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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 OSTM1 ORF mammalian expression plasmid, C-GFPSpark tag||MG51952-ACG|
|Mouse OSTM1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG51952-ACR|
|Mouse OSTM1 ORF mammalian expression plasmid, C-Flag tag||MG51952-CF|
|Mouse OSTM1 ORF mammalian expression plasmid, C-His tag||MG51952-CH|
|Mouse OSTM1 ORF mammalian expression plasmid, C-Myc tag||MG51952-CM|
|Mouse OSTM1 ORF mammalian expression plasmid, C-HA tag||MG51952-CY|
|Mouse OSTM1 Gene cDNA clone plasmid||MG51952-G|
|Mouse OSTM1 ORF mammalian expression plasmid, N-Flag tag||MG51952-NF|
|Mouse OSTM1 ORF mammalian expression plasmid, N-His tag||MG51952-NH|
|Mouse OSTM1 ORF mammalian expression plasmid, N-Myc tag||MG51952-NM|
|Mouse OSTM1 ORF mammalian expression plasmid, N-HA tag||MG51952-NY|
|Mouse OSTM1 natural ORF mammalian expression plasmid||MG51952-UT|
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Osteopetrosis-associated transmembrane protein 1 (OSTM1) is a Single-pass type I membrane protein. It is expressed in many hematopoietic cells of the myeloid and lymphoid B- and T-lineages. The analysis of OSTM1 association with CLCN7 demonstrated that OSTM1 requires CLCN7 to localize to lysosomes, whereas the formation of a CLCN7-OSTM1 complex is required to stabilize CLCN7. The researches found that OSTM1 plays a major role in myelopoiesis and lymphopoiesis and provided evidence of a crosstalk mechanism between hematopoietic cells for osteoclast activation. Thus, OSTM1 has a important role in osteoclast function and activation. The loss of function of OSTM1 results in deregulation of multiple hematopoietic lineages in addition to osteoclast lineage, OSTM1-defect patients display the most severe recessive osteopetrotic phenotype and die at early ages. Furthermore, it is suggested that OSTM1 has a primary role in neural development not related to lysosomal dysfunction. The canonical Wnt/beta-catenin signaling pathway may be a molecular basis for OSTM1 mutations and severe autosomal recessive osteopetrosis (ARO).
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