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BRAND / VENDOR: Abcam

Abcam, ab242243, Mouse FAK ELISA Kit

CATALOG NUMBER: ab242243
Precio habitual$0.99
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Product Description

Size: 1 x 96Tests
Mouse FAK ELISA Kit is a single-wash 90-min Simplestep used to quantify Mouse FAK with a sensitivity of 4.5 pg/ml. The assay uses a simple mix-wash-read protocol with just one incubation and one wash step. - Colorimetric Sandwich ELISA - 450 nm readout : works on any standard plate reader - Design your own immunoassay: we also offer the conjugation-ready antibody pair
Key facts
Detection method:Colorimetric,
Sample types:Cell culture extracts, Tissue Extracts,
Reacts with:Mouse,
Assay type:Sandwich (quantitative),
Sensitivity:= 4.5 pg/mL,
Range:46.88 - 3000 pg/mL,
Assay time:1h 30m,
Assay Platform:Pre-coated microplate (12 x 8 well strips)

Product details:
Mouse FAK ELISA Kit (ab242243) is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of FAK protein in cell culture extracts and tissue extracts. It uses our proprietary SimpleStep ELISA® technology. Quantitate Mouse FAK with 4.5 pg/ml sensitivity.
SimpleStep ELISA® technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our SimpleStep ELISA® plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time. See the SimpleStep ELISA® protocol summary in the image section for further details. Our SimpleStep ELISA® technology provides several benefits:
- Single-wash protocol reduces assay time to 90 minutes or less
- High sensitivity, specificity and reproducibility from superior antibodies
- Fully validated in biological samples
- 96-wells plate breakable into 12 x 8 wells strips
A 384-well SimpleStep ELISA® microplate (
ab203359
) is available to use as an alternative to the 96-well microplate provided with SimpleStep ELISA® kits.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.

Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C, Storage information-+4°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
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.
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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Collaboration

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