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BRAF (v-Raf murine sarcoma viral oncogene homolog B, or proto-oncogene B-Raf) is one of the human RAF genes (the other two are ARAF and CRAF), encoding the B-Raf protein. B-Raf is activated by binding to Ras-GTP and participates in RAS/MAPK signal transduction in cells, which affects cell division, differentiation, and secretion. B-Raf can catalyze the phosphorylation of serine and threonine on target proteins and convert ATP to ADP.
The B-Raf protein contains three conserved domains, Ras-GTP binding self-regulatory domain (CR1), a serine-rich region (CR2, that can serve as a hinge on the molecule), and a catalytic protein kinase domain (CR3). CR3 phosphorylates specific sequences on protein targets. Studies have shown that CR1 can inhibit the activity of the kinase domain CR3 to regulate the overall signaling activity of the molecule. The binding of Ras-GTP to 155-227 amino acid residues in CR1 can activate B-Raf.
In addition, CR3 is also inhibited when certain serine and tyrosine residues in the CR2 hinge region are untranslated and phosphorylated. By phosphorylation of the activation loop, the CR3 kinase domain is converted into its active form.
Mutations in this gene (most commonly the V600E mutation) are the most common carcinogenic mutations in melanoma and have also been identified in a variety of other cancers, including
➢ Non-Hodgkin's lymphoma
➢ Colorectal cancer
➢ Thyroid cancer
➢ Non-small cell lung cancer
➢ hairy cell leukemia
➢ Lung adenocarcinoma
Mutations in this gene have also been linked to cardiac facial skin, noonan, and costello syndrome, which exhibit overlapping phenotypes.
Figure 1: Oncogenic BRAF signaling pathway (Paolo A Ascierto. 2012). RTK: receptor tyrosine kinase.
As a key element of MAPK signaling, B-Raf kinase is considered a convincing target in oncology. B-Raf inhibitors have shown clinical efficacy in melanomas containing B-Raf V600E. Two drugs, vemurafenib, and dabrafenib have been approved by the FDA for the treatment of advanced melanoma. Vemurafenib is the first fragment-based drug discovery method.
BRAF Gene Editing Service
CRISPR/Cas9 PlatformCB has extensive experience in incorporating CRISPR/Cas9 technology into >200 different cell lines, including easy-to-transfect cell lines and hard-to-transfect cells, and different animals. To support your research, we provide you with end-to-end BRAF gene editing service from strategy design to final models.
Mutation via CRISPR Gene Editing
We are able to perform specific DNA deletions, mutations or substitutions to study gene function with CRISPR/Cas9 gene editing technology with high precision. Available services:
➢ Point Mutation
➢ Conditional knockout/knock-in
➢ Floxed allele insertion
Mark by CRISPR Gene Editing
Using the CRISPR/Cas9 gene editing technology, CRISPR/Cas9 PlatformCB is able to tag your genes at the endogenous locus and visualize them with fluorescent proteins or immune-tags for biochemical studies. Available services:
➢ Fluorescent tag
➢ Custom tags and combinations are also available
➢ Strategy design
➢ gRNA design and synthesis, donor DNA design and synthesis (if needed)
➢ CRISPR/Cas9 vector construction
➢ Transfection into the cell lines or microinjection into embryo single cell
➢ Validate by PCR and sequencing
|Blood Lineage Cells||RAW264.7, HMC1.2, K562, U937, etc.|
|Cancer Cell Lines||HEK293, HEK293T, Hela, MCF7, Neuro2a, HepG2, U87, etc.|
|Other Cell Lines||NIH3T3, MCF10, HEME, SW10, etc.|
|Animal models we offered||mouse, rat, rabbit, zebrafish, C. elegans, etc.|
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