PCSK9 (NM_174936) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC220000L4V

Lenti ORF particles, PCSK9 (mGFP-tagged) - Human proprotein convertase subtilisin/kexin type 9 (PCSK9), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: mGFP
• Symbol: PCSK9
• Synonyms: FH3; FHCL3; HCHOLA3; LDLCQ1; NARC-1; NARC1; PC9
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-mGFP-P2A-Puro
• ACCN: NM_174936
• ORF Size: 2076 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC220000).
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.

Reference Data

• RefSeq: NM_174936.2
• RefSeq Size: 3636 bp
• RefSeq ORF: 2079 bp
• Locus ID: 255738
• UniProt ID: Q8NBP7
• Cytogenetics: 1p32.3
• Domains: Peptidase_S8
• Protein Families: Secreted Protein
• MW: 71 kDa
• Gene Summary: This gene encodes a member of the subtilisin-like proprotein convertase family, which includes proteases that process protein and peptide precursors trafficking through regulated or constitutive branches of the secretory pathway. The encoded protein undergoes an autocatalytic processing event with its prosegment in the ER and is constitutively secreted as an inactive protease into the extracellular matrix and trans-Golgi network. It is expressed in liver, intestine and kidney tissues and escorts specific receptors for lysosomal degradation. It plays a role in cholesterol and fatty acid metabolism. Mutations in this gene have been associated with autosomal dominant familial hypercholesterolemia. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2014]