|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 HRAS Gene ORF cDNA clone expression plasmid, C-GFPSpark tag||HG12059-ACG|
|Human HRAS Gene ORF cDNA clone expression plasmid, C-OFPSpark tag||HG12059-ACR|
|Human HRAS Gene ORF cDNA clone expression plasmid, C-Flag tag||HG12059-CF|
|Human HRAS Gene ORF cDNA clone expression plasmid, C-His tag||HG12059-CH|
|Human HRAS Gene ORF cDNA clone expression plasmid, C-Myc tag||HG12059-CM|
|Human HRAS Gene ORF cDNA clone expression plasmid, C-HA tag||HG12059-CY|
|Human HRAS Gene ORF cDNA clone in cloning vector||HG12059-G|
|Human HRAS Gene ORF cDNA clone expression plasmid, N-Flag tag||HG12059-NF|
|Human HRAS Gene ORF cDNA clone expression plasmid, N-His tag||HG12059-NH|
|Human HRAS Gene ORF cDNA clone expression plasmid, N-Myc tag||HG12059-NM|
|Human HRAS Gene ORF cDNA clone expression plasmid, N-HA tag||HG12059-NY|
|Human HRAS Gene ORF cDNA clone expression plasmid||HG12059-UT|
|Learn more about expression Vectors|
HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is arare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Defects in HRAS are the cause of oral squamous cell carcinoma.