AccuStart II Taq DNA Polymerase
High purity recombinant Taq DNA polymerase preparation with high avidity monoclonal antibody hot start
Features & Benefits
- High-yielding, ultrapure modified Taq DNA polymerase delivers robust, reliable assay sensitivity
- Stringent, ultrapure antibody hotstart enables precise target amplification and ambient room temperature setup
AccuStart II Taq DNA Polymerase is intended for molecular biology applications. This product is not intended for the diagnosis, prevention or treatment of a disease.
AccuStart II Taq DNA Polymerase is a high purity, recombinant Taq DNA polymerase preparation with high avidity monoclonal antibodies that bind the polymerase and keep it inactive prior to the initial PCR denaturation step. Upon heat activation (1 minute at 94ºC), the antibodies denature irreversibly, releasing fully active, unmodified Taq DNA polymerase. This enables specific and efficient primer extension with the convenience of room temperature reaction assembly. Non-specific extension of primers at low temperatures is a common cause of artifacts and poor sensitivity in PCR. The AccuStart II automatic hot-start enables specific and efficient primer extension in the PCR process with the added convenience of room temperature reaction assembly. The included 10X PCR Buffer II is optimized for higher yields, improved specificity, and enhanced multiplexing capability. Activated AccuStart II Taq DNA polymerase possesses 5'->3' DNA polymerase activity and a double-strand specific 5'->3' exonuclease. The polymerase does not have 3'-exonuclease activity and is free of any contaminating endo or exonuclease activities. One unit is defined as the amount of enzyme that will incorporate 10 nmol of dNTP into acid-insoluble material in 30 minutes at 74°C. AccuStart II Taq DNA polymerase contains extremely low levels of residual host, E. coli genomic DNA.
- AccuStart II Taq DNA polymerase 5 units/μL in 50% glycerol, 20 mM Tris-HCl, 40 mM NaCl, 0.1 mM EDTA, and stabilizers.
- 10X PCR Buffer II
- 50 mM MgCl2
Storage & HandlingStore components in a constant temperature freezer at -25°C to -15°C upon receipt. For lot specific expiry date, refer to package label, Certificate of Analysis or Product Specification Form.
Related ResourcesProduct ManualsPublicationsThe 5-HTTLPR and BDNF polymorphisms moderate the association between uncinate fasciculus connectivity and antidepressants treatment response in major depressionErica L. Tatham, European Archives of Psychiatry and Clinical Neuroscience - 2016AbstractSymptom improvement in depression due to antidepressant treatment is highly variable and clinically unpredictable. Linking neuronal connectivity and genetic risk factors in predicting antidepressant response has clinical implications. Our investigation assessed whether indices of white matter integrity, serotonin transporter-linked polymorphism (5-HTTLPR) and brain-derived neurotrophic factor (BDNF) val66met polymorphism predicted magnitude of depression symptom change following antidepressant treatment. Fractional anisotropy (FA) was used as an indicator of white matter integrity and was assessed in the uncinate fasciculus and superior longitudinal fasciculus using tract-based spatial statistics (TBSS) and probabilistic tractography. Forty-six medication-free patients with major depressive disorder participated in a diffusion tensor imaging scan prior to completing an 8-week treatment regime with citalopram or quetiapine XR. Indexed improvements in Hamilton Depression Rating Scale score from baseline to 8-week endpoint were used as an indicator of depression improvement. Carriers of the BDNF met allele exhibited lower FA values in the left uncinate fasciculus relative to val/val individuals [F(1, 40) = 7.314, p = 0.009]. Probabilistic tractography identified that higher FA in the left uncinate fasciculus predicted percent change in depression severity, with BDNF moderating this association [F(3, 30) = 3.923, p = 0.018]. An interaction between FA in the right uncinate fasciculus and 5-HTTLPR also predicted percent change in depression severity [F(5, 25) = 5.315, p = 0.002]. Uncorrected TBSS results revealed significantly higher FA in hippocampal portions of the cingulum bundle in responders compared to non-responders (p = 0.016). The predictive value of prefrontal and amygdala/hippocampal WM connectivity on antidepressant treatment response may be influenced by 5-HTTLPR and BDNF polymorphisms in MDD.Elevated Levels of SOX10 in Serum from Vitiligo and Melanoma Patients, Analyzed by Proximity Ligation AssayAndries Blokzijl, PLOS ONE - 2016AbstractBackground The diagnosis of malignant melanoma currently relies on clinical inspection of the skin surface and on the histopathological status of the excised tumor. The serum marker S100B is used for prognostic estimates at later stages of the disease, but analyses are marred by false positives and inadequate sensitivity in predicting relapsing disorder. Objectives To investigate SOX10 as a potential biomarker for melanoma and vitiligo. Methods In this study we have applied proximity ligation assay (PLA) to detect the transcription factor SOX10 as a possible serum marker for melanoma. We studied a cohort of 110 melanoma patients. We further investigated a second cohort of 85 patients with vitiligo, which is a disease that also affects melanocytes. Results The specificity of the SOX10 assay in serum was high, with only 1% of healthy blood donors being positive. In contrast, elevated serum SOX10 was found with high frequency among vitiligo and melanoma patients. In patients with metastases, lack of SOX10 detection was associated with treatment benefit. In two responding patients, a change from SOX10 positivity to undetectable levels was seen before the response was evident clinically. Conclusions We show for the first time that SOX10 represents a promising new serum melanoma marker for detection of early stage disease, complementing the established S100B marker. Our findings imply that SOX10 can be used to monitor responses to treatment and to assess if the treatment is of benefit at stages earlier than what is possible radiologically.Epigenome-wide analysis of sperm cells identifies IL22 as a possible germ line risk locus for psoriatic arthritisRemy A. Pollock, PLOS ONE - 2019AbstractPsoriasis and its associated inflammatory arthritis, psoriatic arthritis (PsA), have a clear heritable component, but a large proportion of the heritable risk remains unexplained by gene sequence variation. This study aimed to determine if epigenetic factors contribute to the missing heritability in psoriatic disease. DNA methylation profiling was performed on sperm cells from 23 probands with psoriasis without PsA (PsC), 13 PsA probands, and 18 unaffected controls. Differentially methylated CpGs and regions (DMRs) were identified and validated by pyrosequencing. Underlying AluY and copy number variation (CNV) in the HCG26 and IL22 genes, respectively, were assessed by genotyping. Array, subject’s age, age of psoriasis onset, psoriasis severity, and medication usage were found to influence methylation at many genes and were included as covariates in the analysis. Between PsC probands vs. controls, 169 DMRs were found; 754 DMRs were found between PsA probands vs. controls, and 86 between PsA and PsC probands (adjusted p<0.05). Differences in methylation across DMRs were generally subtle (<10%) but correlated well with pyrosequencing. Biological inference prioritized notable DMRs associated with skin disease (SIGLEC14, JAM3, PCOLCE, RXRB), skin and/or joint disease (MBP, OSBPL5, SNORD115, HCG26), and joint disease (IL22, ELF5, PPP2R2D, PTPRN2, HCG26). Hypermethylation of the DMR within the first exon of arthritis-associated IL22 showed significant correlation (rho = 0.34, 95% CI 0.06–0.57, p = 0.01) between paired sperm and blood samples, independent of a CNV within the same region. Further studies are needed to rule out underlying genetic causes and determine if these represent heritable, constitutional epimutations, or are the result of exposure of germ cells to endogenous or exogenous environmental factors.The influence of 5-HTTLPR and Val66Met polymorphisms on cortical thickness and volume in limbic and paralimbic regions in depression: a preliminary studyClick here to see all PublicationsNatalia Jaworska, BMC Psychiatry - 2016AbstractStructural brain abnormalities have been investigated in multi-genetic and complex disorders such as major depressive disorder (MDD). Among the various candidate genes implicated in MDD, the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and 5-HT transporter gene linked polymorphism (5-HTTLPR) have garnered the most attention due to their putative roles in neural plasticity and antidepressant response. However, relatively few studies have assessed the influence of these polymorphysims on cortical thickness or brain volume in para-limbic and limbic regions in MDD, which was the aim of this study.Safety Data Sheets (SDS)CofA (PSF)PSF-95141-01K-Lot#022569PSF-95141-01K-Lot#022570PSF-95141-01K-Lot#023147PSF-95141-01K-Lot#023148PSF-95141-05K-Lot#022881PSF-95141-05K-Lot#023614PSF-95141-05K-Lot#024889PSF-95141-250-Lot#024483PSF-95141-250-Lot#024484PSF-95141-250-Lot#024485PSF-95141-01K-Lot#025608PSF-95141-01K-Lot#025608PSF-95141-05K-Lot#025791PSF-95141-250-Lot#026137PSF-95141-250-Lot#026337PSF-95141-250-Lot#026338PSF-95141-05K-Lot#026745PSF-95141-01K-Lot#026874PSF-95141-250-Lot#026867PSF-95141-250-Lot#026869PSF-95141-250-Lot#026870PSF-95141-05K-Lot#027514PSF-95141-01K-Lot#027513PSF-95141-05K-Lot#027836PSF-95141-250-Lot#027896PSF-95141-01K-Lot#027941PSF-95141-01K-Lot#027942PSF-95141-01K-Lot#028181PSF-95141-250-Lot#028180PSF-95141-05K-Lot#028523PSF-95141-05K-Lot#029343PSF-95141-250-LOT#66141472