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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
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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
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Plk4 phosphorylates Ana2 at S38 and STAN motif and promotes Ana2 recruitment to the centriole.
When Asl (显示 ADSL 抗体) reduction is attenuated by Asl (显示 ADSL 抗体) overexpression, plk4 mutations, Plk4 RNAi, or Slimb overexpression, Asl (显示 ADSL 抗体) 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 (显示 SASS6 抗体) 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 (显示 PLK1 抗体), Pericentrin-like protein (Dplp (显示 PCNT 抗体)), Asterless (显示 CEP152 抗体) (Asl (显示 ADSL 抗体)), Plk4 kinase, Centrosomin (显示 EIF3A 抗体) (Cnn) and gamma-tubulin (显示 TUBG1 抗体).
SAK/PLK4 is required for centriole duplication and flagella development.
PLK4 played important roles in regulating cell cycle- and DNA replication-related pathways. E2F (显示 E2F1 抗体) could upregulate the expression levels of PLK4 by deregulating the methylations of their promoters to promote the relapse of Acute Lymphoblastic Leukemia.
PLK4 specifically phosphorylates CP110 (显示 CCP110 抗体) at the S98 position and is an essential step for centriole assembly.
These data show that complementary mechanisms, such as mother-daughter centriole proximity and CDK1 (显示 CDK1 抗体)-CyclinB (显示 CCNB1 抗体) 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 (显示 CDK7 抗体) polo-like kinase 4 (PLK4) and the two proteins STIL (显示 STIL 抗体) and SAS-6 (显示 SASS6 抗体) 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.
Aurora A (显示 AURKA 抗体) 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 (显示 TP53 抗体)-deficient cells
Transient knockdown of KLF14 (显示 SP6 抗体) 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 (显示 TP53 抗体)-Dependent and cell specific epigenetic regulation of the polo (显示 PLK1 抗体)-like kinases under oxidative stress.
The Plk4-Cep152 (显示 CEP152 抗体) 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 (显示 PPP2R2B 抗体) (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 (显示 NUTF2 抗体), suggesting a role for PLK4 during the initiation of spermatogenesis.
Aberrant Plk (显示 PLK1 抗体) 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