PLK2 (SNK) Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q9NYY3 |
| Other Accession | Q9R012 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 78237 Da |
| Antigen Region | 375-406 aa |
| Gene ID | 10769 |
|---|---|
| Other Names | Serine/threonine-protein kinase PLK2, Polo-like kinase 2, PLK-2, hPlk2, Serine/threonine-protein kinase SNK, hSNK, Serum-inducible kinase, PLK2, SNK |
| Target/Specificity | This PLK2 (SNK) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 375-406 amino acids from the C-terminal region of human PLK2 (SNK). |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | PLK2 (SNK) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | PLK2 |
|---|---|
| Synonyms | SNK |
| 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 that are already phosphorylated on a specific motif recognized by the POLO box domains. Phosphorylates CPAP, 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 CPAP and NPM1, respectively. Its induction by p53/TP53 suggests that it may participate in the mitotic checkpoint following stress. |
| Cellular 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 |
| Tissue Location | Expressed at higher level in the fetal lung, kidney, spleen and heart. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Plks (polo-like kinases) encode serine/threonine kinases that are closely related to polo and CDC5, genes that are required for passage through mitosis in Drosophila and Saccharomyces, respectively. Polo-like kinases, which include Plk, Snk (for serum-inducible kinase, also designated Plk2) and Fnk (for FGF-inducible kinase, also designated Plk3 or PRK), play a role in cell proliferation. Plk protein accumulates in the cell during S and G2 phases of the cell cycle, and both protein content and catalytic activity peak at the onset of mitosis, followed by a rapid reduction after mitosis. Snk and Fnk are immediate-early response genes that are first expressed during G1 phase. SNK may play a role in the division of at least some cell types, such as fibroblasts, and could function in embryogenesis, wound healing or neoplasia SNK mRNA is rapidly induced in human lung fibroblasts upon reintroduction of serum following 36 hours of serum deprivation.
REFERENCES
Strausberg, R.L., et al., Proc. Natl. Acad. Sci. U.S.A. 99(26):16899-16903 (2002).
Liby, K., et al., DNA Seq. 11:527-533 (2001).
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