SAB4504403
Anti-phospho-FAK (pTyr397) antibody produced in rabbit
affinity isolated antibody
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About This Item
Codice UNSPSC:
12352203
NACRES:
NA.41
Prodotti consigliati
Origine biologica
rabbit
Livello qualitativo
Coniugato
unconjugated
Forma dell’anticorpo
affinity isolated antibody
Tipo di anticorpo
primary antibodies
Clone
polyclonal
Stato
buffered aqueous solution
PM
antigen 119 kDa
Reattività contro le specie
rat, mouse, human
Concentrazione
~1 mg/mL
tecniche
ELISA: 1:5000
western blot: 1:500-1:1000
N° accesso NCBI
N° accesso UniProt
Condizioni di spedizione
wet ice
Temperatura di conservazione
−20°C
modifica post-traduzionali bersaglio
phosphorylation (pTyr397)
Informazioni sul gene
human ... PTK2(5747)
Descrizione generale
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.
Immunogeno
The antiserum was produced against synthesized peptide derived from human FAK around the phosphorylation site of Tyr397.
Immunogen Range: 364-413
Immunogen Range: 364-413
Azioni biochim/fisiol
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.
Caratteristiche e vantaggi
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.
Stato fisico
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Esclusione di responsabilità
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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Codice della classe di stoccaggio
10 - Combustible liquids
Classe di pericolosità dell'acqua (WGK)
WGK 1
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
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I documenti relativi ai prodotti acquistati recentemente sono disponibili nell’Archivio dei documenti.
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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