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When Asl (show ADSL Proteins) reduction is attenuated by Asl (show ADSL Proteins) overexpression, plk4 mutations, Plk4 RNAi, or Slimb overexpression, Asl (show ADSL Proteins) 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 Proteins) 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, Pericentrin-like protein (Dplp), Asterless (Asl), Plk4 kinase, Centrosomin (Cnn) and gamma-tubulin.
SAK/PLK4 is required for centriole duplication and flagella development.
These data show that complementary mechanisms, such as mother-daughter centriole proximity and CDK1 (show CDK1 Proteins)-CyclinB (show CCNB1 Proteins) interaction with centriolar components, ensure that centriole biogenesis occurs once and only once per cell cycle, raising parallels to the cell-cycle regulation of DNA replication and centromere formation.
Homozygous splicing acceptor site transition (c.31-3 A>G) in PLK4 was identified in a family with Seckel syndrome. PLK4 is essential for centriole biogenesis and DNA damage response.
the interaction between Cep78 and the N-terminal catalytic domain of Plk4 is a new and important element in the centrosome overduplication process.
Our results validate Plk4 as a therapeutic target in cancer patients
Heterozygous missense mutation in PLK4 identified in a patient with microcephaly and chorioretinopathy. Aberrant spindle formation was observed in a LCL derived from this patient. Mutant PLK4 proteins demonstrated altered mobility pattern on a western blot suggesting alterations in post-translation modification.
Studies indicate that depletion of any one of the protein kinase (show CDK7 Proteins) polo-like kinase 4 (PLK4) and the two proteins STIL and SAS-6 (show SASS6 Proteins) blocks centriole duplication, and, conversely, overexpression causes centriole amplification.
Common PLK4 variant rs2305957 is associated with blastocyst formation and early recurrent miscarriage in Chinese women.
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 Proteins) 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 Proteins) overexpression, a common occurrence in hematological malignancies.
Aurora A (show AURKA Proteins) and Plk4 are rate-limiting factors contributing to microtubule growth as the acentriolar oocyte resumes meiosis.
that aneuploidy induced by transient centrosome amplification can accelerate tumorigenesis in p53 (show TP53 Proteins)-deficient cells
Transient knockdown of KLF14 (show SP6 Proteins) 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-Dependent and cell specific epigenetic regulation of the polo-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 (show PPP2R2B Proteins) (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 Proteins), suggesting a role for PLK4 during the initiation of spermatogenesis.
Aberrant Plk methylation is correlated with the development of hepatocellular carcinoma in mice.
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