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PTK2 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 4 and 17 bp deletion in exon 4.

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Images

Western blot - Human PTK2 (FAK) knockout HEK-293T cell line (AB255421), expandable thumbnail
  • Western blot - Human PTK2 (FAK) knockout HEK-293T cell line (AB255421), expandable thumbnail
  • Sanger Sequencing - Human PTK2 (FAK) knockout HEK-293T cell line (AB255421), expandable thumbnail
  • Sanger Sequencing - Human PTK2 (FAK) knockout HEK-293T cell line (AB255421), expandable thumbnail

Key facts

Cell type
HEK-293T
Species or organism
Human
Tissue
Kidney
Form
Liquid
Knockout validation
Sanger Sequencing, Western blot
Mutation description
Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 4 and 17 bp deletion in exon 4

Alternative names

FADK, FADK 1, FAK related non kinase polypeptide, FAK1_HUMAN, FRNK, Focal adhesion Kinase, Focal adhesion kinase 1, Focal adhesion kinase isoform FAK Del33, Focal adhesion kinase related nonkinase, PPP1R71, PTK2 protein tyrosine kinase 2, Protein phosphatase 1 regulatory subunit 71, Protein-tyrosine kinase 2, Ptk2, p125FAK, pp125FAK

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PTK2 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 4 and 17 bp deletion in exon 4.

Key facts

Cell type
HEK-293T
Form
Liquid
Mutation description
Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 4 and 17 bp deletion in exon 4
Concentration
Loading...

Properties

Gene name
PTK2
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Sanger Sequencing, Western blot

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

Recommended control: Human wild-type HEK293T cell line (Human wild-type HEK-293T cell line ab255449). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.

We will provide viable cells that proliferate on revival.

This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant 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

Focal Adhesion Kinase (FAK) also known as Protein Tyrosine Kinase 2 (PTK2) is a non-receptor tyrosine kinase. This protein has a molecular weight of approximately 125 kDa. FAK is expressed at high levels in brain muscle and liver tissues. Mechanically FAK plays a role in cellular adhesion and migration by regulating integrin signaling and cell-extracellular matrix interactions. FAK auto-phosphorylates at tyrosine residue 397 creating a binding site for Src family kinases and promoting downstream signaling pathways.

Biological function summary

Focal Adhesion Kinase participates in the formation of focal adhesions which are complexes that connect the cytoskeleton to the extracellular matrix. The FAK protein functions as an important signaling node in these structures allowing for the assembly of multiprotein signal transduction complexes. FAK also controls cellular processes such as spreading motility and survival. The interaction with proteins such as Src kinases paxillin and talin facilitates its biological roles in cell signaling.

Pathways

Focal Adhesion Kinase engages in the regulation of the MAPK/ERK signaling pathway and the PI3K/AKT pathway. These pathways are instrumental for cell proliferation survival and migration. In these pathways FAK interacts with proteins such as PI3K Grb2 and Sos linking integrin-mediated signals with downstream effects that influence cell behavior and survival.

Associated diseases and disorders

Altered FAK signaling has ties to cancer progression and metastasis as well as cardiovascular diseases. In cancer the overexpression of FAK and its interaction with proteins like Src and VEGFR can drive tumor growth and angiogenesis. In cardiovascular diseases improper FAK activation can lead to aberrant heart tissue remodeling and associated pathologies. Abnormalities in FAK signaling pathways can therefore contribute significantly to the development and progression of these diseases.

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