Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

PAG1 Mouse anti-Human, Clone: MEM-255, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA119289

Catalog No. 01-676-045


Add to cart

Description

Description

This antibody will not cross-react with mouse, rat or bovine.

PAG (phosphoprotein associated with GEMs), also known as Cbp (Csk-binding protein), is a ubiquitously expressed 46 kDa transmembrane adaptor protein present in membrane rafts (glycosphingolipid-enriched microdomains), which however migrates on SDS PAGE gels anomalously as an 80 kDa molecule. Following tyrosine phosphorylation by Src family kinases, PAG binds and thereby activates the protein tyrosine kinase Csk, the major negative regulator of the Src family kinases. Signaling via the B-cell receptor in B cells or high affinity IgE receptor (FcepsilonRI) in mast cells leads to PAG increased tyrosine phosphorylation and Csk binding, while T cell receptor signaling causes PAG dephosphorylation, loss of Csk binding and increased activation of the protein tyrosine kinase Lck.
Specifications

Specifications

PAG1
Monoclonal
1 mg/mL
PBS with 15mM sodium azide; pH 7.4
Q9NWQ8
PAG
Mouse
IgG2a
100 μg
4° C, do not freeze
Primary
55824
Flow Cytometry, Immunohistochemistry (Paraffin), Western Blot
MEM-255
Unconjugated
PAG1
Liquid
PAG1
Recombit intracellular fragment (aa 97-432) of human Cbp (PAG).
Protein A
RUO
Antibody
Monoclonal
Human
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit