|Datasheet||Specific References||Reviews||Related Products||Protocols|
The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|Human FKBP14 Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||HG13522-G-F|
|Human FKBP14 Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG13522-G-H|
|Human FKBP14 Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG13522-G-M|
|Human FKBP14 Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG13522-G-N|
|Human FKBP14 Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG13522-G-Y|
FKBP14 belongs to the FK506-binding protein family. It contains 2 EF-hand domains and one PPIase FKBP-type domain. FKBP14 can be detected in the lumen of the endoplasmic reticulum where it is thought to accelerate the folding of proteins during protein synthesis. Truncation of the amino-terminus of FKBP14 significantly decreases peptidyl prolyl cis-trans isomerase activity, therefore implicating that the PPIase FKBP-type domain must be located at the N-terminus. Defects in FKBP14 can cause Ehlers-Danlos syndrome with progressive kyphoscoliosis, myopathy, and hearing loss. A syndrome with features of Ehlers-Danlos syndrome types VIA and VIB on the one hand, and the collagen VI-related congenital myopathies Ullrich congenital muscular dystrophy and Bethlem myopathy on the other hand.