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Depositing Lab
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Publication
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Sequence Information
Ordering
Item | Catalog # | Description | Quantity | Price (USD) | |
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Plasmid | 11130 | Standard format: Plasmid sent in bacteria as agar stab | 1 | $85 |
Backbone
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Vector backbonepbabe
- Backbone size w/o insert (bp) 4500
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Vector typeMammalian Expression, Retroviral
Growth in Bacteria
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Bacterial Resistance(s)Ampicillin, 100 μg/mL
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Growth Temperature37°C
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Growth Strain(s)DH5alpha
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Copy numberUnknown
Gene/Insert
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Gene/Insert namec-myc, HRas
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Alt namec-myc
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Alt nameHRas
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SpeciesH. sapiens (human), M. musculus (mouse)
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Insert Size (bp)2300
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Mutationc-myc T58A, A156T, and G438R; and H-Ras G12V
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Entrez GeneHRAS (a.k.a. C-BAS/HAS, C-H-RAS, C-HA-RAS1, CTLO, H-RASIDX, HAMSV, HRAS1, RASH1, p21ras)
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Entrez GeneMyc (a.k.a. Myc2, Niard, Nird, bHLHe39)
Cloning Information
- Cloning method Restriction Enzyme
- 5′ cloning site BamHI(c-myc), HindIII(H-Ras) (not destroyed)
- 3′ cloning site EcoRI(c-myc), ClaI(H-Ras) (not destroyed)
- 5′ sequencing primer pBABE 5' (Common Sequencing Primers)
Resource Information
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Articles Citing this Plasmid
Terms and Licenses
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Academic/Nonprofit Terms
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Industry Terms
- Not Available to Industry
Trademarks:
- Zeocin® is an InvivoGen trademark.
Depositor Comments
Contains mouse c-myc and human Hras. This plasmid was generated by cloning c-MycT58A cDNA with flanking BamHI-EcoRI restriction sites added by PCR into the same sites of the polylinker of pBABEpuro or pBABEblast and by excising the selectable marker from the HindIII/ClaI sites and ligating into the same site H-RasG12V cDNA in which HindIII/ClaI sites were again added by PCR.
These plasmids were created by your colleagues. Please acknowledge the Principal Investigator, cite the article in which the plasmids were described, and include Addgene in the Materials and Methods of your future publications.
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For your Materials & Methods section:
pbabe-c-mycT58A+HRasG12V was a gift from Christopher Counter (Addgene plasmid # 11130 ; http://n2t.net/addgene:11130 ; RRID:Addgene_11130) -
For your References section:
A network of genetic events sufficient to convert normal human cells to a tumorigenic state. Kendall SD, Linardic CM, Adam SJ, Counter CM. Cancer Res. 2005 Nov 1. 65(21):9824-8. 10.1158/0008-5472.CAN-05-1543 PubMed 16267004