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Validated All-in-One™ qPCR Primer for CDK1(NM_001786.4) Search again
Product ID:
HQP088360
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CDC2, CDC28A, P34CDC2
Gene Description:
cyclin dependent kinase 1
Target Gene Accession:
NM_001786.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- Cyclin b1 promoter activity and functional cdk1 complex formation in G1 phase of human breast cancer cells
- Abolishment of the Tyr-15 inhibitory phosphorylation site on cdc2 reduces the radiation-induced G(2) delay, revealing a potential checkpoint in early mitosis.
- effects of ergosterol and cholesteron on Cdk1 activation
- role in regulating peroxiredoxin I activity by phosphorylation
- activation in cells depleted of Plk1 by siRNA
- Syncytia from cells expressing the HIV-1 Env gene fused with cells expressing CD4/CXCR4 undergo apoptosis after nuclear translocation of mTOR, mTOR-mediated p53 phosphorylation, p53-dependent Bax upregulation & mitochondrial death pathway activation.
- mediates phosphorylation and mobilizes microtubule-organizing centers from the apical intermediate filament scaffold in CACO-2 epithelial cells
- cdc2 might be involved in the abnormal hyperphosphorylation of tau and aggregation of tau into paired helical filaments at an early stage and increased cdc2 activity is not consequent to the deposition of beta-amyloid in Alzheimer disease brain.
- in a complex with cyclin B, regulates function of WARTS on the mitotic apparatus
- SET protein regulates G(2)/M transition by modulating cyclin B-CDK1 activity.
- Cdc2 provides a signal that triggers inactivation of S6K1 in mitosis.
- deregulation of cdc2 kinase activity can trigger apoptotic machinery that leads to caspase-3 activation and apoptosis.
- Cdc2 is important regulator for cell cycle as well as for apoptosis
- alphavbeta3 expression in LNCaP (beta3-LNCaP) prostate cancer cells causes increased cdc2 mRNA levels as evaluated by gene expression analysis, and increased cdc2 protein and kinase activity levels
- CDC2 phosphorylates emi1 on a consensus site, is recognized by bTrCP ubiquitin ligase and is destroyed, thus delaying activation of the anaphase promoting complex.
- The immunohistochemical expression of p34(cdc2) is independently associated with lymph node metastasis in colorectal carcinoma
- nonphosphorylated CDC2 has a role in stimulating DNA replication, histone H3 phosphorylation, and cell division even after DNA damage
- CDK1 phosphorylates hamartin at three sites, one of which (Thr417) is in the hamartin-tuberin interaction domain; phosphorylation of hamartin regulates the function of the hamartin-tuberin complex during the G2/M phase of the cell cycle
- data suggest the maintenance of Cdk1/cyclin B1 activity in HCMV-infected cells can be explained by 3 mechanisms: accumulation of cyclin B1, inactivation of negative regulatory pathways for Cdk1, accumulation of positive factors that promote Cdk1 activity
- could play an important role in gastric carcinoma progression and would be a novel target for the treatment of gastric carcinomas as well as a strong prognostic marker.
- Increased expression of CDK1 may have important causative role in decreasing levels of p25 in patients with aggressive colorectal carcinoma
- At the onset of mitosis, Cdk1 phosphorylates the peripheral Golgi protein Nir2 at multiple sites.
- the induction of Cdc2 phosphorylation due to the increase of Wee1 and Myt1 as well as the reduction of Cdc2 and cyclin B1 are involved in 1,25[OH]2VD3-induced G2/M arrest of keratinocytes.
- exposure to nonrepairable DNA damage leads to nuclear accumulation of inactive cyclin B1-Cdk1 complexes
- role in regulating Fas ligand transcription
- results suggest that centrosome-associated Chk1 shields centrosomal Cdk1 from unscheduled activation by cytoplasmic Cdc25B, thereby contributing to proper timing of the initial steps of cell division, including mitotic spindle formation
- expression of pdcd4 as an indirect suppressor of CDK1/cdc2 is lost in progressed carcinomas of lung, breast, colon, and prostate.
- models of cyclin-dependent kinase 1 complexed with flavopiridol and roscovitine
- protein 4.1R mitotic regulation involves phosphorylation by cdc2 kinase
- Inhibition of Cdc2 activity and the subsequent downregulation of survivin and XIAP by subtoxic doses of rottlerin contribute to amplification of caspase cascades.
- in tumor cells lacking functional p53 and/or p21, p14(ARF) impaired mitotic entry and enforced a primarily cytoplasmic localization of p34(cdc2) that was associated with a decrease in p34(cdc2) kinase activity and reduced p34(cdc2) protein expression
- Abi enhances Abl-mediated downregulation and phosphorylation of Cdc2 kinase
- The level of mitotic Bloom syndrome protein phosphorylation reflects the level of cdc2 activity.
- Cellular differentiation in squamous cell carcinoma of the esophagus may be mediated by an intracellular localization of p34(cdc2).
- Cdk1-cyclin B is the major kinase phosphorylating GRASP65 in mitosis
- results show that human papillomavirus type 16 E1 E4 does not inhibit the kinase activity of the Cdk1/cyclin B1 complex; instead, 16E1 E4 uses a novel mechanism in which it sequesters Cdk1/cyclin B1 onto the cytokeratin network
- results strongly indicate that in response to genotoxic stress, Cdk5 activator-binding protein C53(C53) serves as an important regulatory component of DNA damage checkpoint through modulating cyclin dependent kinase 1-cyclin B1 function
- Cdc2 inhibits growth factor receptor-mediated ERK activation during mitosis by primarily targeting signaling proteins that are upstream of MEK1
- Our results demonstrate that differential regulation of Cdc2 and Cdk2 activity by different doses of doxorubicin may contribute to the induction of two modes of cell death in hepatoma cells, either apoptosis or cell death through mitotic catastrophe.
- Cdk1 inactivation is sufficient to activate a signaling pathway leading to cytokinesis, which emanates from mitotic spindles and is regulated by ECT2, MgcRacGAP, and RhoA
- in nasopharyngeal carcinoma cells, SarCNU-induced apoptosis is p53-dependent while SarCNU-induced G2/M arrest is mediated by the cyclin B1-cdc-2 complex
- Chk1 deficiency resulted in a premature onset of mitosis because of abnormal activation of cyclin B-Cdc2 and led to the activation of caspases 3 and 9 triggered by cytoplasmic release of cytochrome c.
- Results highlight the centrosome as a site to organize phosphorylation of Cep55 by Erk2/Cdk1 and Plk1, enabling it to relocate to the midbody to function in mitotic exit and cytokinesis.
- Cdc2/cyclin B1 interacts with and modulates inositol 1,4,5-trisphosphate receptor (type 1) functions.
- ECT2 is regulated by CDK1
- A new concept indicates in this review that both Cdk2 and/or Cdc2 can drive cells through G1/S phase in parallel.
- These data indicate that phosphorylation of tubulin by Cdk1 could be involved in the regulation of microtubule dynamics during mitosis.
- Phosphorylation of I-2 is catalyzed by cdk1::cyclinB1 and staining with a specific antibody should prove useful as a selective marker of cells in the early stages of mitosis.
- RUNX2 phosphorylation by cdc2 may facilitate cell cycle progression possibly through regulation of G(2) and M phases, thus promoting endothelial cell proliferation required for tumor angiogenesis
- These results suggest that p27(KIP1) interacts with cdc2 in the M-phase of human retinoblastoma cells.
- GAPDH might be involved in cell cycle regulation by modulating cyclin B-cdk1 activity.
- our studies indicate that the 2-ME(2)-induced upregulation of wee1 and subsequent cdc2 phosphorylation are mediated through mitogen-activated protein kinase (MAPK)-ERK-JNK signaling pathways.
- These observations imply the regulation of mitotic Chk1 function through Chk1 phosphorylation at novel sites by Cdk1.
- hCdc14A is differentially expressed in human cancer cells and can interact with both p53 and the Cdk1/cyclin B complex; it may play a role in carcinogenesis
- DNA damage-induced down-regulation of human Cdc2
- BLM helicase is a new substrate for cdc2, which may have potential physiological implications for the role of BLM in mitosis.
- Cdk1-mediated phosphorylation of S439 stabilizes mature SREBP1 during mitosis, thereby preserving a critical pool of active transcription factors to support lipid synthesis.
- first pathway is by changing the expression levels of nuclear factor-I C(NFI-C) and secretin proteins while the second pathway is by modifying the phosphorylation status of both NFI-C and Sp proteins via cyclin-dependent kinase 1
- The reduced CDK7 kinase activity is responsible for the inactivation of CDC2/p34 kinase and the irreversible G(2)/M phase cell-cycle arrest of a human gastric carcinoma cell line.
- These novel findings suggest that CDK1 is activated by unscheduled accumulation of cyclin B1 in G1 phase cells exposed to X-ray.
- increased Cdk1 activity is a mechanism for increasing androgen receptor expression and stability in response to low androgen levels in androgen-independent prostate cancer
- Mip/LIN-9 is required for the expression of B-Myb, and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A, cyclin B, and CDK1
- Results show that CDK1 can directly interact with RUNX2 and CDK1/cyclin B kinase complex phosphorylate RUNX2 during mitosis in osteoblastic cells.
- Cdc14A may be involved in the cell cycle regulation of Cdc25A stability.
- ATM regulates G(2)/M checkpoint recovery through inhibitory phosphorylations of Artemis that occur soon after DNA damage, thus setting a molecular switch that, hours later upon completion of DNA repair, allows activation of the Cdk1-cyclin B complex.
- The activation state of Cdk1 controls the switch of Plk1 localization from centrosomes and kinetochores during metaphase, to the central spindle during anaphase.
- data strongly argue against mutational events of CDK1, cyclinB1 and cyclinA2 to play a role in gangliogliomas or focal cortical dysplasia
- Both Cdk1 and -2 require cyclin binding and T loop phosphorylation for full activity.
- Partial or complete loss of Lzts1 downregulates Cdc25C and inhibits Cdk1 activity during mitosis, leading to premature transition from metaphase to anaphase.
- the apoptotic initiator protease caspase-9 is regulated during the cell cycle through periodic phosphorylation at an inhibitory site, Thr125. This site is phosphorylated by CDK1/cyclin B1 during mitosis.
- Cyclin B1-Cdk1 activation continues after centrosome separation to control mitotic progression.
- inhibition of radiation-induced CDC2 kinase activity by purvalanol A induces apoptosis through the enhancement of active fragments of caspase 3
- These results identify a GEF-H1-dependent mechanism to modulate localized RhoA activation during cytokinesis under the control of mitotic kinases.
- study suggests that the I-G-T haplotype of the CDC2 gene increases the risk of Alzheimer's disease in APOE epsilon4 carriers
- Differential repression of c-myc and cdc2 gene expression by ERF and PE-1/METS.
- These findings suggest novel Cdk1/cyclin A phosphorylation sites, which appear to be associated with p53-independent cell death following etoposide treatment.
- Cdc2 and homeodomain-interacting protein kinase-2 (HIPK2) phosphorylate chromosomal high-mobility group A protein HMGA1 at the same site but show different site preferences.
- cdk phosphorylation of RUNX1 potentially couples stem/progenitor proliferation and lineage progression
- Mitosis persisits in the absence of CDC2 activity when proteolysis or protein phosphatase activity is suppressed.
- PP2A:B56delta as a key upstream regulator of Cdk1 activity upon exit from mitosis
- the correct attachment of microtubules to kinetochores and efficient alignment of the chromosomes, most likely through localized phosphorylation of specific substrates by cyclin B1-CDK1.
- phosphorylates MgcRacGAP in conjunction with aurora B kinase and is dephosphorylated by PP2A
- CDC2 gene plays an important role in the proliferation of human gliomas.
- lithium arrest of hepatocellular carcinoma cells at G2/M checkpoint
- both U(L)13 and U(S)3 viral kinases phosphorylate cdc25C and ICP22; however, in infected cells, the ability of cdc25C to activate cdc2 by dephosphorylation of the inactive cdc2 protein is reduced
- cdc25C phosphatase plays a role in viral replication and that this role extends beyond its function of activating cdc2 for initiation of the ICP22-dependent cascade for upregulation of gamma(2) gene expression.
- These data closely match the control of Ser359 phosphorylation and indicate that cdc2 may be regulated by mTORC1.
- Our work uncovers a unique regulatory mechanism of MT organization by PP4c through its targets Cdk1 and NDEL1 via regulation of katanin p60 distribution.
- findings define a conserved signaling link between Cdk1 and FOXO1 that may have a key role in diverse biological processes, including the degeneration of postmitotic neurons
- G2 phase cyclin A/cdk2 controls the timing of entry into mitosis by controlling the subsequent activation of cyclin B/cdk1, but also has an unexpected role in coordinating the activation of cyclin B/cdk1 at the centrosome and in the nucleus
- Aberrant activation of CDK1 may contribute to tumorigenesis by promoting cell proliferation and survival via phosphorylation and inhibition of FOXO1.
- Cdk1/cyclin B has a role in regulating B-raf activation at mitosis
- Data show that DAP5 promotes cap-independent translation of Bcl-2 and CDK1 to facilitate cell survival during mitosis.
- analysis of rapid cycling and precocious termination of G1 phase in cells expressing CDK1AF, a mutant of CDK1
- Study concludes that the increase in cyclin A/Cdk1 activity at the end of S phase triggers degradation of SLBP at S/G(2).
- Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition
- Cdk1 phosphorylates HuR during G2, thereby helping to retain it in the nucleus in association with 14-3-3 and hindering its post-transcriptional function and anti-apoptotic influence.
- Cyclin A-CDK activity during G(1) would result in an inhibition of progression into the S phase.
- IE62 is a substrate for CDK1/cyclin B1, and virions could deliver the active cellular kinase to nondividing cells that normally do not express it
- LMP1 regulates Op18/stathmin signaling by cdc2 mediation.
- Cyclin A assembles with Cdk1 only after complex formation with Cdk2 reaches a plateau during late S and G2 phases.
- These findings establish phosphorylation events by CDKs 1 and 2 as key regulators of Discs Large 1 localisation and function.