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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.
|Mouse ATL1 ORF mammalian expression plasmid, C-GFPSpark tag||MG50784-ACG|
|Mouse ATL1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50784-ACR|
|Mouse ATL1 ORF mammalian expression plasmid, C-Flag tag||MG50784-CF|
|Mouse ATL1 ORF mammalian expression plasmid, C-His tag||MG50784-CH|
|Mouse ATL1 ORF mammalian expression plasmid, C-Myc tag||MG50784-CM|
|Mouse ATL1 ORF mammalian expression plasmid, C-HA tag||MG50784-CY|
|Mouse ATL1 ORF mammalian expression plasmid, N-Flag tag||MG50784-NF|
|Mouse ATL1 ORF mammalian expression plasmid, N-His tag||MG50784-NH|
|Mouse ATL1 ORF mammalian expression plasmid, N-Myc tag||MG50784-NM|
|Mouse ATL1 ORF mammalian expression plasmid, N-HA tag||MG50784-NY|
|Mouse ATL1 natural ORF mammalian expression plasmid||MG50784-UT|
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Atlastin-1, also known as Spastic paraplegia 3 protein A, Guanine nucleotide-binding protein 3, GTP-binding protein 3, GBP3, ATL1 and SPG3A, is a multi-pass membrane protein which belongs to the GBP family and atlastin subfamily. ATL1 / SPG3A is expressed predominantly in the adult and fetal central nervous system. Expression of ATL1 / SPG3A in adult brain is at least 50-fold higher than in other tissues. ATL1 / SPG3A is detected predominantly in pyramidal neurons in the cerebral cortex and the hippocampus of the brain. ATL1 / SPG3A is also expressed in upper and lower motor neurons (at protein level). A distinguishing feature of ATL1 / SPG3A is its frequent early onset, raising the possibility that developmental abnormalities may be involved in its pathogenesis. Missense SPG3A mutant atlastin-1 proteins have impaired GTPase activity and may act in a dominant-negative, loss-of-function manner by forming mixed oligomers with wild-type atlastin-1. Defects in ATL1 / SPG3A are the cause of spastic paraplegia autosomal dominant type 3 (SPG3), also known as Strumpell-Lorrain syndrome. Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs.