Knockout Vector Construction
Service Details
Service Types | Knockout Lentiviral Vector / Knockout Adenoviral Vector / Knockout Adeno-Associated Viral (AAV) Vector / Knockout Plasmid |
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Delivery Standards | Plasmid map / Plasmid sequencing results / Plasmid amplification instructions / Plasmids (3 sgRNAs provided separately) |
Timeline/Pricing | Consult online for details |
Knockout Strategies
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Frameshift Knockout
Design sgRNA targeting the 5' coding region of the gene to induce indels that are not in multiples of three, resulting in a frameshift mutation.
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Large Fragment Deletion
Design sgRNA to induce the deletion of large segments within the gene.
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Fragment Deletion
Design sgRNA to delete short segments within the gene, causing frameshift mutations.
Service Advantages
High-Activity Cas9 Plasmid
Efficient sgRNA Design
Diverse Knockout Plasmid Types
Scientific Design
Delivery Standards
1 | Plasmid map |
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2 | Plasmid sequencing results |
3 | Plasmid amplification protocol |
4 | Plasmids (three sgRNAs provided separately) |
Plasmid Map
Advantage and Characteristic
Optimazied Strategy
Optimazied Strategy
Optimazied Strategy
Optimazied Strategy
Genetic Reference Book
FUT8 Gene Knockout in MIA PaCa-2 and PANC-1 Cells.
Pancreatic ductal adenocarcinoma (PDAC) is an extremely malignant tumor, accounting for 90% of all pancreatic cancers. Studies have shown that abnormal glycosylation changes on the surface of cancer cells are positively correlated with tumor progression and metastasis. α1,6-fucosyltransferase (FUT8) is a key enzyme responsible for catalyzing core fucosylation, and its abnormal expression and activation in various malignant tumors are associated with multiple physiological and pathological processes. Although the role of FUT8 in other types of cancer has been observed, its specific molecular mechanisms in PDAC malignancy transformation and potential as a therapeutic target remain unclear.
Researchers used the CRISPR/Cas9 system to knock out the FUT8 gene in MIA PaCa-2 and PANC-1 cells. The migration ability of FUT8-KO cells was evaluated using Transwell migration assays and wound healing assays, while the proliferation ability was assessed using MTT assays and colony formation assays. The expression levels of cancer stem cell markers in FUT8-KO cells were also detected. The results showed that compared to wild-type cells, FUT8-KO cells exhibited significantly reduced migration ability, proliferation, and colony formation, along with decreased expression of cancer stem cell markers. FUT8 knockout cells revealed the important role of FUT8 in pancreatic cancer and indicated that FUT8 may be a potential target for pancreatic cancer treatment, providing new insights for future therapeutic strategies against PDAC.