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pBud-EGFP/PrP V180I (Met 129)
(Plasmid #23190)

Ordering

This material is available to academics and nonprofits only.
Item Catalog # Description Quantity Price (USD)
Plasmid 23190 Standard format: Plasmid sent in bacteria as agar stab 1 $94

Backbone

  • Vector backbone
    pBudCE4.1-EGFP
  • Backbone manufacturer
    Invitrogen
  • Backbone size w/o insert (bp) 5303
  • Vector type
    Mammalian Expression, Bacterial Expression
  • Selectable markers
    Zeocin

Growth in Bacteria

  • Bacterial Resistance(s)
    Bleocin (Zeocin), 50 μg/mL
  • Growth Temperature
    37°C
  • Growth Strain(s)
    DH5alpha
  • Growth instructions
    DH5α in Low-Salt LB
  • Copy number
    High Copy

Gene/Insert

  • Gene/Insert name
    Human Prion Protein
  • Alt name
    hPrP
  • Alt name
    PRNP
  • Species
    H. sapiens (human)
  • Insert Size (bp)
    762
  • Mutation
    hPrP Mutations: V180I, Met 129 polymorphism.
  • Entrez Gene
    PRNP (a.k.a. ASCR, AltPrP, CD230, CJD, GSS, KURU, PRIP, PrP, PrP27-30, PrP33-35C, PrPc, p27-30)

Cloning Information

  • Cloning method Restriction Enzyme
  • 5′ cloning site ScaI (destroyed during cloning)
  • 3′ cloning site XbaI (not destroyed)
  • 5′ sequencing primer unknown
  • (Common Sequencing Primers)

Terms and Licenses

  • Academic/Nonprofit Terms
  • Industry Terms
    • Not Available to Industry

Trademarks:

  • Zeocin® is an InvivoGen trademark.

Depositor Comments

Bigenic vector: EGFP under EF-1α promoter, Human Prion Protein under CMV promoter. Ref Plasmid 23027.

Reference:
Jodoin J, Laroche-Pierre S, Goodyer CG, LeBlanc AC.(2007) J Neurosci.27:5081-91.

How to cite this plasmid ( Back to top)

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.

  • For your Materials & Methods section:

    pBud-EGFP/PrP V180I (Met 129) was a gift from Andrea LeBlanc (Addgene plasmid # 23190)
  • For your References section:

    Defective retrotranslocation causes loss of anti-Bax function in human familial prion protein mutants. Jodoin J, Laroche-Pierre S, Goodyer CG, LeBlanc AC. J Neurosci. 2007 May 9. 27(19):5081-91. 10.1523/JNEUROSCI.0957-07.2007 PubMed 17494694