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shRNA-CAB39 Lentivirus Plasmid (SH1001-02)

Availability: In stock


Quick Overview

ATCGbio Life Technology Inc. provides the function-validated shRNA-CAB39 (Calcium binding protein 39) lentivirus plasmid. 
The plasmids product contains 2-tubes:
1. Negative-control shRNA lentivirus plasmid  20 µl (~50 ng/µl)
2. shRNA-CAB39 (Calcium binding protein 39) lentivirus plasmid   20 µl (~50 ng/µl)
CAB39 also has been known as MO25 (Mouse Protein-25).

shRNA-CAB39 Lentivirus Plasmid (SH1001-02)


                           Produtct Name:         shRNA-CAB39 Lentivirus Plasmid
        Official Gene Symbol:
        Gene ID:         51719  
        Official Full Name:         Calcium binding protein 39  
        Also Known As:         MO25; CGI-66  
        Target Species:         Human
        Product Validation:         shRNA Function validated  
        Technique Information:         Instruction PDF| Web Page|MSDS  
        Product Size:         20µl (~50ng/µl), store at 4°C  
        Product Category:         RNAi, Cat#1001-02  
        Price (USD):         $350.00  

Lentivirus plasmids will be shipped in 0.5 ml tube, and users are free to amplify. Upon receiving the tubes, keep it at 4 °C till amplification.

CAB39 protein, also known as mouse protein-25 (MO25), a scaffold protein, isoforms bind to the STRAD pseudokinase and stabilize it in a conformation that can activate the LKB1 tumour suppressor kinase. CAB39/MO25 has been addressed to be a novel regulatory component of the LKB1 complex that was found to interact with STRAD to play a crucial role in allowing LKB1 to phosphorylate and activate AMPK.

CAB39/MO25 has roles beyond controlling LKB1.These new CAB39/MO25 targets are SPAK/OSR1 kinases, regulators of ion homeostasis and blood pressure, and MST3/MST4/YSK1, involved in controlling development and morphogenesis.MO25α and MO25β associate with these STE20 kinases in a similar manner to STRAD. MO25 isoforms induce approximately 100-fold activation of SPAK/OSR1 dramatically enhancing their ability to phosphorylate the ion cotransporters NKCC1, NKCC2 and NCC, leading to the identification of several new phosphorylation sites. siRNA-mediated reduction of expression of CAB39/MO25 isoforms in mammalian cells inhibited phosphorylation of endogenous NKCC1 at residues phosphorylated by SPAK/OSR1, which is rescued by re-expression of MO25α. MO25α/β binding to MST3/MST4/YSK1 also stimulated kinase activity three- to four-fold. CAB39/MO25 has evolved as a key regulator of a group of STE20 kinases and may represent an ancestral mechanism of regulating conformation of pseudokinases and activating catalytically competent protein kinases (EMBO J. 2011 May 4;30(9):1730-41).

The following figure is the results of experiments to prove our shRNA performance

(One shRNA sequence was selected for one target in each design)

         shRNA-lentivirus-performance                   Non-target   Gene-specific
               shRNA           shRNA
• shRNA Lentivirus were created to target 10 transcription factors expressed in HepG2 cells.
• 64 hrs after infection without antibiotic selection, the target gene mRNAs were down to 28.8% in average of 10 shRNA target (p<0.0001 by paired t-test). 9 out of 10 design shRNA were able to suppress more than 70%, and only one out of 10 shRNA suppressed more modestly about 60%.
• Suppression will be greater, when the cells would be cultured longer time with antibiotics selection.

Ten transcription factors expressed in HepG2 cells were selected for this experiment. The lentivirus plasmids expressing shRNA were made for each target gene using our propriety design scheme (One shRNA sequence was selected for one target in each design). Lentivirus was created in 12-well plates using our Lentivirus Production kit, which produces a high titer stable lentivirus solution in 48hrs. HepG2 cells were grown in 96-well palate and infected with each virus including negative control shRNA by adding 50µl crude virus solution into HepG2 cells cultured with100µl culture medium for overnight(16hrs.). The cells were incubated further 48hrs., and harvested for Direct RT real-time PCR.  As shown in the right figure, 64 hrs. after infection, target gene mRNAs were down to 28.8% in average of 10 shRNA target. 9 out of 10 design shRNA were able to suppress more than 70%, and only one out of 10 shRNA suppressed more modestly about 60%.


 1. Y. Ido, et al., PLoS ONE, 2012 Apr 07( 4): e35092
 2. Lan F, et al., J Biol Chem. 2008 Oct 10;283(41):27628-35.

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