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kras gene fragment  (New England Biolabs)


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    New England Biolabs kras gene fragment
    A ) CRISPR screening strategy to identify regulators of <t>KRAS</t> protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.
    Kras Gene Fragment, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 95/100, based on 286 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kras gene fragment/product/New England Biolabs
    Average 95 stars, based on 286 article reviews
    kras gene fragment - by Bioz Stars, 2026-02
    95/100 stars

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    1) Product Images from "Phosphorylation Protects Oncogenic RAS from LZTR1-Mediated Degradation"

    Article Title: Phosphorylation Protects Oncogenic RAS from LZTR1-Mediated Degradation

    Journal: bioRxiv

    doi: 10.64898/2026.01.07.698128

    A ) CRISPR screening strategy to identify regulators of KRAS protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.
    Figure Legend Snippet: A ) CRISPR screening strategy to identify regulators of KRAS protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.

    Techniques Used: CRISPR, Expressing, Mass Spectrometry, Control, Western Blot, Transduction, shRNA, Plasmid Preparation, Comparison, Activity Assay, Disruption



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    kras gene fragment  (New England Biolabs)
    95
    New England Biolabs kras gene fragment
    A ) CRISPR screening strategy to identify regulators of <t>KRAS</t> protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.
    Kras Gene Fragment, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kras gene fragment/product/New England Biolabs
    Average 95 stars, based on 1 article reviews
    kras gene fragment - by Bioz Stars, 2026-02
    95/100 stars
    		  Buy from Supplier

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    A ) CRISPR screening strategy to identify regulators of KRAS protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.

    Journal: bioRxiv

    Article Title: Phosphorylation Protects Oncogenic RAS from LZTR1-Mediated Degradation

    doi: 10.64898/2026.01.07.698128

    Figure Lengend Snippet: A ) CRISPR screening strategy to identify regulators of KRAS protein stability. B ) Volcano plot of average KRAS stability scores (n=3). Significant hits for genes that either decrease (pink) or increase (purple) KRAS expression are indicated. Callouts represent genes identified as RAS interaction partners by mass spectrometry . C ) Venn diagram of overlapping genes from KRAS stability screen (≤-0.8 KRAS stability score and P≤0.05), RAS BioID2 proteomics (≥1.0 log2 enrichment vs. control, from ref: ), and genes essential in RAS-dependent MM cell lines (≤-1.0 CSS, from ref: ). D ) Western blot analysis of RAS, PPP1R2, and GAPDH 3 days after transduction with control shRNA (shCTRL) or PPP1R2-targeting shRNAs in XG7, RPMI 8226, and MM.1S MM lines, n=3. E ) PPP1R2-BioID2 enrichment over empty vector in RPMI 8226 cells. F ) Western blot analysis of RAS, PPP1R2, PP1C, and GAPDH 3 days after transduction with shCTRL, shPPP1R2.1, and/or ectopic expression of DN PP1C, n=3. G ) Comparison of protein expression levels between KRAS (x-axis) and average PP1C (PPP1CA, PPP1CB, PPP1CC, and PPP1CC;PPP1CB) in 115 MM patient tumors. Display line is simple linear regression; R 2 =0.1593, P<0.0001. I ) Model of PPP1R2 and PP1C regulation of KRAS protein expression. Under a normal state, PPP1R2 inhibits PP1C activity. Following PPP1R2 disruption, PP1C activity reduces KRAS levels. In contrast, PP1C disruption increases KRAS expression.

    Article Snippet: Briefly, 150 ng of KRAS gene fragment was combined with 1 μL of SnaBI-linearized BioID-2 vector and 4 μL of 2× NEBuilder HiFi DNA Assembly Master Mix (New England Biolabs) and incubated for 1 h at 50 °C.

    Techniques: CRISPR, Expressing, Mass Spectrometry, Control, Western Blot, Transduction, shRNA, Plasmid Preparation, Comparison, Activity Assay, Disruption