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Merck

SAB4504403

Sigma-Aldrich

Anti-phospho-FAK (pTyr397) antibody produced in rabbit

affinity isolated antibody

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Mol-Gew.

antigen 119 kDa

Speziesreaktivität

rat, mouse, human

Konzentration

~1 mg/mL

Methode(n)

ELISA: 1:5000
western blot: 1:500-1:1000

NCBI-Hinterlegungsnummer

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

phosphorylation (pTyr397)

Angaben zum Gen

human ... PTK2(5747)

Verwandte Kategorien

Allgemeine Beschreibung

Protein tyrosine kinase 2 (PTK2), also known as FAK (focal adhesion kinase), is encoded by the gene mapped to human chromosome 8q24-qter. The encoded protein is localized to cell adhesion sites and extracellular matrix.

Immunogen

The antiserum was produced against synthesized peptide derived from human FAK around the phosphorylation site of Tyr397.

Immunogen Range: 364-413

Biochem./physiol. Wirkung

Protein tyrosine kinase 2 (PTK2) is a non-receptor tyrosine kinase which is known to regulate cell migration, proliferation, cell survival and invasiveness. Increased expression of FAK (focal adhesion kinase) leads to metastatic breast tumors and lung cancer. Inhibition of FAK tyrosine kinase activity stops various cellular process necessary for tumor growth. Hence, FAK inhibitors are considered to be potential therapeutic methods for cancer treatment. FAK is one of the important components of integrin adhesion complexes (IACs)and it plays a vital role in maintaining IAC dynamics. Cell interactions with components of extracellular matrix and a number of agonists, such as neuropeptides, activate Ptk2. Ptk2, mediates cell signaling through its kinase dependent/independent functions. Upregulation of the gene is observed in hepatocellular carcinoma, which is accompanied with portal venous invasion and intrahepatic metastasis.

Leistungsmerkmale und Vorteile

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physikalische Form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Haftungsausschluss

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 1

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

MicroRNA-7 inhibits cell proliferation, migration and invasion in human non-small cell lung cancer cells by targeting FAK through ERK/MAPK signaling pathway.
Cao Q, et al.
Oncotarget, 7(47), 77468-77468 (2016)
Focal adhesion kinase inhibitors in combination with erlotinib demonstrate enhanced anti-tumor activity in non-small cell lung cancer.
Howe G A, et al.
PLoS ONE, 11(3), e0150567-e0150567 (2016)
F T Fiedorek et al.
Mammalian genome : official journal of the International Mammalian Genome Society, 6(2), 123-126 (1995-02-01)
Focal adhesion kinase (pp125FAK or FAK) is a cytoplasmic protein-tyrosine kinase stimulated in response to cell interactions with extracellular matrix components and by exposure to a variety of agonists, including neuropeptides. FAK lacks Src-homology SH2 and SH3 domains, is highly
Focal adhesion kinase depletion reduces human hepatocellular carcinoma growth by repressing enhancer of zeste homolog 2.
Gnani D, et al.
Cell Death and Differentiation, 24(5), 889-889 (2017)
Grant A Howe et al.
PloS one, 11(3), e0150567-e0150567 (2016-03-11)
Blockade of epidermal growth factor receptor (EGFR) activity has been a primary therapeutic target for non-small cell lung cancers (NSCLC). As patients with wild-type EGFR have demonstrated only modest benefit from EGFR tyrosine kinase inhibitors (TKIs), there is a need

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