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human kinome crispr pooled library  (Addgene inc)


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    Addgene inc human kinome crispr pooled library
    Human Kinome Crispr Pooled Library, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+kinome+crispr+knockout+library+brunello/Human+Kinome+CRISPR+Knockout+Library+(Brunello)+(Pooled+Libraries+%2375312%2C+%2375313%2C+%2375314%2C+%2375315%2C+%231000000082%2C+%231000000083)/pmc12730985-5-8-15
    Average 93 stars, based on 22 article reviews
    human kinome crispr pooled library - by Bioz Stars, 2026-09
    93/100 stars

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    CRISPR:

    Article Title: Loss of JAK1 Function Causes G2/M Cell Cycle Defects Vulnerable to Kif18a Inhibition
    Article Snippet: Lentivirus was produced as above, and cells were transduced followed by Puromycin (Gibco Cat# A11138-03) selection. gRNA sequences are listed in Supplemental Table 2. .. The Human Kinome CRISPR Knockout Library (Brunello) was purchased from Addgene (# 1000000082) and was generated as previously described . .. Library amplification and sequencing were performed according to the manufacturer’s protocol (Addgene/Broad Institute).

    Article Title: Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting RLoop Accumulation and DNA Repair Deficiencies.
    Article Snippet: .. Human kinome CRISPR knockout library (Brunello) was obtained from Addgene (#73179) and was packaged into lentivirus. ..

    Article Title: Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R‐Loop Accumulation and DNA Repair Deficiencies
    Article Snippet: .. Human kinome CRISPR knockout library (Brunello) was obtained from Addgene (#73179) and was packaged into lentivirus. ..

    Knock-Out:

    Article Title: Loss of JAK1 Function Causes G2/M Cell Cycle Defects Vulnerable to Kif18a Inhibition
    Article Snippet: Lentivirus was produced as above, and cells were transduced followed by Puromycin (Gibco Cat# A11138-03) selection. gRNA sequences are listed in Supplemental Table 2. .. The Human Kinome CRISPR Knockout Library (Brunello) was purchased from Addgene (# 1000000082) and was generated as previously described . .. Library amplification and sequencing were performed according to the manufacturer’s protocol (Addgene/Broad Institute).

    Article Title: Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting RLoop Accumulation and DNA Repair Deficiencies.
    Article Snippet: .. Human kinome CRISPR knockout library (Brunello) was obtained from Addgene (#73179) and was packaged into lentivirus. ..

    Article Title: Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R‐Loop Accumulation and DNA Repair Deficiencies
    Article Snippet: .. Human kinome CRISPR knockout library (Brunello) was obtained from Addgene (#73179) and was packaged into lentivirus. ..

    Generated:

    Article Title: Loss of JAK1 Function Causes G2/M Cell Cycle Defects Vulnerable to Kif18a Inhibition
    Article Snippet: Lentivirus was produced as above, and cells were transduced followed by Puromycin (Gibco Cat# A11138-03) selection. gRNA sequences are listed in Supplemental Table 2. .. The Human Kinome CRISPR Knockout Library (Brunello) was purchased from Addgene (# 1000000082) and was generated as previously described . .. Library amplification and sequencing were performed according to the manufacturer’s protocol (Addgene/Broad Institute).



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    human kinome crispr pooled library  (Addgene inc)
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    <t>CRISPR</t> screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout <t>kinome</t> library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).
    Human Kinome Crispr Knockout Library Brunello, 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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    <t>CRISPR</t> screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout <t>kinome</t> library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).
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    <t>CRISPR</t> screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout <t>kinome</t> library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).
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    john doench  (Addgene inc)
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    <t>CRISPR</t> screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout <t>kinome</t> library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).
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    Image Search Results


    CRISPR screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout kinome library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).

    Journal: Advanced Science

    Article Title: Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R‐Loop Accumulation and DNA Repair Deficiencies

    doi: 10.1002/advs.202512074

    Figure Lengend Snippet: CRISPR screening revealed that co‐targeting WEE1 and AKT as a potential combination strategy in ARID1A/TP53 concurrent mutant CRC. A) Schematic description of the CRISPR knockout kinome library screen. (B) Results of CRISPR screen in SNUC5 cells. Scatter plots present the Z‐scores of average log 2 (fold change) for MK‐1775 vs DMSO ( x ‐axis) and for ZN‐c3 vs DMSO ( y ‐axis). (C) Immunoblot analysis confirming AKT2 knockout in SNUC5 cells (n=2). (D) Dose‐response curves of SNUC5 cells, treated with MK‐1775 (left) or ZN‐c3 (right) for 5 days. The results are representative of three independent experiments, each done in triplicate. Bars represent mean ± SD. (E) Immunoblot analysis of HCT15, SNUC5, COLO205, and HRT18 cell lines treated with 0.25 or 0.5 µ m MK‐1775 (n = 2). (F) GDSC2 analysis of indicated PI3K or AKT inhibitors according to ARID1A mutation status. Data are presented as scatter plots. Mean values are indicated by red lines. * p < 0.05, ** p < 0.01 (two‐tailed Wilcoxon rank‐sum test).

    Article Snippet: Human kinome CRISPR knockout library (Brunello) was obtained from Addgene (#73179) and was packaged into lentivirus.

    Techniques: CRISPR, Mutagenesis, Knock-Out, Western Blot, Two Tailed Test