Purposelentiviral expression of dominant negative mouse Akt1 and EGFP
Full plasmid sequence is not available for this item.
|Item||Catalog #||Description||Quantity||Price (USD)|
|Plasmid||53597||Standard format: Plasmid sent in bacteria as agar stab||1||$75|
This material is available to academics and nonprofits only.
Vector backbonepHR-IG (pHR’tripCMV-IRES-eGFP)
Vector typeMammalian Expression, Lentiviral
Growth in Bacteria
Alt nameAkt1 DN
SpeciesM. musculus (mouse)
MutationDominant negative (K179M)
Entrez GeneAkt1 (a.k.a. Ak, Akt, LTR-akt, PK, PKB, PKB/A, PKB/Akt, PKBalpha, Rac)
- Promoter CMV
/ Fusion Proteins
- HA (N terminal on insert)
- IRES-EGFP (C terminal on backbone)
- Cloning method Restriction Enzyme
- 5′ cloning site SalI (not destroyed)
- 3′ cloning site BamHI (not destroyed)
- 5′ sequencing primer CMV-F
- 3′ sequencing primer pCDH-rev (Common Sequencing Primers)
Terms and Licenses
- Not Available to Industry
Articles Citing this Plasmid
AktDN was purchased from Addgene (plasmid # 16243).
The AktDN gene is an Akt gene where a point mutation in the 179th amino acid from the N terminal converts a lysine to a methionine. This mutated form of the Akt protein can still be phosphorylated at the S473 site but loses its ability to affect downstream factors.
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:pHRIG-AktDN was a gift from Heng Zhao (Addgene plasmid # 53597 ; http://n2t.net/addgene:53597 ; RRID:Addgene_53597)
For your References section:Akt isoforms differentially protect against stroke-induced neuronal injury by regulating mTOR activities. Xie R, Cheng M, Li M, Xiong X, Daadi M, Sapolsky RM, Zhao H. J Cereb Blood Flow Metab. 2013 Dec;33(12):1875-85. doi: 10.1038/jcbfm.2013.132. Epub 2013 Aug 14. 10.1038/jcbfm.2013.132 PubMed 23942361
Map uploaded by the depositor.