Western blot analysis of Phospho-P27Kip1 pThr198 using Phospho-P27Kip1 pThr198 polyclonal antibody (Product # PA5-36862) at a dilution of 1:500. Lane 1: HEK293T cell lysate treated with EGF (0.1ng/ml, 30min), Lane 2: Raw264.7 cell lysate treated with EGF (0.1ng/ml, 30min), Lane 3: H9C2 cell lysate treated with EGF (0.1ng/ml, 30min).
|Tested species reactivity||Human, Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic phosphopeptide derived from human p27 Kip1 around the phosphorylation site of Threonine 198|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.2|
|Contains||0.05% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:500-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
This antibody detects endogenous protein at a molecular weight of 27 kDa.
Purity is >95% by SDS-PAGE.
Cell cycle progression is regulated by a series of cyclin-dependent kinases that consist of catalytic subunits, designated Cdks, and activating subunits, designated cyclins. Orderly progression through the cell cycle requires the activation and inactivation of different cyclin-Cdks at appropriate times. A series of proteins has been recently described that function as "mitotic inhibitors." These include p21, the levels of which are elevated upon DNA damage in G1 in a p53-dependent manner, p16 and a more recently described p16 related inhibitor designated p15. A p21 related protein, p27, has been described as a negative regulator of G1 progression and has been speculated to function as a possible mediator of TGF beta-induced G1 arrest. p27 interacts strongly with D-type cyclins and Cdk4 in vitro and to a lesser extent with cyclin E and Cdk2.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.