ARF5 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 1 bp insertion in exon 1.
Images
Key facts
- Cell type
- HEK-293T
- Species or organism
- Human
- Tissue
- Kidney
- Form
- Liquid
- Knockout validation
- Sanger Sequencing
- Mutation description
- Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 1 bp insertion in exon 1
Alternative names
ADP-ribosylation factor 5, ARF5_HUMAN
Recommended products
ARF5 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 1 bp insertion in exon 1.
Key facts
- Cell type
- HEK-293T
- Species or organism
- Human
- Tissue
- Kidney
- Form
- Liquid
- Knockout validation
- Sanger Sequencing
- Mutation description
- Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 1 bp insertion in exon 1
- Concentration
Properties
- Gene name
- ARF5
- Gene editing type
- Knockout
- Gene editing method
- CRISPR technology
- Knockout validation
- Sanger Sequencing
Quality control
- STR analysis
- CSF1PO, D13S317, D7S820, D5S818, TH01, D16S539, TPOX
Cell culture
- Biosafety level
- EU: 2 US: 2
- Adherent/suspension
- Adherent
- Gender
- Female
Handling procedures
- Initial handling guidelines
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.- Subculture guidelines
- All seeding densities should be based on cell counts gained by established methods.
- A guide seeding density of 2x104 cells/cm2 is recommended.
- Cells should be passaged when they have achieved 80-90% confluence.
- Culture medium
- DMEM (High Glucose) + 10% FBS
- Cryopreservation medium
- Cell Freezing Medium-DMSO Serum free media, contains 8.7% DMSO in MEM supplemented with methyl cellulose.
Storage
- Shipped at conditions
- Dry Ice
- Appropriate short-term storage conditions
- -196°C
- Appropriate long-term storage conditions
- -196°C
Notes
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our limited use license and patent pages.
Supplementary info
- This supplementary information is collated from multiple sources and compiled automatically.
- Activity summary
The ADP-ribosylation factor 5 (ARF5) protein also known by its primary name is an important part of the ARF family. It has a mass of around 20 kDa. ARF5 plays a role in regulating vesicle trafficking systems particularly linked with the Golgi apparatus. It is found broadly expressed in numerous tissues with high levels observed in the brain and testes. This small GTP-binding protein is associated with intracellular signaling cascades and cellular communication.
- Biological function summary
ARF5 is involved in modulating key cellular processes including membrane trafficking and lipid metabolism. It directly participates in the formation of vesicle coats by aiding the recruitment of coat protein complexes. ARF5 also interacts within cellular complexes impacting the transport of cargo in the secretory pathway. It also affects actin cytoskeleton remodeling thereby influencing cell shape and motility.
- Pathways
The ARF5 protein contributes to both the COPI and clathrin-coated vesicle formation pathways. It functions within intricate signaling networks coordinating with other small GTPases such as ARF1. ARF5's activity links to pivotal roles within these pathways affecting protein and lipid sorting. These pathways are vital for maintaining cellular homeostasis and facilitating effective intracellular transport.
- Associated diseases and disorders
ARF5's dysfunction has been linked to neurodegenerative disorders including Alzheimer's disease. Variations in the expression or mutations of ARF5 might contribute to the disease pathology by impairing vesicular transport and potentially interacting with proteins like tau. Furthermore ARF5 may relate to metabolic syndromes due to its involvement in lipid metabolism with implications for body fat distribution and lipid-related diseases.
Product promise
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In the unlikely event of one of our products not working as expected, you are covered by our product promise.
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Terms & Conditions.
3 product images
Cell Culture - Human ARF5 knockout HEK-293T cell line (ab266614)
Representative images of ARF5 knockout HEK293T cells, low and high confluency examples (top left and right respectively) and wild-type HEK293T cells, low and high confluency (bottom left and right respectively) showing typical adherent, epithelial-like morphology. Images were captured at 10X magnification using a EVOS XL Core microscope.
Sanger Sequencing - Human ARF5 knockout HEK-293T cell line (ab266614)
Allele-1: 13 bp deletion in exon1
Sanger Sequencing - Human ARF5 knockout HEK-293T cell line (ab266614)
Allele-2: 1 bp insertion in exon 1.
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