lenticrisprv2 Search Results


92
Addgene inc lenticrisprv2 plasmids

Lenticrisprv2 Plasmids, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc paper n a lenticrisprv2 puro addgene

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Addgene inc lenticrisprv2 hygro

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Addgene inc lenticrispr v2 blast

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Addgene inc plenticrisprv2 backbones carrying neomycin

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95
Addgene inc atg5
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Atg5, supplied by Addgene inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc lenticrisprv2 beclin1 plasmid
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Lenticrisprv2 Beclin1 Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Addgene inc lenticrisprv2 grna plasmid
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Lenticrisprv2 Grna Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc plenticrisprv2 msting grna 1
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Plenticrisprv2 Msting Grna 1, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Addgene inc lenticrisprv2 plasmid 2
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Lenticrisprv2 Plasmid 2, supplied by Addgene inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
Addgene inc lenticrisprv2 plasmid
( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR <t>ATG5</t> KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .
Lenticrisprv2 Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Journal: Cell Reports Medicine

Article Title: CDK12 loss drives prostate cancer progression, transcription-replication conflicts, and synthetic lethality with paralog CDK13

doi: 10.1016/j.xcrm.2024.101758

Figure Lengend Snippet:

Article Snippet: LentiCRISPRv2 Plasmids , – , Addgene Plasmid #107402.

Techniques: Virus, Recombinant, Plasmid Preparation, Blocking Assay, Lysis, Protease Inhibitor, Membrane, Transfection, SYBR Green Assay, Cell Viability Assay, Avidin-Biotin Assay, cDNA Synthesis, Software

( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR ATG5 KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .

Journal: bioRxiv

Article Title: Autophagy is suppressed in peripheral blood mononuclear cells during chronic obstructive pulmonary disease

doi: 10.1101/2024.04.27.591479

Figure Lengend Snippet: ( A ) Basal level LC3B-II observation densities show a near-zero distribution for both groups, while the COPD group exhibited a significant reduction in LC3B-II accumulation with chloroquine (QC), vs the controls. ( B ) A representative blot (n=6 in total) comparing no-treatment and CQ outcomes for LC3B-I/II and Actin-β (ACTB). C ). Measures of autophagic flux (ΔLC3B-II) showed a significant reduction in autophagic competency for the COPD group. ( D ) The LC3B-I/II antibody was validated using protein isolated from 16HBE14o-cells transduced with a CRISPR ATG5 KO construct. As expected, the depletion of ATG5 caused a large reduction in the LC3B-II signal (the lipidated form of LC3B-I), and substantial increases in the LC3B-I and p62/Sequestosome-1 (SQSTM1) signals. Pink-purple color within the LC3B-I and Sequestosome-1/p62 blots indicate signal saturation beyond the linear range determined for these proteins. Outcomes for LC3B-II were normalized to the Actin-β signal. Control, n=16 and COPD, n= 22. “**” denoted P < 0 . 01. Outcomes for the violin graphs were from non-parametric analyses; Wilcoxon matched pairs rank were used when comparing no-treatment and CQ, and Kruskall-Wallis rank test for comparisons between control vs COPD. Violin graphs boxplots show ± standard error and whiskers denote ± 95% CI .

Article Snippet: Briefly, HEK-293T cells were co-transfected with lentivirus construct encoding Cas9 and a sgRNA targeting exon 7 of ATG5 (LentiCRISPRv2- ATG5 ; Addgene, 99573 [ ]; deposited by Edward Campbell), pMDLg/pRRE (Addgene, 12251), pMD2.G (Addgene, 12259), and pRSV-REV (Addgene, 12253) (Packaging vectors deposited by Didier Trono) using Lipofectamine 3000 (ThermoFisher Scientific, L3000150).

Techniques: Isolation, Transduction, CRISPR, Construct