|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
Human influenza hemagglutinin (HA) is a surface glycoprotein required for the infectivity of the human virus. The HA tag is derived from the HA-molecule corresponding to amino acids 98-106 has been extensively used as a general epitope tag in expression vectors. Many recombinant proteins have been engineered to express the HA tag, which does not appear to interfere with the bioactivity or the biodistribution of the recombinant protein. This tag facilitates the detection, isolation, and purification of the proteins.
The actual HA tag is as follows: 5' TAC CCA TAC GAT GTT CCA GAT TAC GCT 3' or 5' TAT CCA TAT GAT GTT CCA GAT TAT GCT 3' The amino acid sequence is: YPYDVPDYA.
|Human CTRL ORF mammalian expression plasmid, C-GFPSpark tag||HG13748-ACG|
|Human CTRL ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG13748-ACR|
|Human CTRL ORF mammalian expression plasmid, C-Flag tag||HG13748-CF|
|Human CTRL ORF mammalian expression plasmid, C-His tag||HG13748-CH|
|Human CTRL ORF mammalian expression plasmid, C-Myc tag||HG13748-CM|
|Human CTRL ORF mammalian expression plasmid, C-HA tag||HG13748-CY|
|Human CTRL Gene cDNA clone plasmid||HG13748-G|
|Human CTRL ORF mammalian expression plasmid, N-Flag tag||HG13748-NF|
|Human CTRL ORF mammalian expression plasmid, N-His tag||HG13748-NH|
|Human CTRL ORF mammalian expression plasmid, N-Myc tag||HG13748-NM|
|Human CTRL ORF mammalian expression plasmid, N-HA tag||HG13748-NY|
|Human CTRL natural ORF mammalian expression plasmid||HG13748-UT|
|Learn more about expression Vectors|
CTRL-1, also known as chymotrypsin-like protease, belongs to the peptidase S1 family. CTRL-1 contains 1 peptidase S1 domain. Its expression is increased in preeclampsia (PE). Placental-derived chymotrypsin-like protease is responsible for inducing endothelial inflammatory phenotypic changes possibly by upregulation of cell adhesion molecule expressions, activation of cellular protease, and induction of extracellular regulated kinase phosphorylation. Activated microglia have been observed in various neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis, and multiple sclerosis. Five structurally distinct inhibitors that are known to inhibit chymotrypsin-like proteases were partially protective. They might represent a novel class of drugs with benefit in diseases where overactivity of microglia contributes to the pathogenesis.