|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A myc tag can be used in many different assays that require recognition by an antibody. If there is no antibody against the studied protein, adding a myc-tag allows one to follow the protein with an antibody against the Myc epitope. Examples are cellular localization studies by immunofluorescence or detection by Western blotting.
The peptide sequence of the myc-tag is: N-EQKLISEEDL-C (1202 Da). It can be fused to the C-terminus and the N-terminus of a protein. It is advisable not to fuse the tag directly behind the signal peptide of a secretory protein, since it can interfere with translocation into the secretory pathway.
|Rat TNFSF11 ORF mammalian expression plasmid, C-GFPSpark tag||RG80165-ACG|
|Rat TNFSF11 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80165-ACR|
|Rat TNFSF11 ORF mammalian expression plasmid, C-Flag tag||RG80165-CF|
|Rat TNFSF11 ORF mammalian expression plasmid, C-His tag||RG80165-CH|
|Rat TNFSF11 ORF mammalian expression plasmid, C-Myc tag||RG80165-CM|
|Rat TNFSF11 ORF mammalian expression plasmid, C-HA tag||RG80165-CY|
|Rat TNFSF11 Gene cDNA clone plasmid||RG80165-G|
|Rat TNFSF11 ORF mammalian expression plasmid, N-Flag tag||RG80165-NF|
|Rat TNFSF11 ORF mammalian expression plasmid, N-His tag||RG80165-NH|
|Rat TNFSF11 ORF mammalian expression plasmid, N-Myc tag||RG80165-NM|
|Rat TNFSF11 ORF mammalian expression plasmid, N-HA tag||RG80165-NY|
|Rat TNFSF11 natural ORF mammalian expression plasmid||RG80165-UT|
|Learn more about expression Vectors|
Tumor necrosis factor ligand superfamily member 11, also known as Receptor activator of nuclear factor kappa-B ligand, Osteoprotegerin ligand, TNFSF11, RANKL, TRANCE, OPGL and CD254, is a single-pass type II membrane protein which belongs to the tumor necrosis factor family. The receptor activator of nuclear factor-kappaB ligand (RANKL), its cognate receptor RANK, and its natural decoy receptor osteoprotegerin have been identified as the final effector molecules of osteoclastic bone resorption. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy. Genetically, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Inhibition of RANKL function via the natural decoy receptor osteoprotegerin (OPG, TNFRSF11B) prevents bone loss in postmenopausal osteoporosis and cancer metastases. Importantly, RANKL appears to be the pathogenetic principle that causes bone and cartilage destruction in arthritis. RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. In addition, RANKL and RANK have essential roles in lymph node formation, establishment of the thymic microenvironment, and development of a lactating mammary gland during pregnancy.