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Cdk1 waves are not controlled by the mitotic switch but by a double-negative feedback between Cdk1 and Chk1 (show CHEK1 ELISA Kits). In Drosophila embryos, Cdk1 positive feedback serves primarily to ensure the rapid onset of mitosis, while wave propagation is regulated by S phase events.
Cdk1 phosphorylates the conserved centriole protein Sas-4 during mitosis. This creates a Polo (show PLK1 ELISA Kits)-docking site that helps recruit Polo (show PLK1 ELISA Kits) to daughter centrioles.
Our results indicate that the cyclic changes in Gwl localization at mitotic entry and exit are directly regulated by the antagonistic cyclin B-Cdk1 and PP2A-Tws enzymes
Cdk1 mediates the role of TARA (show TRIOBP ELISA Kits) and CycA (show CCNA2 ELISA Kits) in sleep regulation.
Y15 phosphorylation can both inhibit Cdk1 catalytic activity and de-stabilize Cdk1/Cyclin (show PCNA ELISA Kits) complexes, whereas T161 phosphorylation facilitates stable interactions between cyclin B and Cdk1.
Phosphorylation of Cdk1 on Y15 appeared to be crucial for developmental and DNA damage-induced G2-phase checkpoint arrest, consistent with other evidence that Myt1 (show MYT1 ELISA Kits) is the major Y15-directed Cdk1 inhibitory kinase at this stage of development.
nonmuscle myosin II regulation by Cdc2 activity
CDK1 activation may be the cell cycle regulated event that determines the timing of emi1 destruction.
Data show that down-regulation of Cdc2 delayed pI mitosis and altered the polarity and the number of subsequent cell divisions.
Data suggest that Cks30A interacts with Cdk1, and may regulate Cyclin A (show CCNA2 ELISA Kits) levels through the activity of a female germline-specific anaphase-promoting complex, CDC20 (show CDC20 ELISA Kits)-Cortex.
TRAP1 (show TRAP1 ELISA Kits) is relevant in the control of key cell cycle regulators in tumor cells. TRAP1 (show TRAP1 ELISA Kits)/TBP7 (show PSMC4 ELISA Kits) quality control of CDK1 and MAD2 (show MAD2L1 ELISA Kits) contributes mechanistically to the regulation of mitotic entry and transit.
The Vgll4 is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induced mitotic arrest and also in normal mitosis.
Cdk-dependent phosphorylation of TRF1 on threonine 371 promotes TRF1 to interact with APBs in S and G2 phases independently of its binding to telomeric DNA. We have demonstrated that the interaction of (pT371)TRF1 with APBs is dependent upon ATM and homologous-recombination-promoting factors such as Mre11 and BRCA1.
XIAP (show XIAP ELISA Kits) is stable during mitotic arrest, but its function is controlled through phosphorylation by the mitotic kinase CDK1-cyclin-B1 (show CCNB1 ELISA Kits) at S40.
Results suggest that the cyclin-dependent kinase I (CDK1) phosphotyrosine (pTyr15) protein is a potential indicator of the progression of colorectal cancer.
These results suggest that inhibition of CDK-1 in G2 causes unpredicted effects in mitosis, even after CDK-1 inhibition is relieved.
Date show that when Wee1 (show WEE1 ELISA Kits) alone is inhibited, Chk1 (show CHEK1 ELISA Kits) suppresses CDC45 loading and thereby limits the extent of unscheduled replication initiation and subsequent S-phase DNA damage, despite very high CDK (show CDK4 ELISA Kits)-activity.
CDK1 is a positive regulator of the IFN signaling pathway. The overexpression of CDK1 might contribute to the abnormally amplified type I IFN signaling in systemic lupus erythematosus.
the mechanism of Plk1 (show PLK1 ELISA Kits) activation and the potential role of Bora phosphorylation by Cdk1, is reported.
The data presented here suggest that the temporal separation of pro- and anti-apoptotic pathways by selective inhibition of CDK2 (show CDK2 ELISA Kits) disrupts coherent signaling modules and may synergize with anti-proliferative drugs, averting toxic side effects from CDK1 inhibition.
Oligosaccharides of hyaluronan induce angiogenesis through distinct CD44 (show CD44 ELISA Kits) and RHAMM (show HMMR ELISA Kits)-mediated signalling pathways involving Cdc2 and gamma-adducin (show ADD3 ELISA Kits).
loss of LAR (show PTPRF ELISA Kits) activity resulted in reduced activity of CDK1.
Cdk1-induced desmin (show DES ELISA Kits) phosphorylation is required for efficient separation of desmin (show DES ELISA Kits)-IFs and generally detected in muscular mitotic cells in vivo.
using in vitro dephosphorylation assays, we demonstrate that Mastl (show MASTL ELISA Kits) promotes persistent MPS1 phosphorylation by inhibiting PP2A/B55 (show MINK1 ELISA Kits)-mediated MPS1 dephosphorylation rather than affecting Cdk1 kinase activity. Our findings establish a key regulatory function of the Greatwall (show MASTL ELISA Kits) kinase/Mastl (show MASTL ELISA Kits) - PP2A/B55 (show MINK1 ELISA Kits) pathway in preventing premature SAC (show ADCY10 ELISA Kits) silencing
oxidative stress-induced (show SQSTM1 ELISA Kits) DNA damage of mouse zygotes triggers the cell cycle checkpoint, which results in G2/M cell cycle arrest, and that phospho-Cdc25B (show CDC25B ELISA Kits) (Ser323), phospho-Cdc25C (show CDC25C ELISA Kits) (Ser216), and phospho-Cdc2 (Tyr15) participate in activating the G2/M checkpoint.
CDK1 is required upstream of a checkpoint-associated cell death as well as meiotic metaphase progression in mouse spermatocytes.
CDK1 is a synthetic lethal target for KRAS mutant tumors.
Our data demonstrate that ES cells are uniquely sensitive to CDK1 inhibition via a p53 (show TP53 ELISA Kits)/NOXA (show PMAIP1 ELISA Kits)/MCL1 (show MCL1 ELISA Kits) pathway.
Ubiquitin-dependent degradation of GATA 2 (show GATA2 ELISA Kits) is promoted by Fbw7 (show FBXW7 ELISA Kits), is cyclin B-CDK1-mediated Thr176 phosphorylation-dependent, and influences hematopoietic cell differentiation.
HDAC3 (show HDAC3 ELISA Kits) controls G2/M phase progression mainly through posttranslational stabilization of the G2/M cyclin-dependent kinase 1.
intestinal clock controls the expression of key cell cycle regulators, such as cdc2, wee1 (show WEE1 ELISA Kits), p21 (show CDKN1A ELISA Kits), PCNA (show PCNA ELISA Kits) and cdk2 (show CDK2 ELISA Kits), but only weakly influences cyclin B1 (show CCNB1 ELISA Kits), cyclin B2 (show CCNB2 ELISA Kits) and cyclin E1 (show CCNE1 ELISA Kits) expression.
CDK7 (show CDK7 ELISA Kits) and CCNH (show CCNH ELISA Kits) activate CDC2 by T161 phosphorylation and make up CDK-activating kinase (show CDK7 ELISA Kits), which is required for normal meiotic progression during porcine oocyte maturation.
Results describe the expression of maternal cyclin B1 (show CCNB1 ELISA Kits) and Cdc2 during in vitro maturation of porcine oocytes.
Data demonstrate the presence of a novel structure in the cortex of porcine oocytes that comprises ERES and transiently accumulates CDC2 prior to germinal vesicle breakdown.
insufficient amount of Cdc2 and continuous activation of Wee1 B are the cause of meiotic failure of small oocytes in pigs
These results suggest that the inhibitory phosphorylation of CDC2, which is catalyzed by pigWee1B (show WEE2 ELISA Kits), but not pigMyt1, is involved in the meiotic arrest of porcine oocytes.
the fine-tuning of Cdc6 (show CDC6 ELISA Kits) accumulation is essential to ensure two meiotic waves of Cdk1 activation and to avoid unscheduled DNA replication during meiotic maturation.
equilibrium between CDK1 and PP2A specifies the timing of M-phase entry and exit and regulates the dynamics of cyclin B degradation upon M-phase exit in Xenopus laevis first embryonic mitosis.
CDK1 activation proceeds with concomitant inhibition by CDC6 (show CDC6 ELISA Kits), which tunes the timing of the M-phase entry during the embryonic cell cycle
Xenopus Cdk1-AS rescues HT2-19 cells from apoptosis.
Ras suppresses cyclin-dependent kinase 1 in a complex manner: It induces continuous accumulation of cyclin B2 (show CCNB2 ELISA Kits), but also causes persistent inhibitory phosphorylation of tyr (show TYR ELISA Kits)-15-cyclin-dependent kinase 1.
By promoting CtIP (show RBBP8 ELISA Kits)-dependent resection of double-strand break (DSB) ends while preventing Rad51 chromatin assembly, Cdk1 inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.
Examination of H1 histones reveals isoform-specific regulation by Cdk1 and RanGTP; mitotic Cdk1 functions to enhance H1 binding in egg extracts and embryos
Cdc2 displays cytoskeleton-dependent localization in blastomere cortex during Xenopus embryonic cell cycle.
Results suggest that the specific synthesis of either B-type cyclins or c-Mos (show MOS ELISA Kits), induced by progesterone, is required to induce meiotic maturation and Cdc2 activation.
Cyclin B dissociation from CDK1 precedes cyclins B degradation upon CDK1 inactivation in mitotic embryo extracts and that proteasome proteolytic activity is dispensable for both activation and inactivation of CDK1 in such extracts.
Cyclin-dependent kinase A (CDKA) phosphorylates eukaryotic initiation factor 4A (show DDX39 ELISA Kits) (eIF4A)eIF4A1 (show EIF4A1 ELISA Kits) and eIF4A2 (show EIF4A2 ELISA Kits) on a conserved threonine residue (threonine-164) within the RNA-binding motif.
CDKA;1 and CYCD3;2 are required for the terminal division in the stomatal lineage.
Data indicate that the in vivo confirmation of substrates of CDKA;1 showing a direct link between cell proliferation and the control of the redox state.
The crucial function of CDKA;1 is the control of the plant Retinoblastoma homolog RBR1 and codepletion of RBR1 and CDKA;1 rescued most defects of cdka;1 mutants.
Expression of a dominant negative CDKA;1 allele under the control of the STM (show SHMT1 ELISA Kits) promoter perturbs post-embryonic development. Inhibition of CDK (show CDK4 ELISA Kits) activity at the shoot apex (show APEX1 ELISA Kits) results in premature differentiation of shoot apical meristem cells.
When a single cdka;1 sperm was delivered, either female gamete could be fertilized leading to similar proportions of seeds containing either a single endosperm or a single embryo.
However, we show here that the DNA damage checkpoint in Arabidopsis can also operate independently of the phosphorylation of CDKA;1.
CDC2A participates in the fertilization process of endosperm
The balance between cell division and differentiation is regulated through the interaction between CDKA;1 and the antiphosphatase PAS2. [CDKA;1]
The Arabidopsis thaliana Cdc2(+)/Cdc28 homolog CDKA;1 is also phosphorylated in the T-loop and that phosphorylation at the conserved Thr (show TRH ELISA Kits)-161 residue is essential for its function.
These results reveal a crucial and conserved role of phosphorylation of the N terminus of Bora for Plk1 (show PLK1 ELISA Kits) activation and mitotic entry.
CDK-1 regulates PLK-1 (show PLK1 ELISA Kits) activity during mitosis in C. elegans embryos through multisite phosphorylation of the PLK-1 (show PLK1 ELISA Kits) activator SPAT (show AGXT ELISA Kits)-1
Conversion of microtubule-organizing center state involves the conserved C. elegans centrosome protein SPD-2/CEP192 and cell-cycle-dependent kinase activity from the mitotic cell.
Our results support a model in which CYB (show CSTB ELISA Kits)-2.1/2/CDK-1 antagonize CUL-2 (show CUL2 ELISA Kits) activity to promote stabilization of PAR-6 (show PARD6A ELISA Kits) levels during polarization of the early C. elegans embryo.
CDK-1 activates PLK-1 (show PLK1 ELISA Kits) via SPAT (show AGXT ELISA Kits)-1 phosphorylation to promote entry into mitosis.
model in which Wnt signaling and CDK-1 modify WRM-1 in a temporal and spatial manner to unmask an intrinsic polarity cue required for proper orientation of the endomesoderm cell division axis
results indicate that CDC-25.1 is required for maintaining proper rate of germline mitotic cell cycle; propose that CDC-25.1 regulates the rate of germline mitotic cell cycle by counteracting WEE (show WEE1 ELISA Kits)-1.3 and by positively controlling CDK-1
CDK-1 blocks rotation by inhibiting dynein association with microtubules.
Use of loss- and gain-of-function genetic approaches demonstrates that CYY-1, a cyclin (show PCNA ELISA Kits) box-containing protein, drives synapse removal in this process.
NPP-16 and CDK-1 function to arrest prophase blastomeres in C. elegans embryos
The protein encoded by this gene is a member of the Ser/Thr protein kinase family. This protein is a catalytic subunit of the highly conserved protein kinase complex known as M-phase promoting factor (MPF), which is essential for G1/S and G2/M phase transitions of eukaryotic cell cycle. Mitotic cyclins stably associate with this protein and function as regulatory subunits. The kinase activity of this protein is controlled by cyclin accumulation and destruction through the cell cycle. The phosphorylation and dephosphorylation of this protein also play important regulatory roles in cell cycle control. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
cyclin-dependent kinase 1
, cell division control protein 2 homolog
, protein cdc2 kinase
, putative cyclin-dependent kinase A family protein
, cdc2 kinase
, cyclin dependent kinase
, cyclin-dependent kinase
, cell cycle controller CDC2
, cell division cycle 2, G1 to S and G2 to M
, cell division protein kinase 1
, p34 protein kinase
, cell cycle p34 CDC2 kinase protein
, cell division cycle 2 homolog A
, cell division cycle control protein 2a
, Cell division cycle control protein 2
, cell division cycle 2
, cell division cycle 2 protein
, Cell division control protein 2 homolog 1
, cell division control protein 2-A
, cell division cycle 2 like
, cell division protein kinase 1-A
, cyclin-dependent kinase 1-A
, p34 protein kinase 1
, DNA polymerase delta
, DNA-directed DNA polymerase delta 1
, polymerase (DNA directed), delta 1, catalytic subunit 125kDa