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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.
|Human Smad3 Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||HG10892-M-F|
|Human Smad3 Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG10892-M-H|
|Human Smad3 Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG10892-M-M|
|Human Smad3 Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG10892-M-N|
|Human Smad3 Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG10892-M-Y|
SMAD3 belongs to the SMAD family. Members of this family mediate signal transduction by the TGF-beta/activin/BMP-2/4 cytokine superfamily from receptor Ser/Thr protein kinases at the cell surface to the nucleus. SMAD3 is involved in cell signalling. It modulates signals of activin and TGFβ's. Binding of SMAD3 with SMAD4 enables its transmigration into the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD3 is a receptor-regulated SMAD (R-SMAD). In mice, mutation of SMAD3 has been linked to colorectal adenocarcinoma, increased systemic inflammation, and accelerated wound healing. Increased SMAD3 activity has been implicated in the pathogenesis of scleroderma. Smad3 is also a multifaceted regulator in adipose physiology and the pathogenesis of obesity and type 2 diabetes.