APOB Easy KO Kit

Name: APOB Easy KO Kit
SKU: CC-145
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CC-145

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Product Information

Gene Information

Cat. No.	CC-145
Description	A complete kit for efficient gene knockout in mammalian cells, combining chemically synthesized sgRNAs with Cas9 RNPs to induce targeted DNA cleavage and generate frameshift mutations or deletions. All essential reagents for transfection and knockout validation are included for rapid, high-efficiency gene disruption.
Gene Abbr	APOB
Species	Human
Ensembl ID	ENSG00000084674
NCBIGene ID	338
Uni Prot ID	P04114
Features	All-in-One workflow from gene editing to knockout validation for users with no prior experience. Pre-validated sgRNAs and primers for rapid setup. Streamlined experiment handling. CRISPR RNP method ensures precise and efficient gene knockout.
Applications	This kit enables in vitro gene knockout in human-derived cells using chemically synthesized sgRNAs and Cas9-gRNA RNP complexes. Transfected RNPs cleave early exons of the target gene, inducing deletions or frameshift mutations for efficient and rapid knockout.
Reactions	5–10 reactions per target gene
Kit Components	2–3 chemically synthesized sgRNAs (200pmol each) 3 PCR/Sequencing primers (500pmol each) LM cell lysate (500µL) Cas9 protein (12µg) LM RNP transfection reagent (50µL)
Storage	Store at -80°C for up to 1 year or at -20°C for up to 6 months. Avoid repeated freeze-thaw cycles.

Target Gene

APOB

Background

This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins (LDL), and is the ligand for the LDL receptor. It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut and the latter in the liver. The intestinal and the hepatic forms of apoB are encoded by a single gene from a single, very long mRNA. The two isoforms share a common N-terminal sequence. The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA->UAA), resulting in the creation of a stop codon, and early translation termination. Mutations in this gene or its regulatory region cause hypobetalipoproteinemia, normotriglyceridemic hypobetalipoproteinemia, and hypercholesterolemia due to ligand-defective apoB, diseases affecting plasma cholesterol and apoB levels. [provided by RefSeq, Dec 2019]

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