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Human Polyclonal PLK4 Primary Antibody for ELISA, WB - ABIN257858
Hudson, Chen, Fode, Binkert, Dennis: Sak kinase gene structure and transcriptional regulation. in Gene 2000
Show all 2 Pubmed References
Human Polyclonal PLK4 Primary Antibody for WB - ABIN524159
Hori, Peddie, Collinson, Toda: Centriolar satellite- and hMsd1/SSX2IP-dependent microtubule anchoring is critical for centriole assembly. in Molecular biology of the cell 2015
Show all 2 Pubmed References
When Asl (show ADSL Antibodies) reduction is attenuated by Asl (show ADSL Antibodies) overexpression, plk4 mutations, Plk4 RNAi, or Slimb overexpression, Asl (show ADSL Antibodies) 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 Antibodies) 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 Antibodies), Pericentrin-like protein (Dplp (show PCNT Antibodies)), Asterless (show CEP152 Antibodies) (Asl (show ADSL Antibodies)), Plk4 kinase, Centrosomin (show EIF3A Antibodies) (Cnn) and gamma-tubulin (show TUBG1 Antibodies).
SAK/PLK4 is required for centriole duplication and flagella development.
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 Antibodies) polo-like kinase 4 (PLK4) and the two proteins STIL (show STIL Antibodies) and SAS-6 (show SASS6 Antibodies) 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 Antibodies) 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 Antibodies) overexpression, a common occurrence in hematological malignancies.
KLF14 transcription is signi (show SP6 Antibodies)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 Antibodies)-coiled-coil region/PLK4 interaction mediates PLK4 activation as well as stabilization of centriolar PLK4 and plays a key role in centriole duplication.
that aneuploidy induced by transient centrosome amplification can accelerate tumorigenesis in p53 (show TP53 Antibodies)-deficient cells
Transient knockdown of KLF14 (show SP6 Antibodies) 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 Antibodies)-Dependent and cell specific epigenetic regulation of the polo (show PLK1 Antibodies)-like kinases under oxidative stress.
The Plk4-Cep152 (show CEP152 Antibodies) 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 Antibodies) (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 Antibodies), suggesting a role for PLK4 during the initiation of spermatogenesis.
Aberrant Plk (show PLK1 Antibodies) 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