LDL Receptor (LDLR) (NM_000527) Human Tagged ORF Clone Lentiviral Particle

SKU RC200006L3V

Lenti ORF particles, LDLR (Myc-DDK tagged) - Human low density lipoprotein receptor (LDLR), transcript variant 1, 200ul, >10^7 TU/mL

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: LDL Receptor
• Synonyms: FH; FHC; FHCL1; LDLCQ2
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• Mammalian Cell Selection: Puromycin
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC200006).
• ACCN: NM_000527
• ORF Size: 2580 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_000527.2, NP_000518.1
• RefSeq Size: 5175 bp
• RefSeq ORF: 2583 bp
• Locus ID: 3949
• UniProt ID: P01130
• Cytogenetics: 19p13.2
• Domains: EGF, EGF_CA, ldl_recept_a, ldl_recept_b
• Protein Families: Druggable Genome, ES Cell Differentiation/IPS, Transmembrane
• Protein Pathways: Endocytosis
• MW: 95.38 kDa
• 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]