LDL Receptor (LDLR) Human Gene Knockout Kit (CRISPR)

CAT#: KN200006BN

LDLR - human gene knockout kit via CRISPR, HDR mediated




 HDR-mediated knockout kit validation

  See Other Versions

CNY 12,260.00


货期*
6周

规格
    • 1 kit

Product images

经常一起买 (3)
pCAS-Scramble, pCas-Guide vector with a scrambled sequence as a negative control (10 µg)
    • 10 ug

CNY 3,710.00


LDLR mouse monoclonal antibody,clone OTI7C5
    • 100 ul

CNY 1,999.00
CNY 2,700.00


LDLR (Myc-DDK-tagged)-Human low density lipoprotein receptor (LDLR), transcript variant 1
    • 10 ug

CNY 9,448.00

Specifications

Product Data
Format 2 gRNA vectors, 1 mBFP-Neo donor, 1 scramble control
Donor DNA mBFP-Neo
Symbol LDL Receptor
Locus ID 3949
Kit Components

KN200006G1, LDL Receptor gRNA vector 1 in pCas-Guide CRISPR vector

KN200006G2, LDL Receptor gRNA vector 2 in pCas-Guide CRISPR vector

KN200006BN-D, donor DNA containing left and right homologous arms and mBFP-Neo 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_000527, NM_001195798, NM_001195799, NM_001195800, NM_001195802, NM_001195803
Synonyms FH; FHC; LDLCQ2
Summary The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. Low density lipoprotein (LDL) is normally bound at the cell membrane and taken into the cell ending up in lysosomes where the protein is degraded and the cholesterol is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants.[provided by RefSeq, Sep 2010]
*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen complexities in the preparation of your product. International customers may expect an additional 1-2 weeks in shipping.

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