PLK2 (SNK) Antibody (C-term) [AMM07252G]

Product Specifications

Background

Tissue Location: Expressed at higher level in the fetal lung, kidney, spleen and heart.

Overview

We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality PLK2 (SNK) Antibody (C-term) [AMM07252G].

Synonyms

Serine/threonine-protein kinase PLK2, Polo-like kinase 2, PLK-2, hPlk2, Serine/threonine-protein kinase SNK, hSNK, Serum-inducible kinase, PLK2, SNK

Gene Name

PLK2

Gene ID

10769

UniProt

Q9NYY3

Chromosomal Location

Cytoplasm, cytoskeleton, microtubule organizing center, centrosome, centriole. Cell projection, dendrite Note=Localizes to centrosomes during early G1 phase where it only associates to the mother centriole and then distributes equally to both mother and daughter centrioles at the onset of S phase

Applications

WB, IHC-P

Dilution

WB--1:1000 IHC-P--1:100~500

Form

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.

Function

Tumor suppressor serine/threonine-protein kinase involved in synaptic plasticity, centriole duplication and G1/S phase transition. Polo-like kinases act by binding and phosphorylating proteins are that already phosphorylated on a specific motif recognized by the POLO box domains. Phosphorylates CENPJ, NPM1, RAPGEF2, RASGRF1, SNCA, SIPA1L1 and SYNGAP1. Plays a key role in synaptic plasticity and memory by regulating the Ras and Rap protein signaling: required for overactivity-dependent spine remodeling by phosphorylating the Ras activator RASGRF1 and the Rap inhibitor SIPA1L1 leading to their degradation by the proteasome. Conversely, phosphorylates the Rap activator RAPGEF2 and the Ras inhibitor SYNGAP1, promoting their activity. Also regulates synaptic plasticity independently of kinase activity, via its interaction with NSF that disrupts the interaction between NSF and the GRIA2 subunit of AMPARs, leading to a rapid rundown of AMPAR-mediated current that occludes long term depression. Required for procentriole formation and centriole duplication by phosphorylating CENPJ and NPM1, respectively. Its induction by p53/TP53 suggests that it may participate in the mitotic checkpoint following stress.