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pUC19 is a small, high-copy number E. coli plasmid cloning vector, of which multiple cloning sites as shown below. The molecule is a small double-stranded circle, 2686 base pairs in length. pUC19 encodes the N-terminal fragment of b-galactosidase (lacZa), which allows for blue/white colony screening (i.e., a-complementation), as well as a pUC origin of replication.
The coding sequence can be amplified by PCR with M13-47 and RV-M primers.
|Rat IGF1 ORF mammalian expression plasmid, C-GFPSpark tag||RG80503-ACG|
|Rat IGF1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80503-ACR|
|Rat IGF1 ORF mammalian expression plasmid, C-Flag tag||RG80503-CF|
|Rat IGF1 ORF mammalian expression plasmid, C-His tag||RG80503-CH|
|Rat IGF1 ORF mammalian expression plasmid, C-Myc tag||RG80503-CM|
|Rat IGF1 ORF mammalian expression plasmid, C-HA tag||RG80503-CY|
|Rat IGF1 ORF mammalian expression plasmid, N-Flag tag||RG80503-NF|
|Rat IGF1 ORF mammalian expression plasmid, N-His tag||RG80503-NH|
|Rat IGF1 ORF mammalian expression plasmid, N-Myc tag||RG80503-NM|
|Rat IGF1 ORF mammalian expression plasmid, N-HA tag||RG80503-NY|
|Rat IGF1 Gene cDNA clone plasmid||RG80503-U|
|Rat IGF1 natural ORF mammalian expression plasmid||RG80503-UT|
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IGF I, also known as mechano growth factor, somatomedin-C, IGF-I and IGF1, is a secreted protein which belongs to the?insulin family. The insulin family, comprised of insulin, relaxin, insulin-like growth factors I and II ( IGF-I and IGF-II ) and possibly the beta-subunit of 7S nerve growth factor, represents a group of structurally related polypeptides whose biological functions have diverged. The IGFs, or somatomedins, constitute a class of polypeptides that have a key role in pre-adolescent mammalian growth. IGF-I expression is regulated by GH and mediates postnatal growth, while IGF-II appears to be induced by placental lactogen during prenatal development. IGF1 / IGF-I may be a physiological regulator of [1-14C]-2-deoxy-D-glucose (2DG) transport and glycogen synthesis in osteoblasts. IGF1 / IGF-I stimulates glucose transport in rat bone-derived osteoblastic (PyMS) cells and is effective at much lower concentrations than insulin, not only regarding glycogen and DNA synthesis but also with regard to enhancing glucose uptake. Defects in IGF1 / IGF-I are the cause of insulin-like growth factor I deficiency (IGF1 deficiency) which is an autosomal recessive disorder characterized by growth retardation, sensorineural deafness and mental retardation.