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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 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+kinome+crispr+pooled+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 23 article reviews
    human kinome crispr pooled library - by Bioz Stars, 2026-10
    93/100 stars

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    CRISPR:

    Article Title: A Kinome-Wide Synthetic Lethal CRISPR/Cas9 Screen Reveals That mTOR Inhibition Prevents Adaptive Resistance to CDK4/CDK6 Blockade in HNSCC
    Article Snippet: The viral titer of lentivirus was analyzed using the qRT-PCR titer kit (#631235, Takara, Mountain View, CA) and functional titration. .. The human kinome CRISPR pooled library (Brunello) was a gift from John Doench and David Root (RRID: Addgene_75312). ..

    Article Title: CRISPR Screening Identifies WEE1 as a Combination Target for Standard Chemotherapy in Malignant Pleural Mesothelioma
    Article Snippet: 77367 and 77368) and Cas9 expression vector (catalog no. 52962) were obtained from Addgene. .. Human kinome CRISPR pooled library (Brunello) was a gift from John Doench & David Root (Addgene, catalog no. 75314; ref. 26). ..

    Article Title: A Kinome-Wide Synthetic Lethal CRISPR/Cas9 Screen Reveals That mTOR Inhibition Prevents Adaptive Resistance to CDK4/CDK6 Blockade in HNSCC
    Article Snippet: The viral titer of lentivirus was analyzed using the qRT-PCR titer kit (#631235, Takara, Mountain View, CA) and functional titration. .. The human kinome CRISPR pooled library (Brunello) was a gift from John Doench and David Root (RRID: Addgene_75312). ..

    Article Title: CRISPR-MIP replaces PCR and reveals GC and oversampling bias in pooled CRISPR screens
    Article Snippet: .. Human Kinome CRISPR pooled library (Brunello) was a gift from John Doench & David Root (Addgene #75314) . .. Backbone plasmid in the library is lentiCRISPRv2 (Addgene #52961), which contains a U6-sgRNA expression cassette coupled with Cas9 gene as well as puromycin resistance gene for the selection of transduced cells.

    Article Title: Combined blockade of polo-like kinase and pan-RAF is effective against NRAS-mutant non-small cell lung cancer cells.
    Article Snippet: NRAS mutation is rarely observed in non-small cell lung cancer (NSCLC) patients, and there are no approved treatments for NRAS-mutant NSCLC.. Here, we evaluated the effect of pan-RAF inhibitors on human NRASmutant NSCLC cell lines and performed high-throughput screening using human kinome small interfering (si) RNA or CRISPR/Cas9 libraries to identify new targets for combination NSCLC treatment.. Our results indicate that human NRAS-mutant NSCLC cells are moderately sensitive to pan-RAF inhibitors.



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    Addgene inc human kinome crispr pooled library
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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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    <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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    Addgene inc john doench
    <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).
    John Doench, 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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    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