Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : SHH422717
| Cat. No. | SHH422717 |
| Description | The SureSilencing trade; shRNA Plasmids are designed to specifically knock down the expression of individual genes by RNA interference under either transient (with GFP) or stable transfection (for hygromycin, neomycin or puromycin-resistance) conditions after performance of the appropriate enrichment or selection procedures, respectively. Each vector contains the shRNA under control of the U1 promoter and either the GFP gene, for the enrichment of transiently transfected cells, or the neomycin or puromycin resistance genes, for the selection of stably transfected cells. |
| Gene Abbr | TAF4 |
| Species | Mouse |
| Resistance | Hygromycin |
| Selection | Hygromycin |
| Storage | The SureSilencing shRNA Plasmids are shipped on dry ice or cold packs. Store all tubes at -20°C. |
| Target Gene | TAF4 |
| Background | Initiation of transcription by RNA polymerase II requires the activities of more than 70 polypeptides. The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position the polymerase properly, serves as the scaffold for assembly of the remainder of the transcription complex, and acts as a channel for regulatory signals. TFIID is composed of the TATA-binding protein (TBP) and a group of evolutionarily conserved proteins known as TBP-associated factors or TAFs. TAFs may participate in basal transcription, serve as coactivators, function in promoter recognition or modify general transcription factors (GTFs) to facilitate complex assembly and transcription initiation. This gene encodes one of the larger subunits of TFIID that has been shown to potentiate transcriptional activation by retinoic acid, thyroid hormone and vitamin D3 receptors. In addition, this subunit interacts with the transcription factor CREB, which has a glutamine-rich activation domain, and binds to other proteins containing glutamine-rich regions. Aberrant binding to this subunit by proteins with expanded polyglutamine regions has been suggested as one of the pathogenetic mechanisms underlying a group of neurodegenerative disorders referred to as polyglutamine diseases. [provided by RefSeq, Jul 2008] |
If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.
Write a review of your use of Biogene products and services in your research. Your review can help your fellow researchers make informed purchasing decisions.