SignalSilence®VPRBP siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit VPRBP expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence®siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis.
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Description
SignalSilence®VPRBP siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit VPRBP expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence®siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis.
Quality Control
Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
Directions for Use
CST recommends transfection with 100 nM SignalSilence®VPRBP siRNA I 48 to 72 hours prior to cell lysis. For transfection procedure, follow protocol provided by the transfection reagent manufacturer. Please feel free to contact CST with any questions on use.
Each vial contains the equivalent of 100 transfections, which corresponds to a final siRNA concentration of 100 nM per transfection in a 24-well plate with a total volume of 300 μl per well.
Background
The HIV-1 viral protein R (Vpr)-binding protein (VPRBP, DCAF1) is a substrate-specific adaptor for the CUL4-based ubiquitin ligase complex that consists of CUL4A, RBX1, and DDB1 (1). VPRBP protein structure contains a central LIS1 homology (LisH) motif responsible for dimerization, and two carboxy-terminal WD-40 motifs involved in Vpr and DDB1 binding (2-4). Research studies demonstrate that VPRBP plays a role in hepatic lipid metabolism by promoting the ubiquitin-dependent proteasomal degradation of the TR4 nuclear receptor, which is involved in lipid homeostasis (5). The VPRBP protein plays a role in mammalian germ cell development through regulation of TET methylcytosine dioxygenase activation (6). Additional studies show that VPRBP exhibits kinase activity and phosphorylates histone H2A at Ser120, which blocks tumor suppressor gene transcription (7). The tumor suppressor Merlin/NF2 inhibits tumorigenesis through interaction with and suppression of the CUL4A-RBX1-DDB1-VPRBP complex (8).
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