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Human Polyclonal PLK4 Primary Antibody für ELISA, WB - ABIN257858
Hudson, Chen, Fode, Binkert, Dennis: Sak kinase gene structure and transcriptional regulation. in Gene 2000
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Human Polyclonal PLK4 Primary Antibody für 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 (zeige ADSL Antikörper) reduction is attenuated by Asl (zeige ADSL Antikörper) overexpression, plk4 mutations, Plk4 RNAi, or Slimb overexpression, Asl (zeige ADSL Antikörper) 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 (zeige SASS6 Antikörper) 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 (zeige PLK1 Antikörper), Pericentrin-like protein (Dplp (zeige PCNT Antikörper)), Asterless (zeige CEP152 Antikörper) (Asl (zeige ADSL Antikörper)), Plk4 kinase, Centrosomin (zeige EIF3A Antikörper) (Cnn) and gamma-tubulin (zeige TUBG1 Antikörper).
SAK/PLK4 is required for centriole duplication and flagella development.
PLK4 specifically phosphorylates CP110 (zeige CCP110 Antikörper) 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 (zeige CDK1 Antikörper)-CyclinB (zeige CCNB1 Antikörper) 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 (zeige CDK7 Antikörper) polo-like kinase 4 (PLK4) and the two proteins STIL (zeige STIL Antikörper) and SAS-6 (zeige SASS6 Antikörper) 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 (zeige MBD1 Antikörper) and phosphorylates S372. Plk4 depletion leads to the dispersal of centriolar satellites.
Aurora A (zeige AURKA Antikörper) 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 (zeige TP53 Antikörper)-deficient cells
Transient knockdown of KLF14 (zeige SP6 Antikörper) 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 (zeige TP53 Antikörper)-Dependent and cell specific epigenetic regulation of the polo (zeige PLK1 Antikörper)-like kinases under oxidative stress.
The Plk4-Cep152 (zeige CEP152 Antikörper) 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 (zeige PPP2R2B Antikörper) (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 (zeige NUTF2 Antikörper), suggesting a role for PLK4 during the initiation of spermatogenesis.
Aberrant Plk (zeige PLK1 Antikörper) 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