|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A myc tag can be used in many different assays that require recognition by an antibody. If there is no antibody against the studied protein, adding a myc-tag allows one to follow the protein with an antibody against the Myc epitope. Examples are cellular localization studies by immunofluorescence or detection by Western blotting.
The peptide sequence of the myc-tag is: N-EQKLISEEDL-C (1202 Da). It can be fused to the C-terminus and the N-terminus of a protein. It is advisable not to fuse the tag directly behind the signal peptide of a secretory protein, since it can interfere with translocation into the secretory pathway.
|Human TPP1 ORF mammalian expression plasmid, C-GFPSpark tag||HG13619-ACG|
|Human TPP1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG13619-ACR|
|Human TPP1 ORF mammalian expression plasmid, C-Flag tag||HG13619-CF|
|Human TPP1 ORF mammalian expression plasmid, C-His tag||HG13619-CH|
|Human TPP1 ORF mammalian expression plasmid, C-Myc tag||HG13619-CM|
|Human TPP1 ORF mammalian expression plasmid, C-HA tag||HG13619-CY|
|Human TPP1 Gene cDNA clone plasmid||HG13619-G|
|Human TPP1 ORF mammalian expression plasmid, N-Flag tag||HG13619-NF|
|Human TPP1 ORF mammalian expression plasmid, N-His tag||HG13619-NH|
|Human TPP1 ORF mammalian expression plasmid, N-Myc tag||HG13619-NM|
|Human TPP1 ORF mammalian expression plasmid, N-HA tag||HG13619-NY|
|Human TPP1 natural ORF mammalian expression plasmid||HG13619-UT|
|Learn more about expression Vectors|
Tripeptidyl-peptidase 1 (TPP1 / CLN2) is a member of the sedolisin family of serine proteases. The protease functions in the lysosome to cleave N-terminal tripeptides from substrates, and has weaker endopeptidase activity. It is synthesized as a catalytically-inactive enzyme which is activated and auto-proteolyzed upon acidification. TPP1 / CLN2 May act as a non-specific lysosomal peptidase which generates tripeptides from the breakdown products produced by lysosomal proteinases. Defects in TPP1 / CLN2 are the cause of neuronal ceroid lipofuscinosis type 2 (CLN2), a form of neuronal ceroid lipofuscinosis which is associated with the failure to degrade specific neuropeptides and a subunit of ATP synthase in the lysosome. Neuronal ceroid lipofuscinoses are progressive neurodegenerative, lysosomal storage diseases characterized by intracellular accumulation of autofluorescent liposomal material, and clinically by seizures, dementia, visual loss, and/or cerebral atrophy.