LEF1 Easy KO Kit

Name: LEF1 Easy KO Kit
SKU: CC-781
Availability: InStock

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

Cat. No. : CC-781

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Product Information

Gene Information

Cat. No.	CC-781
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	LEF1
Species	Human
EnsemblID	ENSG00000138795
NCBIGeneID	51176
Uni ProtID	Q9UJU2
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

LEF1

Background

This gene encodes a transcription factor belonging to a family of proteins that share homology with the high mobility group protein-1. The protein encoded by this gene can bind to a functionally important site in the T-cell receptor-alpha enhancer, thereby conferring maximal enhancer activity. This transcription factor is involved in the Wnt signaling pathway, and it may function in hair cell differentiation and follicle morphogenesis. Mutations in this gene have been found in somatic sebaceous tumors. This gene has also been linked to other cancers, including androgen-independent prostate cancer. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2009]

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