pCDH-CuO-MCS-EF1α-CymR-T2A-Puro SparQ™ All-in-one Cloning and Expression Lentivector
Simplify your SparQ projects by delivering your gene-of-interest and CymR with the same lentivector – includes co-expression of CymR and a puromycin marker
With SBI’s SparQ™ Cumate Switch System, you can get inducible gene expression in mammalian cells with a range of cloning and expression lentivectors. The pCDH-CuO-MCS-EF1α-CymR-T2A-Puro SparQ All-in-one Cloning and Expression Lentivector (Cat.# QM800A-1) simplifies your SparQ projects by delivering your gene- or miRNA-of-interest with the same vector that delivers CymR. The vector drives your gene-of-interest or miRNA-of-interest with the inducible cumate switch promoter, and constitutively co-expresses CymR and a puromycin resistance marker from an EF1α promoter. Co-expression is mediated by the T2A element.
With SBI’s SparQ™ Cumate Switch System, you can get inducible gene expression in mammalian cells through the binding of cumate, a non-toxic small molecule, to CymR. Expression levels of your gene-of-interest are tightly controlled and increase with increasing cumate concentration until maximum induction is reached—see as much as a 32-fold increase in gene expression. Even better, induction is reversible, so you can turn expression levels on and off. Delivering negligible background expression in the absence of cumate, the SparQ System is an excellent choice for achieving controlled levels of gene expression.
Robust—increase expression up to 32-fold
Adjustable—tune expression levels by titrating the amount of cumate
Reversible—turn expression on, then off, then on again
Versatile—choose from all-in-one formats that co-express CymR and your gene-of-interest, or two-vector systems where CymR is expressed from a different plasmid
Powerful—suitable for in vivo applications
How It Works
Tightly-controlled, inducible gene expression
SBI’s SparQ Cumate Switch System delivers robust, titratable gene expression with low background through three components:
Cumate, a non-toxic, small-molecule inducer
CymR, a repressor that binds to cumate operator sequences in the absence of cumate
SparQ Lentivector that contains an MCS to clone-in your gene-of-interest, the cumate inducible promoter with cumate operator sequences (CuO) upstream of the MCS, and one or more markers
CymR has a high binding affinity for cumate and, as more cumate is added, fewer CymR molecules bind to the CuO sequences in the promoter resulting in increased expression. Exhibiting much lower background expression than similar systems, SBI’s cumate-inducible vectors can provide up to 32-fold induction of gene expression.
Supporting Data
Tight expression control with low background with the SparQ Cumate Switch System
Figure 1. Get lower background and higher induction with the SparQ Cumate Switch System than other inducible systems.
Figure 2. Gene expression with the SparQ Cumate SwitchSystem can be turned on and off, then on again.
Figure 3. Gene expression with the SparQ Cumate Switch System is titratable, with increasing amounts of cumate inducing a linear increase in gene expression.
Figure 4. With the SparQ System, gene expression can also be titrated by increasing the amount of transduced SparQ lentivirus, even up to 30 MOI.
Shinmura, K, et al. (2017) WDR62 overexpression is associated with a poor prognosis in patients with lung adenocarcinoma. Mol. Carcinog.. 2017 Aug 1; 56(8):1984-1991. PM ID: 28277612
Maegawa, KI, et al. (2017) The Highly Dynamic Nature of ERdj5 Is Key to Efficient Elimination of Aberrant Protein Oligomers through ER-Associated Degradation. Structure. 2017 Jun 6; 25(6):846-857.e4. PM ID: 28479060
Park, TS, Kim, SW & Lee, JH. (2017) Efficient transgene expression system using a cumate-inducible promoter and Cre-loxP recombination in avian cells. Asian-australas. J. Anim. Sci.. 2017 Jun 1; 30(6):886-892. PM ID: 27764912
Herrington, KA, et al. (2017) Spatial analysis of Cdc42 activity reveals a role for plasma membrane-associated Cdc42 in centrosome regulation. Mol. Biol. Cell. 2017 May 24;. PM ID: 28539409
Jain, A, et al. (2017) Abl kinase regulation by BRAF/ERK and cooperation with Akt in melanoma. Oncogene. 2017 Apr 3;. PM ID: 28368422
O'Hara, SP, et al. (2017) ETS Proto-oncogene 1 Transcriptionally Up-regulates the Cholangiocyte Senescence-associated Protein Cyclin-dependent Kinase Inhibitor 2A. J. Biol. Chem.. 2017 Mar 24; 292(12):4833-4846. PM ID: 28184004
Ikushima, S & Boeke, JD. (2017) New Orthogonal Transcriptional Switches Derived from Tet Repressor Homologues for Saccharomyces cerevisiae Regulated by 2,4-Diacetylphloroglucinol and Other Ligands. ACS Synth Biol. 2017 Mar 17; 6(3):497-506. PM ID: 28005347
Shinmura, K, et al. (2017) Reduced expression of the DNA glycosylase gene MUTYH is associated with an increased number of somatic mutations via a reduction in the DNA repair capacity in prostate adenocarcinoma. Mol. Carcinog.. 2017 Feb 1; 56(2):781-788. PM ID: 27253753
Liu, L, Huang, W & Huang, JD. (2017) Synthetic circuits that process multiple light and chemical signal inputs. BMC Syst Biol. 2017 Jan 19; 11(1):5. PM ID: 28103878
Ando, T, et al. (2017) Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to Dox via Src-Stat3 inactivation in osteosarcoma. Sci Rep. 2017 Jan 5; 7:40187. PM ID: 28054649
Choi, JS, et al. (2016) cIAPs promote the proteasomal degradation of mutant SOD1 linked to familial amyotrophic lateral sclerosis. Biochem. Biophys. Res. Commun.. 2016 Nov 18; 480(3):422-428. PM ID: 27773815
Barta, T, Peskova, L & Hampl, A. (2016) miRNAsong: a web-based tool for generation and testing of miRNA sponge constructs in silico. Sci Rep. 2016 Nov 18; 6:36625. PM ID: 27857164
Ushioda, R, et al. (2016) Redox-assisted regulation of Ca2+ homeostasis in the endoplasmic reticulum by disulfide reductase ERdj5. Proc. Natl. Acad. Sci. U.S.A.. 2016 Oct 11; 113(41):E6055-E6063. PM ID: 27694578
Welti, J, et al. (2016) Analytical Validation and Clinical Qualification of a New Immunohistochemical Assay for Androgen Receptor Splice Variant-7 Protein Expression in Metastatic Castration-resistant Prostate Cancer. Eur. Urol.. 2016 Oct 1; 70(4):599-608. PM ID: 27117751
Narumi, S, et al. (2016) SAMD9 mutations cause a novel multisystem disorder, MIRAGE syndrome, and are associated with loss of chromosome 7. Nat. Genet.. 2016 Jul 1; 48(7):792-7. PM ID: 27182967
Park, BO, et al. (2016) Selective novel inverse agonists for human GPR43 augment GLP-1 secretion. Eur. J. Pharmacol.. 2016 Jan 15; 771:1-9. PM ID: 26683635
Herrington, KA. (2016) New technologies for a better understanding of the Golgi: FLIM-FRET and click chemistry. Thesis. ;. Link: Thesis
Shinmura, K, et al. (2015) NEIL1 p.Gln282Stop variant is predominantly localized in the cytoplasm and exhibits reduced activity in suppressing mutations. Gene. 2015 Oct 15; 571(1):33-42. PM ID: 26095805
Peterson, MF, et al. (2015) Integrated systems for exosome investigation. Methods. 2015 Oct 1; 87:31-45. PM ID: 25916618
