|Datasheet||Specific References||Reviews||Related Products||Protocols|
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 BDNF transcript variant 4 cDNA ORF Clone, expression ready, FLAG-tagged||HG10068-M-F|
|Human BDNF transcript variant 4 Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG10068-M-H|
|Human BDNF transcript variant 4 Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG10068-M-M|
|Human BDNF transcript variant 4 Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG10068-M-N|
|Human BDNF transcript variant 4 Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG10068-M-Y|
BDNF is a member of the nerve growth factor family. It is highly expressed in hippocampus, amygdala, cerebral cortex and cerebellum. It also can be detected in heart, lung, skeletal muscle, testis, prostate and placenta. BDNF is induced by cortical neurons, and is necessary for survival of striatal neurons in the brain. During development, BDNF promotes the survival and differentiation of selected neuronal populations of the peripheral and central nervous systems. It participates in axonal growth, pathfinding and in the modulation of dendritic growth and morphology. It functions as the major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS. The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability.