|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A polyhistidine-tag is an amino acid motif in proteins that consists of at least five histidine (His) residues, often at the N- or C-terminus of the protein.
Polyhistidine-tags are often used for affinity purification of polyhistidine-tagged recombinant proteins expressed in Escherichia coli and other prokaryotic expression systems.
|Human HRAS ORF mammalian expression plasmid, C-GFPSpark tag||HG12059-ACG|
|Human HRAS ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG12059-ACR|
|Human HRAS ORF mammalian expression plasmid, C-Flag tag||HG12059-CF|
|Human HRAS ORF mammalian expression plasmid, C-His tag||HG12059-CH|
|Human HRAS ORF mammalian expression plasmid, C-Myc tag||HG12059-CM|
|Human HRAS ORF mammalian expression plasmid, C-HA tag||HG12059-CY|
|Human HRAS Gene cDNA clone plasmid||HG12059-G|
|Human HRAS ORF mammalian expression plasmid, N-Flag tag||HG12059-NF|
|Human HRAS ORF mammalian expression plasmid, N-His tag||HG12059-NH|
|Human HRAS ORF mammalian expression plasmid, N-Myc tag||HG12059-NM|
|Human HRAS ORF mammalian expression plasmid, N-HA tag||HG12059-NY|
|Human HRAS natural ORF mammalian 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.