AccuStart II GelTrack PCR SuperMix
Features & Benefits
- Contains premixed loading dye to streamline gel electrophoresis
- User-friendly 2X concentrated master mix simplifies reaction setup with exceptional room-temperature stability (≥30 days at 22°C) and withstands to repetitive freeze-thaw (≥ 20X)
- High-yielding, ultrapure modified Taq DNA polymerase delivers robust, reliable assay sensitivity
- Stringent, ultrapure antibody hotstart ensures sensitive and precise assay performance
AccuStart II GelTrack PCR SuperMix is a 2X concentrated, ready-to-use reaction cocktail for routine PCR amplification of DNA fragments up to 4 kb. It contains all components, except primers and template. This kit improves assay reproducibility, and reduces the risk of contamination. A key component is AccuStart II Taq DNA polymerase which contains ultra-pure monoclonal antibodies that arrest polymerase prior to the initial PCR denaturation step. Hot start antibodies are rapidly and irreversibly denatured (1 minute at 94ºC), releasing a high yielding Taq DNA polymerase mutant with absolute maximum processivity and velocity from the first cycle. This enables specific and efficient primer extension with the convenience of room temperature reaction assembly.
GelTrack Loading Dye is a mixture of blue and yellow electrophoresis-tracking dyes that migrate at approximately 4kb and 50 bp, and comes pre-mixed with the PCR reagents.
2X reaction buffer containing
- MgCl2 (3 mM)
- dATP, dCTP, dGTP, dTTP (0.4 mM each)
- AccuStart II Taq DNA Polymerase
- GelTrack loading dye and stabilizers.
Storage & HandlingStore components in a constant temperature freezer at -25°C to -15°C upon receipt. Repeated freezing and thawing does not impair product performance. For lot specific expiry date, refer to package label, Certificate of Analysis or Product Specification Form.
Related ResourcesProduct ManualsSafety Data Sheets (SDS)CofA (PSF)PSF-95136-100-Lot#014838PSF-95136-500-Lot#021003PSF-95136-04K-Lot#022349PSF-95136-04K-Lot#023288PSF-95136-500-Lot#021880PSF-95136-500-Lot#022445PSF-95136-500-Lot#022446PSF-95136-500-Lot#023235PSF-95136-500-Lot#024746PSF-95136-500-Lot#024747PSF-95136-04K-Lot#025280PSF-95136-500-Lot#025282PSF-95136-500-Lot#027065PSF-95136-500-Lot#027066PSF-95136-100-Lot#027659PSF-95136-500-Lot#027601PSF-95136-04K-Lot#027744PSF-95136-04K-Lot#028116PSF-95136-100-Lot#028174PSF-95136-500-Lot#028175PSF-95136-500-Lot#028461PSF-95136-04K-Lot#027852PSF-95136-100-Lot#029539PublicationsHETEROZYGOUS MODIFICATIONS OF TUMOR SUPPRESSOR GENES - Recombinetics, Inc.Adrienne Leigh Biggar, United States Patent - 2016AbstractAnimals genomically modified to have heterozygous modifications of one or more tumor suppressor genes are disclosed.A molecular understanding of d-homoestrone-induced G2/M cell cycle arrest in HeLa human cervical carcinoma cellsClick here to see all PublicationsRenáta Minorics, Journal of Cellular and Molecular Medicine - 2015Abstract2-Methoxyestradiol (ME), one of the most widely investigated A-ring-modified metabolites of estrone, exerts significant anticancer activity on numerous cancer cell lines. Its pharmacological actions, including cell cycle arrest, microtubule disruption and pro-apoptotic activity, have already been described in detail. The currently tested d-ring-modified analogue of estrone, d-homoestrone, selectively inhibits cervical cancer cell proliferation and induces a G2/M phase cell cycle blockade, resulting in the development of apoptosis. The question arose of whether the difference in the chemical structures of these analogues can influence the mechanism of anticancer action. The aim of the present study was therefore to elucidate the molecular contributors of intracellular processes induced by d-homoestrone in HeLa cells. Apoptosis triggered by d-homoestrone develops through activation of the intrinsic pathway, as demonstrated by determination of the activities of caspase-8 and -9. It was revealed that d-homoestrone-treated HeLa cells are not able to enter mitosis because the cyclin-dependent kinase 1-cyclin B complex loses its activity, resulting in the decreased inactivation of stathmin and a concomitant disturbance of microtubule formation. However, unlike 2-ME, d-homoestrone does not exert a direct effect on tubulin polymerization. These results led to the conclusion that the d-homoestrone-triggered intracellular processes resulting in a cell cycle arrest and apoptosis in HeLa cells differ from those in the case of 2-ME. This may be regarded as an alternative mechanism of action among steroidal anticancer compounds.