Transfection, Construct, Plasmid Preparation