|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.
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-GFPSpark tag||CG90065-ACG|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-OFPSpark tag||CG90065-ACR|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-Flag tag||CG90065-CF|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-His tag||CG90065-CH|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-Myc tag||CG90065-CM|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, C-HA tag||CG90065-CY|
|Rhesus BMPR2 Gene ORF cDNA clone in cloning vector||CG90065-G|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, N-Flag tag||CG90065-NF|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, N-His tag||CG90065-NH|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, N-Myc tag||CG90065-NM|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid, N-HA tag||CG90065-NY|
|Rhesus BMPR2 Gene ORF cDNA clone expression plasmid||CG90065-UT|
|Learn more about expression Vectors|
The bone morphogenetic protein type II receptor (BMPR-II, or BMPR2), a receptor for the transforming growth factor (TGF)-beta/bone morphogenetic protein (BMP) superfamily. Reduced expression or function of BMPR2 signaling leads to exaggerated TGF-beta signaling and altered cellular responses to TGF-beta. In endothelial cells, BMPR2 mutation increases the susceptibility of cells to apoptosis. BMPR2 transduces BMP signals by forming heteromeric complexes with and phosphorylating BMP type I receptors. The intracellular domain of BMPR2 is both necessary and sufficient for receptor complex interaction. It had been identified that BMPR2 plays a key role in cell growth. Its mutations lead to hereditary pulmonary hypertension, and knockout of Bmpr-II results in early embryonic lethality. The C-terminal tail of BMPR2 provides binding sites for a number of regulatory proteins that may initiate Smad-independent signalling. BMPR2 mutations were predicted to alter the BMP and TGF-b1/SMAD signalling pathways, resulting in proliferation rather than apoptosis of vascular cells, and greatly increase the risk of developing severe pulmonary arterial hypertension. BMPR2 gene result in familial Primary pulmonary hypertension (PPH) transmitted as an autosomal dominant trait, albeit with low penetrance. Heterozygous germline mutations of BMPR2 gene have been identified in patients with familial and sporadic PPH, indicating that BMPR2 may contribute to the maintenance of normal pulmonary vascular structure and function. Tctex-1, a light chain of the motor complex dynein, interacts with the cytoplasmic domain of BMPR2 and demonstrate that Tctex-1 is phosphorylated by BMPR-II, a function disrupted by PPH disease causing mutations within exon 12. BMPR2 and Tctex-1 co-localize to endothelium and smooth muscle within the media of pulmonary arterioles, key sites of vascular remodelling in PPH.