Pcsk9 (NM_153565) Mouse Tagged ORF Clone Lentiviral Particle

SKU MR210088L1V

Lenti ORF particles, Pcsk9 (Myc-DDK-tagged) - Mouse proprotein convertase subtilisin/kexin type 9 (Pcsk9), 200ul, >10^7 TU/mL

Product Data

• Type: Mouse Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: Pcsk9
• Synonyms: AI415265; AI747682; FH3; HCHOLA3; Narc1; PC9
• Vector: pLenti-C-Myc-DDK
• Mammalian Cell Selection: None
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR210088).
• ACCN: NM_153565
• ORF Size: 2082 bp
• 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.
• Shipping: Dry Ice

Reference Data

• RefSeq: NM_153565.2, NP_705793.1
• RefSeq Size: 3512 bp
• RefSeq ORF: 2085 bp
• Locus ID: 100102
• UniProt ID: Q80W65
• Cytogenetics: 4 C7
• Summary: Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.[UniProtKB/Swiss-Prot Function]