kras gene fragment Search Results


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
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Average 95 stars, based on 1 article reviews
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synthetic fsei-ha-krab-asci dna fragment  (GenScript corporation)
90
GenScript corporation synthetic fsei-ha-krab-asci dna 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.
Synthetic Fsei Ha Krab Asci Dna Fragment, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/synthetic fsei-ha-krab-asci dna fragment/product/GenScript corporation
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dna fragment encoding dcas9 bfp krab domain  (Addgene inc)
95
Addgene inc dna fragment encoding dcas9 bfp krab domain
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.
Dna Fragment Encoding Dcas9 Bfp Krab Domain, 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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0.8-kb viral harvey ras (v-ha-ras) oncogene sstii2psti fragments  (Lofstrand)
90
Lofstrand 0.8-kb viral harvey ras (v-ha-ras) oncogene sstii2psti fragments
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.
0.8 Kb Viral Harvey Ras (V Ha Ras) Oncogene Sstii2psti Fragments, supplied by Lofstrand, 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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0.8-kb viral harvey ras (v-ha-ras) oncogene sstii2psti fragments - by Bioz Stars, 2026-02
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Image Search Results


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