Mouse Pcsk9 activation kit by CRISPRa

SKU GA211583

Pcsk9 CRISPRa kit - CRISPR gene activation of mouse proprotein convertase subtilisin/kexin type 9

Product Data

• Format: 3 gRNAs (5ug each), 1 scramble ctrl (10ug) and 1 enhancer vector (10ug)
• Target Symbol: Pcsk9
• Locus ID: 100102
• Components:

  GA211583G1, Pcsk9 gRNA vector 1 in pCas-Guide-GFP-CRISPRa

  GA211583G2, Pcsk9 gRNA vector 2 in pCas-Guide-GFP-CRISPRa

  GA211583G3, Pcsk9 gRNA vector 3 in pCas-Guide-GFP-CRISPRa

  1 CRISPRa-Enhancer vector, SKU GE100056

  1 CRISPRa scramble vector, SKU GE100077

• OTI Disclaimer: These products are manufactured and supplied by OriGene under license from ERS. The kit is designed based on the best knowledge of CRISPRa SAM technology. The efficiency of the activation can be affected by many factors, including nucleosome occupancy status, chromatin structure and the gene expression level of the target, etc.
• Shipping: Ambient

Reference Data

• RefSeq: NM_153565
• UniProt ID: Q80W65
• Synonyms: AI415265; AI747682; FH3; HCHOLA3; Narc1; PC9
• 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]