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PLK4 encodes a member of the polo family of serine/threonine protein kinases. Additionally we are shipping Polo-Like Kinase 4 Antibodies (30) and Polo-Like Kinase 4 Proteins (5) and many more products for this protein.
When Asl (show ADSL ELISA Kits) reduction is attenuated by Asl (show ADSL ELISA Kits) overexpression, plk4 mutations, Plk4 RNAi, or Slimb overexpression, Asl (show ADSL ELISA Kits) levels are higher in spermatozoa, resulting in embryos with reduced viability.
Drosophila Plk4 phosphorylates four conserved serines in the STAN motif of the core centriole protein Ana2 to enable it to bind and recruit its Sas6 (show SASS6 ELISA Kits) partner.
Plk4 directly generates its own phosphodegron.Phosphorylation of only S293 of the Slimb-recognition motif is required for Slimb binding to Plk4.
Regulation of autophosphorylation controls PLK4 self-destruction and centriole number.PLK4 protein levels are controlled by Slimb.
Data indicate that interphase centrioles are closely associated with Sas-4, Spd-2, Polo kinase (show PLK1 ELISA Kits), Pericentrin-like protein (Dplp (show PCNT ELISA Kits)), Asterless (Asl (show ADSL ELISA Kits)), Plk4 kinase, Centrosomin (show EIF3A ELISA Kits) (Cnn) and gamma-tubulin (show TUBG1 ELISA Kits).
SAK/PLK4 is required for centriole duplication and flagella development.
Mutations in human PLK4, the protein of which plays critical role in centriole duplication and normal nuclear formation, could be associated with abnormal spermatogenesis leading to Sertoli cell-only syndrome. Aberrant forms of PLK4 might also cause other types of oligozoospermia or sperm fl agellar abnormalities.
Plk4 directly binds PCM1 (show MBD1 ELISA Kits) and phosphorylates S372. Plk4 depletion leads to the dispersal of centriolar satellites.
Decreased PLK4 protein expression due to promoter hypermethylation was negatively correlated with JAK2 (show JAK2 ELISA Kits) overexpression, a common occurrence in hematological malignancies.
KLF14 transcription is signi (show SP6 ELISA Kits)ficantly downregulated, whereas Plk4 transcription is upregulated in multiple types of cancers, and there exists an inverse correlation between KLF14 and Plk4 protein expression in human breast and colon cancers.
The authors suggest that the STIL (show STIL ELISA Kits)-coiled-coil region/PLK4 interaction mediates PLK4 activation as well as stabilization of centriolar PLK4 and plays a key role in centriole duplication.
We demonstrate that centrioles promote PLK4 activation through its recruitment and local accumulation. Though centriole removal reduces the proportion of active PLK4, this is rescued by concentrating PLK4 to the peroxisome lumen
these results identify the interaction between Mib1 and Plk4 as a new and important element in the control of centriole homeostasis.
PLK4 functions downstream of ROCK2 (show ROCK2 ELISA Kits) to drive centrosome amplification in arrested cells.
PLK4 overexpression induces centrosome amplification and chromosome instability and causes the suppression of primary cilia formation.
Negative feedback by centriolar STIL (show STIL ELISA Kits) regulates bimodal centriolar distribution of Plk4 and seemingly restricts occurrence of procentriole formation to one site on each parental centriole.
that aneuploidy induced by transient centrosome amplification can accelerate tumorigenesis in p53 (show TP53 ELISA Kits)-deficient cells
Transient knockdown of KLF14 (show SP6 ELISA Kits) is sufficient to induce Plk4-directed centrosome amplification.
PLK4 is essential for meiotic resumption but may not influence spindle formation in mouse oocytes during meiotic maturation
p53 (show TP53 ELISA Kits)-Dependent and cell specific epigenetic regulation of the polo (show PLK1 ELISA Kits)-like kinases under oxidative stress.
The Plk4-Cep152 complex has an unexpected role in promoting microtubule nucleation in the vicinity of chromosomes to mediate bipolar spindle formation in the absence of centrioles.
Loss of Plk4 is associated with centrosome amplification causing microcephaly.
PP2A (Protein Phosphatase 2A(Twins)) counteracts Plk4 autophosphorylation, thus stabilizing Plk4 and promoting centriole duplication
the I242N heterozygous mutation in PLK4 is causative for patchy germ cell loss beginning at P10 (show NUTF2 ELISA Kits), suggesting a role for PLK4 during the initiation of spermatogenesis.
Aberrant Plk (show PLK1 ELISA Kits) methylation is correlated with the development of hepatocellular carcinoma in mice.
Plk4 is required for cytokinesis and maintenance of chromosomal stability
These results indicated that PLK4 plays crucial roles in bovine oocyte meiotic maturation and subsequent early embryo development.
results provide the first steps in defining a new role for plk4 in organogenesis and implies a role in planar cell polarity, segmentation, and in recently described PLK4 mutations in human
This gene encodes a member of the polo family of serine/threonine protein kinases. The protein localizes to centrioles, complex microtubule-based structures found in centrosomes, and regulates centriole duplication during the cell cycle. Three alternatively spliced transcript variants that encode different protein isoforms have been found for this gene.
, Snk akin kinase
, serine/threonine kinase 18
, serine/threonine protein kinase SAK
, serine/threonine-protein kinase 18
, serine/threonine-protein kinase PLK4
, serine/threonine-protein kinase Sak