CRISPR-U™ technology (CRISPR based), developed by Ubigene, is more efficient than general
CRISPR/Cas9 technology in double-strand breaking and homologous recombination. With CRISPR-U™, Ubigene has
successfully edited over 3000 genes on more than 200 types of cell lines.
Objective
To create a Mouse Ctnnb1 Knockout
model in cell line by CRISPR-U™-mediated genome engineering.
Target gene info
Official symbol
Ctnnb1
Gene id
12387
Organism
Mus musculus
Gene type
protein-coding
Official full symbol
catenin (cadherin associated protein), beta 1
Also known as
Bfc, Catnb, Mesc
Genomic regions
Chromosome 9
Summary
This gene encodes not only an important cytoplasmic component of the classical cadherin adhesion complex that forms the adherens junction in epithelia and mediates cell-cell adhesion in many other tissues but also a key signaling molecule in the canonical Wnt signaling pathway that controls cell growth and differentiation during both normal development and tumorigenesis. The gene product contains a central armadillo-repeat containing domain through which it binds the cytoplasmic tail of classical cadherins; meanwhile, it also binds alpha-catenin, which further links the cadherin complex to the actin cytoskeleton either directly or indirectly. Beta-catenin is therefore necessary for the adhesive function of classical cadherins. Another key function of this protein is to mediate the canonical Wnt signaling pathway and regulate gene transcription. Without Wnt signal, cytoplasmic beta-catenin that is not associated with the cadherin complex is quickly phosphorylated at the N-terminal Ser/Thr residues by the so called degradation complex containing axin, adenomatous polyposis coli (APC), casein kinase I, and GSK3B, then ubiquitylated by beta-TrCP, and degraded by the proteasome. However, in the presence of Wnt signal, the degradation complex is disrupted and the stabilized cytoplasmic beta-catenin translocates into the nucleus, where it binds various transcription factors and, together with these factors, regulates the transcription of many downstream genes. Mutations of this gene have been linked with various types of tumors. Alternatively spliced variants have been found for this gene.
Strategy Summary
This gene has 0 protein coding transcripts:
Frame-shift
Fragment A
Fragment B
gRNA Detail
Strategy
Project Comprehensive Difficulty Assessment
According to the Red Cotton database: the CRISPR gene-editing strategy design is Unknown. Knockout project comprehensive difficulty is thus assessed as Unknown.
Red Cotton™ Notes
Gene
Ctnnb1
had been KO in hct116 cell line.
EZ-editor™ Gene Dependency
EZ-editor™ Gene Expression Level
EZ-editor™ Gene Copy Number
EZ-editor™ Gene Dependency
Result
The Ctnnb1 gene you inquire is evaluated as high risk
in 13%
cell line.
Cell line is not selected, unable to assess the accurate risk level, for reference only.
In all cell lines, there is
0.3% cells with low expression level,
99.6% cells with medium expression level,
0.1% cells with high expression level
of Ctnnb1 gene.
Cell line is not selected, unable to assess the accurate expression level, for reference only.
In all cell lines, there is
73.5% cells with low copy number,
24.4% cells with medium copy number,
2.1% cells with high copy number
of Ctnnb1 gene.
Cell line is not selected, unable to assess the accurate copy number, for reference only.
Ubigene is an international high-technology enterprise focused on gene-editing cells. Our exclusive CRISPR-U™ technology has 10-20 times more efficient editing than traditional methods, easily achieving gene knockout, point mutation, and knock-in. Based on CRISPR-U™ technology, Ubigene has accumulated over 6000 successful gene-editing cases from more than 300 cell lines including iPSC and ESC, and has established a KO Cell Line Bank with 5000+ KO cell lines and Red Cotton™ gRNA Plasmid Bank with 10000+ gRNA plasmids available in stock.
Ubigene focuses on technological innovation and product development, of which EZ-editor™ series products that cover the whole workflow of gene-editing keep improving. Ubigene will move on toward our goal of "Make genome editing easier" and we won't stop!