|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.
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-GFPSpark 标签||RG80712-ACG|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-OFPSpark 标签||RG80712-ACR|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-Flag 标签||RG80712-CF|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-His 标签||RG80712-CH|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-Myc 标签||RG80712-CM|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), C-HA 标签||RG80712-CY|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), N-Flag 标签||RG80712-NF|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), N-His 标签||RG80712-NH|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), N-Myc 标签||RG80712-NM|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体), N-HA 标签||RG80712-NY|
|大鼠 CTHRC1 基因ORF全长cDNA(克隆载体)||RG80712-U|
|大鼠 CTHRC1 基因ORF全长cDNA克隆(表达载体)||RG80712-UT|
Collagen triple helix repeat-containing protein 1, also known as Protein NMTC1, and CTHRC1, is a secreted protein that is glycosylated and highly conserved from lower chordates to mammals. CTHRC1 expression was not detectable in normal arteries. However, it is transiently expressed in the arterial wall in response to injury where it may contribute to vascular remodeling by limiting collagen matrix deposition and promoting cell migration. A short collagen motif with 12 Gly-X-Y repeats appears to be responsible for trimerization of the CTHRC1 protein and this renders the molecule susceptible to cleavage by collagenase. CTHRC1 overexpression caused a dramatic reduction in collagen type I mRNA and protein levels. Currently available data indicate that Cthrc1 expression in vascular cells regulates transforming growth factor beta responsiveness, thereby impacting transforming growth factor beta target genes, including collagens. Additionally, CTHRC1 increases bone mass as a positive regulator of osteoblastic bone formation and offers an anabolic approach for the treatment of osteoporosis.