qScript One-Step SYBR Green RT-qPCR
1-step SYBR simplicity
Features & Benefits
- Sensitive RNA detection with performance-engineered, RNase H (+) M-MLV reverse transcriptase.
- Stringent ultra-pure antibody hot start ensures precise target amplification.
- Flexible buffer chemistry supports either conventional or accelerated thermal cycling conditions.
qScript One-Step SYBR Green RT-qPCR Kit is intended for molecular biology applications. This product is not intended for the diagnosis, prevention or treatment of a disease.
The qScript One-Step SYBR Green RT-qPCR Kit is a convenient and highly sensitive solution for quantitative RT-PCR of RNA templates (RT-qPCR) using SYBR Green I dye detection and gene-specific primers. cDNA synthesis and PCR amplification are carried out in the same tube without opening between procedures.The proprietary reaction buffer has been specifically formulated to maximize activities of both reverse transcriptase and Taq DNA polymerase while minimizing the potential for primer-dimer and other non-specific PCR artifacts. This reagent is compatible with both fast and standard qPCR cycling protocols. Precise amplification is essential for successful RT-qPCR with SYBR Green I technology since this dye binds to all dsDNA generated during amplification. This 1-step reagent contains ultra-pure AccuStart™ hot start Taq DNA polymerase that is completely arrested prior to the initial PCR denaturation step. Upon heat activation at 95°C, the antibodies are rapidly and irreversibly denatured, releasing a fully active high-yielding Taq DNA polymerase mutant.
Contents50X concentrated qScript One-Step Reverse Transcriptase - Optimized 50X formulation of recombinant MMLV reverse transcriptase for one-step RT-PCR. One-Step SYBR Green Master Mix (2X) - 2X reaction buffer containing dNTPs, magnesium chloride, AccuStart Taq DNA polymerase, stabilizers, and SYBR Green I dye Nuclease-free water
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.
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Related ResourcesProduct ManualsqScript One-Step SYBR® Green qRT-PCR KitqScript One-Step SYBR Green qRT-PCR Kit for iQqScript One-Step SYBR Green qRT-PCR Kit, ROXqScript One-Step SYBR Green qRT-PCR Kit, Low ROXSafety Data Sheets (SDS)qScript One-Step SYBR® Green qRT-PCR KitqScript One-Step SYBR® Green qRT-PCR Kit for iQqScript One-Step SYBR® Green qRT-PCR Kit, ROXqScript One-Step SYBR® Green qRT-PCR Kit, Low ROXCofA (PSF)PSF-95086-200-Lot#022591PSF-95086-200-Lot#023379PSF-95087-050-Lot#022441PSF-95087-050-Lot#023390PSF-95087-200-Lot#022307PSF-95087-200-Lot#022308PSF-95087-200-Lot#023130PSF-95088-050-Lot#022174PSF-95088-050-Lot#023392PSF-95089-050-Lot#022532PSF-95089-200-Lot#023205PSF-95087-200-Lot#023130PSF-95088-200-Lot#022815PublicationsHeterogeneous Nuclear Ribonucleoprotein L is required for the survival and functional integrity of murine hematopoietic stem cells : Scientific ReportsMarie-Claude Gaudreau, Scientific Reports - 2016AbstractThe proliferation and survival of hematopoietic stem cells (HSCs) has to be strictly coordinated to ensure the timely production of all blood cells. Here we report that the splice factor and RNA binding protein hnRNP L (heterogeneous nuclear ribonucleoprotein L) is required for hematopoiesis, since its genetic ablation in mice reduces almost all blood cell lineages and causes premature death of the animals. In agreement with this, we observed that hnRNP L deficient HSCs lack both the ability to self-renew and foster hematopoietic differentiation in transplanted hosts. They also display mitochondrial dysfunction, elevated levels of γH2AX, are Annexin V positive and incorporate propidium iodide indicating that they undergo cell death. Lin-c-Kit+ fetal liver cells from hnRNP L deficient mice show high p53 protein levels and up-regulation of p53 target genes. In addition, cells lacking hnRNP L up-regulated the expression of the death receptors TrailR2 and CD95/Fas and show Caspase-3, Caspase-8 and Parp cleavage. Treatment with the pan-caspase inhibitor Z-VAD-fmk, but not the deletion of p53, restored cell survival in hnRNP L deficient cells. Our data suggest that hnRNP L is critical for the survival and functional integrity of HSCs by restricting the activation of caspase-dependent death receptor pathways.The liver-specific microRNA-122*, the complementary strand of microRNA-122, acts as a tumor suppressor by modulating the p53/mouse double minute 2 homolog circuitryAlina Simerzin, Hepatology - 2016AbstractThe tumor suppressor p53 is a central regulator of signaling pathways that controls the cell cycle and maintains the integrity of the human genome. p53 level is regulated by mouse double minute 2 homolog (Mdm2), which marks p53 for proteasomal degradation. The p53-Mdm2 circuitry is subjected to complex regulation by a variety of mechanisms, including microRNAs (miRNAs). We found a novel effector of this regulatory circuit, namely, miR-122*, the passenger strand of the abundantly expressed liver-specific miR-122. Here, we demonstrate that miR-122* levels are reduced in human hepatocellular carcinoma (HCC). We found that miR-122* targets Mdm2, thus participating as an important player in the p53-Mdm2 circuitry. Moreover, we observed significant negative correlation between levels of miR-122* and Mdm2 in a large set of human HCC samples. In vivo tumorigenicity assays demonstrate that miR-122* is capable of inhibiting tumor growth, emphasizing the tumor-suppressor characteristics of this miRNA. Furthermore, we show that blocking miR-122 in murine livers with an antagomiR-122 (miRNA inhibitor) results in miR-122* accumulation, leading to Mdm2 repression followed by elevated p53 protein levels. Conclusion: We show that miR-122*, the passenger strand of miR-122, regulates the activity of p53 by targeting Mdm2. Importantly, similarly to miR-122, miR-122* is significantly down-regulated in human HCC. We therefore propose that miR-122* is an important contributor to the tumor suppression activity previously attributed solely to miR-122. (Hepatology 2016)The impact of the long-distance transport of a BEL1-Like Messenger RNA on DevelopmentTian Lin, Original Research - 2016AbstractBEL1- and KNOTTED1-type proteins are transcription factors from the three-amino-loop-extension superclass that interact in atandem complex to regulate the expression of target genes. In potato (Solanum tuberosum), StBEL5 and its Knox protein partner regulate tuberization by targeting genes that control growth. RNA movement assays demonstrated that StBEL5 transcripts move through the phloem to stolon tips, the site of tuber induction.StBEL5 messenger RNA originates in the leaf, and its movement to stolons is induced by a short-day photoperiod. Here, we report the movement of StBEL5 RNA to roots correlated with increased growth, changes in morphology, and accumulation of GA2-oxidase1,YUCCA1a, and ISOPENTENYL TRANSFERASE transcripts. Transcription of tBEL5 n leaves is induced by light but insensitive to photoperiod, whereas in stolon tips growing in the dark, romoter activity is enhanced by short days. The heterodimer of StBEL5 and POTH1, a KNOTTED1-type transcription factor,binds to a tandem TTGAC-TTGAC motif that is essential for regulating transcription. The discovery of an inverted tandem motifin the tBEL5 romoter with TTGAC motifs on opposite strands may explain the induction of tBEL5 romoter activity in stolon ips under short days. Using transgenic potato lines, deletion of one of the TTGAC motifs from the tBEL5 romoter results in he reduction of GUS activity in new tubers and roots. Gel-shift assays demonstrate BEL5/POTH1 binding specificity to the otifs present in the tBEL5 promoter and a double tandem motif present in the StGA2-oxidase1 promoter. These results suggest that, in addition to tuberization, the movement of StBEL5 messenger RNA regulates other aspects of vegetative development.Engagement of distinct epitopes on CD43 induces different co-stimulatory pathways in human T cellsMadhura Modak, Immunology - 2016AbstractCo-receptors, being either co-stimulatory or co-inhibitory, play a pivotal role in T-cell immunity. Several studies have indicated that CD43, one of the abundant T-cell surface glycoproteins, acts not only as a potent co-receptor but also as a negative regulator for T-cell activation. Here we demonstrate that co-stimulation of human peripheral blood (PB) T cells through two distinct CD43 epitopes recognized by monoclonal antibodies (mAb) CD43-6E5 (T6E5-act) and CD43-10G7 (T10G7-act) potently induced T-cell proliferation. However, T-cell co-stimulation through two CD43 epitopes differentially regulated activation of nuclear factor of activated T cells (NFAT) and nuclear factor-κB (NF-κB) transcription factors, T-cell cytokine production and effector function. T6E5-act produced high levels of interleukin-22 (IL-22) and interferon-γ (IFN-γ) similar to T cells activated via CD28 (TCD28-act), whereas T10G7-act produced low levels of inflammatory cytokines but higher levels of regulatory cytokines transforming growth factor-β (TGF-β) and interleukin-35 (IL-35). Compared with T6E5-act or to TCD28-act, T10G7-act performed poorly in response to re-stimulation and further acquired a T-cell suppressive function. T10G7-act did not directly inhibit proliferation of responder T cells, but formed stable heterotypic clusters with dendritic cells (DC) via CD2 to constrain activation of responder T cells. Together, our data demonstrate that CD43 is a unique and polarizing regulator of T-cell function.RALFL34 regulates formative cell divisions in Arabidopsis pericycle during lateral root initiationClick here to see all PublicationsEvan Murphy, Journal of Experimental Botany - 2016AbstractIn plants, many signalling molecules, such as phytohormones, miRNAs, transcription factors, and small signalling peptides, drive growth and development. However, very few small signalling peptides have been shown to be necessary for lateral root development. Here, we describe the role of the peptide RALFL34 during early events in lateral root development, and demonstrate its specific importance in orchestrating formative cell divisions in the pericycle. Our results further suggest that this small signalling peptide acts on the transcriptional cascade leading to a new lateral root upstream of GATA23, an important player in lateral root formation. In addition, we describe a role for ETHYLENE RESPONSE FACTORs (ERFs) in regulating RALFL34 expression. Taken together, we put forward RALFL34 as a new, important player in lateral root initiation.