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- Table of Contents
Facts about Serine/threonine-protein kinase PLK3.
Phosphorylates ATF2, BCL2L1, CDC25A, CDC25C, CHEK2, HIF1A, JUN, p53/TP53, p73/TP73, PTEN, TOP2A and VRK1. Involved in cell cycle regulation: required for entrance into S phase and cytokinesis.
Human | |
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Gene Name: | PLK3 |
Uniprot: | Q9H4B4 |
Entrez: | 1263 |
Belongs to: |
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protein kinase superfamily |
CNK; CNKpolo-like kinase 3 (Drosophila); cytokine-inducible kinase; Cytokine-inducible serine/threonine-protein kinase; EC 2.7.11; FNK; FNKEC 2.7.11.21; PLK3; polo-like kinase 3PLK-3; PRK; PRKFGF-inducible kinase; Proliferation-related kinase; serine/threonine-protein kinase PLK3
Mass (kDA):
71.629 kDA
Human | |
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Location: | 1p34.1 |
Sequence: | 1; NC_000001.11 (44799952..44805995) |
Transcripts are highly detected in placenta, lung, followed by skeletal muscle, heart, pancreas, ovaries and kidney and weakly detected in liver and brain. May have a short half-live. In cells of hematopoietic origin, strongly and exclusively detected in terminally differentiated macrophages. Transcript expression appears to be down-regulated in primary lung tumor.
Cytoplasm. Nucleus. Nucleus, nucleolus. Golgi apparatus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Translocates to the nucleus upon cisplatin treatment. Localizes to the Golgi apparatus during interphase. According to a report, PLK3 localizes only in the nucleolus and not in the centrosome, or in any other location in the cytoplasm (PubMed:17264206). The discrepancies in results may be explained by the PLK3 antibody specificity, by cell line-specific expression or post-translational modifications.
If you're searching for an Anti-PLK3 Monoclonal Antibody, then you've come to the right place. This article will discuss the history and potential uses of this antibody. We'll also examine the background of Steven Boster, and how his research may benefit your laboratory. You'll be better able to choose the best PLK3 antibody for you research.
The Anti-P53Tp53 monoclonic by Boster Bio is the best choice if you are looking for an antibody that detects P53 protein. This antibody reacts with Human P53 and has been validated for use in Immunohistochemistry, Immunocytochemistry, and Western Blot. The product description is below.
The TP53 genes encode a tumor suppressor gene that regulates cellular reactions to different cellular stresses. The protein oligomerizes, induces many target genes, and ultimately leads to apoptosis. The MDM2 ubiquitin ligase inhibits the activity of p53 and promotes its degradation. Mutations in p53 cause the majority of cancers. Boster validates its antibody against both known positive samples and those that are negative.
Boster Bio's Anti-PLK3 Molecular Marker for Mitochondrial DNA recognizes a protein that binds directly to Plk1. The target molecule is also known by plk1 and is found in centrosomes. These peptides interact and inhibit cell cycle progression by interfering with centrosomes. This antibody is available at different sizes. Each size is targeted at specific centrososomes.
The FRAP analysis showed that the Anti-PLK3 marker is specific for centrosomes. The protein localizes in centrosomes during G2 and remains at mitotic centrosomes during prometaphase and metaphase. Plk1 D176N, the kinase-dead form, had slower recovery times, lower net fluorescence recovery and a reduced ability to separate from mitotic centrosomes.
Plk1 is vital for mitotic progress. Without this function, cells cannot progress through mitosis properly. Plk1 also plays a crucial role in proper relocalization. A cell that expresses less active Plk1 may experience prometaphase arrest. Boster Bio's antiPLK3Marker recognizes Plk1 kinase activity, and promotes Plk1 release from centrosomes.
Dynamic Plk1 aids in mitotic entry after DNA damage. This protein is found within centrosomes. It allows mitotic entry after DNA injury. Hence, the Anti-PLK3 Marker in Boster Bio is highly specific for mitotic reentry. While anti-PLK3 Antibodies are highly specific, and extremely useful for mitotic entry, they also show other protein targets such cyclin B (or cyclin D2)
Moreover, Plk1-AKAP cells have an unusual mitotic arrest phenotype and exhibit DNA masses in GFP-positive cells at 20 h after thymidine-blocking. EGFP-transfected controls were in interphase while prometaphase was low. The cells that were transfected with the anti-PLK3 AKAP marker had slightly higher mitotic cells than Plk1 AKAP cells.
BoSTER BIO AntiPLK3 Marker is an effective, non-hazardous monoclonal anti-PLK3 antibody that reacts against Human Plk3 Kinase. The antibody is prepared in 10mM PBS. Blocking peptide can be purchased at 1.0 mg/ml. Blocking peptides costs vary depending on their length.
Plk1 kinase regulates PBD involvement at mitotic structures. As such, it is important to identify Plk3 in cells that express it as an alternative marker. The Plk1-AKAP marker may not be able to recognize Plk3 proteins, which is a negative outcome. It could also be indicative of other genetic disorders. To allow mitotic progression, Plk1 kinase domain from the TCF gene is required.
This is the place to go if you want more information about Steve Boster. Public records about Steve Boster include his address and phone numbers as well as his email addresses. His family was also included. You can search for Steve Boster using state, age, and known family members. There are many historic landmarks that honor Steve Boster. You can view Steve Boster’s biography for more information.
Steve Boster was born on December 6, 1952, in Joliet, IL. He was a long-standing manager in retail sales. He was a U.S. Army veteran and a Concordia Hall Member in Staunton. He is survived by his two Daughters, Crystal and Natosha Peck, and 6 Grandchildren. He is also survived by 4 Brothers, Jack and Sandra Blanton, son Jonathan, daughter-in-law Tammy, and niece and nephews.
PMID: 11039900 by Holtrich U., et al. Adhesion induced expression of the serine/threonine kinase Fnk in human macrophages.
PMID: 8702627 by Li B., et al. Prk, a cytokine-inducible human protein serine/threonine kinase whose expression appears to be down-regulated in lung carcinomas.