DNMT3B Easy KO Kit

Name: DNMT3B Easy KO Kit
SKU: CC-416
Availability: InStock

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

Cat. No. : CC-416

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Product Information

Gene Information

Cat. No.	CC-416
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	DNMT3B
Species	Human
EnsemblID	ENSG00000088305
NCBIGeneID	1789
Uni ProtID	Q9UBC3
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

DNMT3B

Background

CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development. This gene encodes a DNA methyltransferase which is thought to function in de novo methylation, rather than maintenance methylation. The protein localizes primarily to the nucleus and its expression is developmentally regulated. Mutations in this gene cause the immunodeficiency-centromeric instability-facial anomalies (ICF) syndrome. Eight alternatively spliced transcript variants have been described. The full length sequences of variants 4 and 5 have not been determined. [provided by RefSeq, May 2011]

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