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Key Documents

SAB4300047

Sigma-Aldrich

Anti-phospho-PTK2 (pTyr861) antibody produced in rabbit

affinity isolated antibody

Synonym(s):

Anti-FADK antibody produced in rabbit, Anti-FAK antibody produced in rabbit, Anti-FAK1 antibody produced in rabbit, Anti-PTK2 protein tyrosine kinase 2 antibody produced in rabbit, Anti-pp125FAK antibody produced in rabbit

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~125 kDa

species reactivity

human

concentration

1 mg/mL

technique(s)

western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(H-I-YP-Q-P)

NCBI accession no.

NP_005598.3

UniProt accession no.

Q05397

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pTyr861)

Gene Information

human ... PTK2(5747)

Immunogen

Peptide sequence around phosphorylation site of tyrosine 861 (H-I-Y(p)-Q-P), according to the protein PTK2.

Features and Benefits

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Target description

Non-receptor protein-tyrosine kinase implicated in signaling pathways involved in cell motility, proliferation and apoptosis. Activated by tyrosine-phosphorylation in response to either integrin clustering induced by cell adhesion or antibody cross-linking, or via G-protein coupled receptor (GPCR) occupancy by ligands such as bombesin or lysophosphatidic acid, or via LDL receptor occupancy. Plays a potential role in oncogenic transformations resulting in increased kinase activity.

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

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Minami Sato et al.
Annals of biomedical engineering, 42(10), 2156-2163 (2014-08-07)
Low-intensity pulsed ultrasound (LIPUS) suppresses synovial hyperplasia and synovial cell proliferation characterized for rheumatoid arthritis, but the molecular mechanisms remain unknown. The purpose of this study was to examine the mechanotransduction pathway via the integrin/mitogen-activated protein kinase (MAPK) pathway in

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