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pMD18-T Simple Vector is a high-efficiency TA cloning vector constructed from pUC18, of which the initial multiple cloning sites (MCS) were destroyed. Thus the cDNA should be amplified by PCR with primers containing a restriction site for subclone. Competent cells appropriate for pUC18 are also appropriated for the Vector, e.g. JM109, DH5α, TOP10. The pMD18-T Simple Vector is 2.6kb in size. Selection of the plasmid in E. coli is conferred by the ampicillin resistance gene. The coding sequence was inserted by TA cloning at site 425.
The coding sequence can be amplified by PCR with M13-47 and RV-M primers.
|Mouse PRLR ORF mammalian expression plasmid, C-GFPSpark tag||MG50457-ACG|
|Mouse PRLR ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50457-ACR|
|Mouse PRLR ORF mammalian expression plasmid, C-Flag tag||MG50457-CF|
|Mouse PRLR ORF mammalian expression plasmid, C-His tag||MG50457-CH|
|Mouse PRLR ORF mammalian expression plasmid, C-Myc tag||MG50457-CM|
|Mouse PRLR ORF mammalian expression plasmid, C-HA tag||MG50457-CY|
|Mouse PRLR ORF mammalian expression plasmid, N-Flag tag||MG50457-NF|
|Mouse PRLR ORF mammalian expression plasmid, N-His tag||MG50457-NH|
|Mouse PRLR ORF mammalian expression plasmid, N-Myc tag||MG50457-NM|
|Mouse PRLR ORF mammalian expression plasmid, N-HA tag||MG50457-NY|
|Mouse PRLR natural ORF mammalian expression plasmid||MG50457-UT|
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Prolactin receptor (PRLR) is a single-pass transmembrane receptor belonging to the type â… cytokine receptor superfamily, and contains two fibronectin type-â…¢ domains. All class 1 ligands activate their respective receptors by clustering mechanisms. Ligand binding results in the transmembrane PRLR dimerization, followed by phosphorylation and activation of the molecules invloved in the signaling pathways, such as Jak-STAT, Ras/Raf/MAPK. The PRLR contains no intrinsic tyrosine kinase cytoplasmic domain but associates with a cytoplasmic tyrosine kinase, JAK2. PRLR mainly serves as the receptor for the pituitary hormone prolactin (PRL), a secreted hormone that affects reproduction and homeostasis in vertebrates. PRLR can be regulated by an interplay of two different mechanisms, PRL or ovarian steroid hormones independently or in combination in a tissue-specific manner. The role of the hormone prolactin (PRL) in the pathogenesis of breast cancer is mediated by its cognate receptor (PRLR). Ubiquitin-dependent degradation of the PRLR that negatively regulates PRL signaling is triggered by PRL-mediated phosphorylation of PRLR on Ser349 followed by the recruitment of the beta-transducin repeats-containing protein (beta-TrCP) ubiquitin-protein isopeptide ligase. which altered PRLR stability may directly influence the pathogenesis of breast cancer.