CSGALNACT1 Human Gene Knockout Kit (CRISPR)
CAT#: KN419296
CSGALNACT1 - KN2.0, Human gene knockout kit via CRISPR, non-homology mediated.
KN2.0 knockout kit validation
KN419296 is the updated version of KN219296.
USD 1,290.00
2 Weeks*
Size
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Specifications
Product Data | |
Format | 2 gRNA vectors, 1 linear donor |
Donor DNA | EF1a-GFP-P2A-Puro |
Symbol | CSGALNACT1 |
Locus ID | 55790 |
Disclaimer | The kit is designed based on the best knowledge of CRISPR technology. The system has been functionally validated for knocking-in the cassette downstream the native promoter. The efficiency of the knock-out varies due to the nature of the biology and the complexity of the experimental process. |
Reference Data | |
RefSeq | NM_001130518, NM_018371, NR_024040, NM_001354475, NM_001354476, NM_001354477, NM_001354480, NM_001354481, NM_001354483, NM_001354484, NM_001354485, NM_001354487, NM_001354488, NM_001354489, NM_001354490, NM_001354491, NM_001354492, NM_001354494, NM_001354495, NM_001354496, NM_001354497, NM_001354498, NM_001354499, NR_148897, NR_148898, NR_148899, NR_148900, NR_148901, NR_148902 |
Synonyms | beta4GalNAcT; ChGn; CSGalNAcT-1 |
Summary | This gene encodes an enzyme that transfers N-acetylglucosamine (GalNAc) to the core tetrasaccharide linker and to elongating chondroitin sulfate chains in proteoglycans. Knockout of the orthologous mouse gene indicates that the protein is necessary for normal cartilage development and aggrecan metabolism. Mutations in this gene are associated with multiple sclerosis progression, and with mild skeletal dysplasia and joint laxity. [provided by RefSeq, Aug 2017] |
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Other Versions
SKU | Description | Size | Price |
---|---|---|---|
GA110972 | CSGALNACT1 CRISPRa kit - CRISPR gene activation of human chondroitin sulfate N-acetylgalactosaminyltransferase 1 |
USD 1,290.00 |
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*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen
complexities in the preparation of your product. International customers may expect an additional 1-2 weeks
in shipping.