Addgene inc phdr cdkn2a ex2 cmv egfp

(A) Strategy for introducing focal knock-in of CMV-EGFP to replace exon 2 of <t>CDKN2A.</t>

Phdr Cdkn2a Ex2 Cmv Egfp, supplied by Addgene inc, 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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(A) Strategy for introducing focal knock-in of CMV-EGFP to replace exon 2 of CDKN2A.

Journal: Cancer cell

Article Title: Bi-allelic loss of CDKN2A initiates melanoma invasion via BRN2 activation

doi: 10.1016/j.ccell.2018.05.014

Figure Lengend Snippet: (A) Strategy for introducing focal knock-in of CMV-EGFP to replace exon 2 of CDKN2A.

Article Snippet: MISSION pLKO.1-puro Non-Mammalian shRNA Control Plasmid (SHC002) and shPOU3F2 MISSION shRNA Bacterial Glycerol Stock (TRCN0000218221) were purchased from Sigma. pHIV-INK4A-zsGreen (Addgene #110728), pHIV-ARF-zsGreen (Addgene #110729), pHIV-ARF-mOrange2 (Addgene #110731), pHIV-INK4A-mOrange2 (Addgene #110730), and pHIV-BRAF V600E -mOrange2 (Addgene #110732) were all generated by inserting the indicated coding sequence into the Ecorl and Xbal sites of the indicated parental pHIV constructs. pSicoR-Efla-mCh-Puro was a gift from Bruce Conklin (Addgene plasmid # 31845)( Salomonis et al., 2010 ). pGL410-BRN2p (Addgene #110733, BRN2 promoter luciferase reporter) was generated by placing 2kb of sequence upstream of the BRN2 transcriptional start site into the Bgl2 and Xhol sites. pHDR-CDKN2A-Ex2-CMV-EGFP (Addgene #110734) was generated by amplifying 2kb left and right arms from human genomic DNA and using Cold Fusion (System Bio) to combine with the CMV promoter, EGFP ORF, and an Amp/Ori cassette. pHDR-CDKN2A-Ex2-EFla-H2B-mOrange2 (Addgene #110735) was constructed similarly but with a EFla promoter and mOrange2 ORF fused to H2B.

Techniques: Knock-In

(A) Schematic of experimental set-up. For each experiment, NHMs are derived from donated tissue and engineered for CDKN2A loss as in Figure 1. After isolation, CDKN2A null and wild-type sibling cells are monitored via digital holographic cytometry for 72 hr. The rate of cell division, motility, morphology, growth arrest and detachment are quantified. Representative holographic phase shift images (bottom left) show colored comet tails tracking cells.

Journal: Cancer cell

Article Title: Bi-allelic loss of CDKN2A initiates melanoma invasion via BRN2 activation

doi: 10.1016/j.ccell.2018.05.014

Figure Lengend Snippet: (A) Schematic of experimental set-up. For each experiment, NHMs are derived from donated tissue and engineered for CDKN2A loss as in Figure 1. After isolation, CDKN2A null and wild-type sibling cells are monitored via digital holographic cytometry for 72 hr. The rate of cell division, motility, morphology, growth arrest and detachment are quantified. Representative holographic phase shift images (bottom left) show colored comet tails tracking cells.

Techniques: Derivative Assay, Isolation, Cytometry

(A) Volcano plot comparing transcriptomes of three independently derived pairs of CDKN2A null NHMs and matched wild-type sibling cells. Differentially expressed transcripts with q-values < 0.05 and log2 fold change > 1.7 are highlighted in aqua. The BRN2 transcript is highlighted in red.

Journal: Cancer cell

Article Title: Bi-allelic loss of CDKN2A initiates melanoma invasion via BRN2 activation

doi: 10.1016/j.ccell.2018.05.014

Figure Lengend Snippet: (A) Volcano plot comparing transcriptomes of three independently derived pairs of CDKN2A null NHMs and matched wild-type sibling cells. Differentially expressed transcripts with q-values < 0.05 and log2 fold change > 1.7 are highlighted in aqua. The BRN2 transcript is highlighted in red.

Techniques: Derivative Assay

(A) Fraction of nevi or melanomas with mono- or bi-allelic CDKN2A disruption. Melanomas are sub-categorized as melanoma in situ (MIS), thin invasive melanoma (Stage T1), thick invasive melanoma (Stage T2+) and distal metastatic melanoma (obtained from the TCGA public database).

Journal: Cancer cell

Article Title: Bi-allelic loss of CDKN2A initiates melanoma invasion via BRN2 activation

doi: 10.1016/j.ccell.2018.05.014

Figure Lengend Snippet: (A) Fraction of nevi or melanomas with mono- or bi-allelic CDKN2A disruption. Melanomas are sub-categorized as melanoma in situ (MIS), thin invasive melanoma (Stage T1), thick invasive melanoma (Stage T2+) and distal metastatic melanoma (obtained from the TCGA public database).

Techniques: In Situ

(A) Gene set enrichment analysis of three CDKN2A null NHM lines compared to three CDKN2A wild-type NHM lines (Engineered NHMs) or CDKN2A wild-type regions compared to CDKN2A null regions of the clinical cohort (Transition case cohort). # indicates both the NOM p value and FDR q-values for the enrichment score < 0.0005.

Journal: Cancer cell

Article Title: Bi-allelic loss of CDKN2A initiates melanoma invasion via BRN2 activation

doi: 10.1016/j.ccell.2018.05.014

Figure Lengend Snippet: (A) Gene set enrichment analysis of three CDKN2A null NHM lines compared to three CDKN2A wild-type NHM lines (Engineered NHMs) or CDKN2A wild-type regions compared to CDKN2A null regions of the clinical cohort (Transition case cohort). # indicates both the NOM p value and FDR q-values for the enrichment score < 0.0005.

Techniques:

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