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Human WNT5A Knockout Cell Line-HeLa

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

Cat. No. :   CSC-RT3233

Target Gene :   WNT5A Host Cell :   HeLa

Size :   >1x106 cells/vial Validation :   Sequencing

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Cell Line Information

Cell Culture Information

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Gene Information

Cat. No. CSC-RT3233
Introduction This cell is a stable cell line with a homozygous knockout of human WNT5A using CRISPR/Cas9.
Target Gene WNT5A
Host Cell HeLa
Host Cell Species Homo sapiens (Human)
Size 1 vial (>10^6 cell/vial)
Validation Sequencing
Storage Liquid Nitrogen
Shipping Dry ice package
Revival Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.
Mycoplasma Negative
Format One frozen vial containing millions of cells
Storage Liquid nitrogen
Safety Considerations The following safety precautions should be observed.
1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum.
2. No eating, drinking or smoking while handling the stable line.
3. Wash hands after handling the stable line and before leaving the lab.
4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells.
5. All waste should be considered hazardous.
6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship Dry ice
Target Gene WNT5A
Background The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene encodes a member of the WNT family that signals through both the canonical and non-canonical WNT pathways. This protein is a ligand for the seven transmembrane receptor frizzled-5 and the tyrosine kinase orphan receptor 2. This protein plays an essential role in regulating developmental pathways during embryogenesis. This protein may also play a role in oncogenesis. Mutations in this gene are the cause of autosomal dominant Robinow syndrome. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jan 2012]
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