Pcsk9 Mouse Gene Knockout Kit (CRISPR)

CAT#: KN312980RB

Pcsk9 - mouse gene knockout kit via CRISPR, HDR mediated

Functional Cassette: GFP-puro Luciferase-Puro RFP-BSD mBFP-Neo



HDR-mediated knockout kit validation

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Specifications

Product Data
Format 2 gRNA vectors, 1 RFP-BSD donor, 1 scramble control
Donor DNA RFP-BSD
Symbol Pcsk9
Locus ID 100102
Components

KN312980G1, Pcsk9 gRNA vector 1 in pCas-Guide CRISPR vector

KN312980G2, Pcsk9 gRNA vector 2 in pCas-Guide CRISPR vector

KN312980RBD, donor DNA containing left and right homologous arms and RFP-BSD functional cassette.

GE100003, scramble sequence in pCas-Guide vector

Disclaimer These products are manufactured and supplied by OriGene under license from ERS. The kit is designed based on the best knowledge of CRISPR technology. The system has been functionally validated for knocking-in the cassette downstream the native promoter. The efficiency of the knock-out varies due to the nature of the biology and the complexity of the experimental process.
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]

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