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PerfeCTa qPCR SuperMix

Features & Benefits
Product
Kit Size
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Product
Kit Size
Order Info
PerfeCTa qPCR SuperMix
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Kit Size:
Order Info:
500 x 50 μL rxns (10 x 1.25 mL)
2000 x 50 μL rxns (1 x 50 mL)
Product
Kit Size
Order Info
PerfeCTa qPCR SuperMix ROX
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Kit Size:
Order Info:
500 x 50 μL rxns (10 x 1.25 mL)
2000 x 50 μL rxns (1 x 50 mL)
Product
Kit Size
Order Info
PerfeCTa qPCR SuperMix Low-ROX
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Kit Size:
Order Info:
500 x 50 μL rxns (10 x 1.25 mL)
2000 x 50 μL rxns (1 x 50 mL)

Description

PerfeCTa qPCR SuperMix is a 2X concentrated, ready-to-use reaction cocktail that contains all components, except primers, probe(s), and template for real-time quantitative PCR systems. The proprietary buffer and stabilizers have been specifically optimized to deliver maximum PCR efficiency, sensitivity, and robust fluorescent signal with TaqMan® or TaqMan MGB probe chemistry. The enhanced specificity of this supermix suppresses cross-reactivity between homologous sequences, improving detection and discrimination in SNP applications. A key component of this supermix is AccuStart™ Taq DNA polymerase, which contains monoclonal antibodies that bind to the polymerase and keep it inactive prior to the initial PCR denaturation step. Upon heat activation (2 minutes at 95ºC), 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.
Details

Details

Contents

PerfeCTa qPCR SuperMix (2X): 2X reaction buffer containing optimized concentrations of MgCl2, dNTPs (dATP, dCTP, dGTP, dTTP), AccuStart Taq DNA Polymerase, and stabilizers.

Instrument Capability

Instrument Capability

ROX

  • Applied Biosystems 5700
  • Applied Biosystems 7000
  • Applied Biosystems 7300
  • Applied Biosystems 7700
  • Applied Biosystems 7900
  • Applied Biosystems 7900HT
  • Applied Biosystems 7900 HT Fast
  • Applied Biosystems StepOne™
  • Applied Biosystems StepOnePlus™

Low ROX

  • Applied Biosystems 7500
  • Applied Biosystems 7500 Fast
  • Stratagene Mx3000P®
  • Stratagene Mx3005P™
  • Stratagene Mx4000™
  • Applied Biosystems ViiA 7
  • Applied Biosystems QuantStudio™
  • Agilent AriaMx
  • Douglas Scientific IntelliQube®

No ROX

  • Quantabio Q
  • BioRad CFX
  • Roche LightCycler 480
  • QIAGEN Rotor-Gene Q
  • Other

Bio-Rad iCycler iQ systems

  • BioRad iCycler iQ™
  • BioRad MyiQ™
  • BioRad iQ™5

Details

Contents

PerfeCTa qPCR SuperMix (2X): 2X reaction buffer containing optimized concentrations of MgCl2, dNTPs (dATP, dCTP, dGTP, dTTP), AccuStart Taq DNA Polymerase, and stabilizers.

Instrument Capability

ROX

  • Applied Biosystems 5700
  • Applied Biosystems 7000
  • Applied Biosystems 7300
  • Applied Biosystems 7700
  • Applied Biosystems 7900
  • Applied Biosystems 7900HT
  • Applied Biosystems 7900 HT Fast
  • Applied Biosystems StepOne™
  • Applied Biosystems StepOnePlus™

Low ROX

  • Applied Biosystems 7500
  • Applied Biosystems 7500 Fast
  • Stratagene Mx3000P®
  • Stratagene Mx3005P™
  • Stratagene Mx4000™
  • Applied Biosystems ViiA 7
  • Applied Biosystems QuantStudio™
  • Agilent AriaMx
  • Douglas Scientific IntelliQube®

No ROX

  • Quantabio Q
  • BioRad CFX
  • Roche LightCycler 480
  • QIAGEN Rotor-Gene Q
  • Other

Bio-Rad iCycler iQ systems

  • BioRad iCycler iQ™
  • BioRad MyiQ™
  • BioRad iQ™5

Resources

Product Manuals

CofA (PSFs)

Click here to see all CofA (PSFs)

SDSs

Publications

p53 regulates skeletal muscle mitophagy and mitochondrial quality control following denervation-induced muscle disuse
Jonathan M. Memme - 2021
Abstract
Persistent inactivity promotes skeletal muscle atrophy, marked by mitochondrial aberrations that affect strength, mobility, and metabolic health leading to the advancement of disease. Mitochondrial quality control (MQC) pathways include biogenesis (synthesis), mitophagy/lysosomal turnover, and the mitochondrial unfolded protein response (UPRmt) which serve to maintain an optimal organelle network. Tumor suppressor p53 has been implicated in regulating muscle mitochondria in response to cellular stress; however, its role in the context of muscle disuse has yet to be explored, and whether p53 is necessary for MQC remains unclear. To address this, we subjected p53 muscle-specific knockout (mKO) and wild-type (WT) mice to unilateral denervation. Transcriptomic and pathway analyses revealed dysregulation of pathways pertaining to mitochondrial function, and especially turnover, in mKO muscle following denervation. Protein and mRNA data of the MQC pathways indicated activation of the UPRmt and mitophagy-lysosome systems along with reductions in mitochondrial biogenesis and content in WT and mKO tissue following chronic denervation. However, p53 ablation also attenuated the expression of autophagy/mitophagy machinery, reduced autophagic flux, and enhanced lysosomal dysfunction. While similar reductions in mitochondrial biogenesis and content were observed between genotypes, MQC dysregulation exacerbated mitochondrial dysfunction in mKO fibers, evidenced by elevated reactive oxygen species (ROS). Moreover, acute experiments indicate that p53 mediates the expression of transcriptional regulators of MQC pathways as early as 1 day following denervation. Together, our data illustrate exacerbated mitochondrial dysregulation with denervation stress in p53 mKO tissue, thus indicating that p53 contributes to organellar maintenance via regulation of MQC pathways during muscle atrophy.
Differential expression of Oct3/4 in human breast cancer and normal tissues
Feng-Qi Zhao - 2018
Abstract
Oct3/4, a transcription factor specifically expressed in mammalian totipotent embryonic stem and germ cells, has a critical role in the regulation and maintenance of pluripotency and self-renewal. However, reactivation of Oct3/4 expression is observed in several human breast cancer cell lines, but not in non‑malignant cells. To examine Oct3/4 expression in human primary breast carcinomas and normal breast tissues, we obtained breast tumor tissues from 28 patients and normal breast tissues from 9 women. According to quantitative polymerase chain reaction, all of the tumor tissues, irrespective of tumor type or clinicopathological status, expressed Oct3/4 mRNA at 10- to 100- fold higher levels than that in the normal breast tissues. Expression of the Oct3/4 protein in tumors was confirmed by western blot analysis and immunofluorescent staining. Additionally, rapid amplification of cDNA ends and DNA sequencing revealed expression of multiple Oct4 gene transcripts from chromosome 6 (POU5F1) in normal breast tissues and the non‑malignant breast epithelial cell line MCF‑10A; by contrast, the breast tumors and malignant breast cancer cell line MCF‑7 predominantly expressed transcripts of an Oct4-like gene (POU5F1B) from chromosome 8, which was termed Oct3 in the current study. The deduced amino acid sequences of full-length Oct3 and Oct4 are 96% identical. The findings of the current study indicated that Oct3, rather than Oct4, may serve as a novel clinical marker and a potential target for gene-specific therapy of breast cancer
Establishment of neomycin phosphotransferase II
Asuka Itaya - 2018
Abstract
Soybean transformation is limited by the lack of multiple efficient selectable marker systems. Biolistic transformation of somatic proliferative embryogenic cultures, one of the commonly used soybean transformation methods, relies largely on hygromycin phosphotransferase II (hptII) selection. The purpose of the present study was to establish another efficient selectable marker system to facilitate multiple gene transformations of soybean. We tested neomycin phosphotransferase II (nptII) that has been used successfully in cotyledonary node transformation, but with limited success in transformation of embryogenic cultures. Transgenic events were obtained using nptII with improved G418 selection without generating escapes. G418 selection required longer recovery and selection periods, and resulted in a lower efficiency of initial transformants compared to hygromycin selection. Six independent fertile transgenic plants were recovered using nptII and G418, a frequency similar to that obtained with hygromycin selection. Soybean embryogenic cultures co-transformed with the hptII and nptII markers showed resistance to both hygromycin B and G418, while regeneration and plant fertility were not adversely affected. The nptII will be useful as a second selectable marker for multiple gene transformations in basic and applied soybean research.
Differential activation of neuronal and glial STAT3 in the spinal cord of the SOD1G93A mouse model of amyotrophic lateral sclerosis
Tomohiro Ohgomori - 2017
Abstract
Signal transducer and activator of transcription (STAT) proteins are activated by phosphorylation in the spinal cord of patients suffering from amyotrophic lateral sclerosis (ALS). The major scope of our study is a comprehensive histological characterization of the mechanisms underlying neuronal and glial STAT3 activation in the pathogenesis of ALS using SOD1G93A mice. We calculated the fold changes (FCs, ratios vs. appropriate controls) of the numerical densities of the following phosphorylated STAT3-positive (pSTAT3)+ cells: choline acetyltransferase (ChAT)+ α-motoneurons, ionized calcium-binding adapter molecule 1 (Iba1)+ microglia, and S100β+ astrocytes in SOD1G93A mice. The FCs of pSTAT3+ microglia and pSTAT3+ astrocytes were increased from 9 to 15 weeks of age and then plateaued until 21 weeks. In contrast, the FCs of pSTAT3+ α-motoneurons peaked at 9 weeks and then decreased until 21 weeks. The immunoreactivity for nonphosphorylated neurofilament protein (SMI-32), a marker of axonal impairment, was decreased in pSTAT3+ α-motoneurons compared with pSTAT3− α-motoneurons at 9 weeks of age. We then compared the following pharmacological models: the chronic administration of 3,3′-iminodipropionitrile (IDPN), which models axonal impairment and the acute administration of lipopolysaccharide (LPS), which is a model of neuroinflammation. The FCs of pSTAT3+ α-motoneurons were increased in IDPN-treated mice, while those of pSTAT3+ microglia were increased in LPS-treated mice. The FCs of pSTAT3+ astrocytes were higher in SOD1G93A mice at 9 weeks compared with IDPN- and LPS-treated mice. Our results indicate that axonopathy and neuroinflammation may trigger the respective activation of neuronal and glial STAT3, which is observed during ALS pathogenesis. This article is protected by copyright. All rights reserved.
The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 at DNA double strand breaks
Kyle S.Sorenson - 2017
Abstract
Double strand breaks (DSBs) represent highly deleterious DNA damage and need to be accurately repaired. Homology directed repair (HDR) and non-homologous end-joining (NHEJ) are the two major DSB repair pathways that are highly conserved from yeast to mammals. The choice between these pathways is largely based on 5′ to 3′ DNA resection, and NHEJ proceeds only if resection has not initiated. In yeast, yKu70/80 (Ku) rapidly localizes to the break, protecting DNA ends from nuclease accessibility and recruits additional NHEJ factors, including Nej1 and Lif1. Cells harboring the nej1-V338A mutant exhibit NHEJ-mediated repair deficiencies and hyper-resection 0.15 kb from the DSB that was dependent on the nuclease activity of Dna2-Sgs1. The integrity of Nej1 is also important for inhibiting long-range resection, 4.8 kb from the break, and for preventing the formation of large genomic deletions at sizes > 700 bp around the break. Nej1V338A localized to an HO-induced DSB similarly to WT Nej1 indicating that the Nej1-Lif1 interaction becomes mainly critical for blocking hyper-resection after their recruitment to the DSB. This work highlights that Nej1 inhibits 5′ DNA hyper-resection mediated by Dna2-Sgs1, a function distinct from its previously reported role in supporting Dnl4 ligase activity and has implications for repair pathway choice and resection regulation upon DSB formation.

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