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

MTA2 Rabbit anti-Human, Mouse, Rat, Polyclonal, Invitrogen™

Rabbit Polyclonal Antibody

Manufacturer:  Invitrogen PA112809

Catalog No. 01-675-801


Add to cart

Description

Description

A suggested positive control for this product is HeLa cell lysate.

The p53 tumor-suppressor gene integrates numerous signals that control cell life and death. Several novel molecules involved in p53 network, including Chk2 , p53R2, p53AIP1, Noxa, PIDD, PID/MTA2 and MTBP, were recently discovered. The transcriptional activity of p53 is modulated by posttranslational regulations of the p53 protein including stabilization and acetylation. P53 transcriptionally activates MDM2 gene then the translated MDM2 protein binds to p53 and promotes the degradation of p53 leading to lowering the concentration of p53 protein. MDM2 inhibits both p53 mediated G1 arrest and apoptosis. A recently discovered protein termed MTBP was found to bind to MDM2 and to inhibit the modulation effect of MDM2 on p53. MTBP is expressed in a variety of normal tissues.
Specifications

Specifications

MTA2
Polyclonal
PBS with 0.02% sodium azide
O94776, Q9R190
MTA2
Rabbit
IgG
100 μg
-20° C, Avoid Freeze/Thaw Cycles
Primary
23942, 361724, 9219
Immunohistochemistry, Western Blot
Unconjugated
MTA2
Liquid
MTA2
Synthetic peptide corresponding to residues 652 to 668 of human PID/MTA2.
Antigen affinity chromatography
RUO
Antibody
Polyclonal
Human, Mouse, Rat
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