Cd81 Mouse shRNA Plasmid (Locus ID 12520)

Specifications

Product Data
Product Name	Cd81 Mouse shRNA Plasmid (Locus ID 12520)
Locus ID	12520
UniProt ID	P35762
Synonyms	Tapa-1; Tapa1; Tspan28
Vector	pRS
Format	Retroviral plasmids
Kit Components	Cd81 - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector(Gene ID = 12520). 5µg purified plasmid DNA per construct 29-mer scrambled shRNA cassette in pRS Vector, TR30012, included for free.
RefSeq	BC011433, NM_133655, NM_133655.1, NM_133655.2
Summary	Structural component of specialized membrane microdomains known as tetraspanin-enriched microdomains (TERMs), which act as platforms for receptor clustering and signaling. Essential for trafficking and compartmentalization of CD19 receptor on the cell surface of activated B cells (PubMed:23499492). Upon initial encounter with a microbial pathogen, enables the assembly of CD19-CR2 and B cell receptor complexes at signaling TERMs, lowering the threshold dose of antigen required to trigger B cell clonal expansion and humoral immune response (By similarity). In T cells, associates with CD4 or CD8 coreceptors and defines the maturation state of antigen-induced synapses with B cells (By similarity). Facilitates localization of CD3 in these immune synapses, required for costimulation and sustained activation of T cells, preferentially triggering T helper type 2 immune response (PubMed:11046035). Can act both as positive and negative regulator of homotypic or heterotypic cell-cell fusion processes. In myoblasts, associates with another tetraspanin CD9 in complex with PTGFRN and inhibits myotube fusion during muscle regeneration (PubMed:23575678). In macrophages, associates with CD9 and beta-1 and beta-2 integrins, and prevents macrophage fusion into multinucleated giant cells specialized in ingesting complement-opsonized large particles. Also prevents the fusion between mononuclear cell progenitors into osteoclasts in charge of bone resorption. Positively regulates sperm-egg fusion and may be involved in the acrosome reaction (PubMed:16380109, PubMed:17290409). Regulates protein trafficking in intracellular compartments. In T cells, associates with dNTPase SAMHD1 and defines its subcellular location, enabling its degradation by the proteasome and thereby controlling intracellular dNTP levels (By similarity). Also regulates integrin-dependent migration of macrophages, particularly relevant for inflammatory response in the lung (PubMed:18662991).[UniProtKB/Swiss-Prot Function]
shRNA Design	These shRNA constructs were designed against multiple splice variants at this gene locus. To be certain that your variant of interest is targeted, please contact techsupport@origene.com. If you need a special design or shRNA sequence, please utilize our custom shRNA service.
Performance Guaranteed	OriGene guarantees that the sequences in the shRNA expression cassettes are verified to correspond to the target gene with 100% identity. One of the four constructs at minimum are guaranteed to produce 70% or more gene expression knock-down provided a minimum transfection efficiency of 80% is achieved. Western Blot data is recommended over qPCR to evaluate the silencing effect of the shRNA constructs 72 hrs post transfection. To properly assess knockdown, the gene expression level from the included scramble control vector must be used in comparison with the target-specific shRNA transfected samples. For non-conforming shRNA, requests for replacement product must be made within ninety (90) days from the date of delivery of the shRNA kit. To arrange for a free replacement with newly designed constructs, please contact Technical Services at techsupport@origene.com. Please provide your data indicating the transfection efficiency and measurement of gene expression knockdown compared to the scrambled shRNA control (Western Blot data preferred).

*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen complexities in the preparation of your product. International customers may expect an additional 1-2 weeks in shipping.