shRNA set against Mouse COL6A3 (NM_001243008.1)

Name: shRNA set against Mouse COL6A3 (NM_001243008.1)
SKU: SHH267405
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : SHH267405

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Product Information

Gene Information

Cat. No.	SHH267405
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	COL6A3
Species	Mouse
Report Gene	GFP
Storage	The SureSilencing shRNA Plasmids are shipped on dry ice or cold packs. Store all tubes at -20°C.

Target Gene

COL6A3

Background

This gene encodes the alpha-3 chain, one of the three alpha chains of type VI collagen, a beaded filament collagen found in most connective tissues. The alpha-3 chain of type VI collagen is much larger than the alpha-1 and -2 chains. This difference in size is largely due to an increase in the number of subdomains, similar to von Willebrand Factor type A domains, that are found in the amino terminal globular domain of all the alpha chains. These domains have been shown to bind extracellular matrix proteins, an interaction that explains the importance of this collagen in organizing matrix components. Mutations in the type VI collagen genes are associated with Bethlem myopathy, a rare autosomal dominant proximal myopathy with early childhood onset. Mutations in this gene are also a cause of Ullrich congenital muscular dystrophy, also referred to as Ullrich scleroatonic muscular dystrophy, an autosomal recessive congenital myopathy that is more severe than Bethlem myopathy. Multiple transcript variants have been identified, but the full-length nature of only some of these variants has been described. [provided by RefSeq, Jun 2009]

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