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Validated All-in-One™ qPCR Primer for CHEK1(NM_001244846.1) Search again
Product ID:
HQP061994
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CHK1
Gene Description:
checkpoint kinase 1
Target Gene Accession:
NM_001244846.1(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.
Gene References into function
- Biochemical studies suggest the functional interactions of this protein with cell cycle regulators. Cdc25A, Cdc25B, and Cdc25C can be phosphoryalted by this protein.
- utilization of peptide library analyses to develop specific, highly preferred substrate motifs for hCds1/Chk2 and Chk1
- radiation induced phosphotylation of chK1 is associated with p53-dependent cell cycle arrest pathways in tumor
- An ATM-independent S-phase checkpoint response involves CHK1 pathway.
- role in mediating G(2)M checkpoint in relation to the cellular resistance to the novel topoisomerase I poison BNP1350
- findings indicate that Chk1 directly phosphorylates Cdc25A during an unperturbed cell cycle, and that phosphorylation of Cdc25A by Chk1 is required for cells to delay cell cycle progression in response to double-strand DNA breaks
- Data suggest that the UVC-induced S checkpoint response of inhibition of replicon initiation is mediated by ATR signaling through Chk-1 and is independent of ATM, Nbs1, and Mre11.
- Chk1 is phosphorylated by ATM and NBS1 and is essential for ionizing radiation-induced inhibition of DNA synthesis and the G(2)/M checkpoint
- targets tousled like kinasese via DNA damage checkpoint
- CHK1 regulates the S phase checkpoint by coupling the physiological turnover and ionizing radiation-induced accelerated proteolysis of Cdc25A.
- Chk1 mediates both S and G2 checkpoint and is thus a more ubiquitous cell cycle checkpoint mediator than previously thought
- Chk1 protein complexes bind to single-stranded DNA and DNA ends and has a role in the repair of double strand breaks
- the G2 checkpoint in irradiated human cells derives from an overactivation of the ATR/CHK1 pathway.
- Chk1 expression is dispensable for somatic cell death and critical for sustaining G2 DNA damage checkpoint
- we show that Chk1 is essential for the suppression of TLK activity after replication block, but that ATR, Chk2 and BRCA1 are dispensable for TLK suppression.
- hyperoxia activates the ATR-Chk1 pathway and phosphorylates p53 at multiple sites in an ATM-independent manner, which is different from other forms of oxidative stress such as H2O2 or UV light.
- Data report the isolation and characterization of the 5' flanking region of the Chk1 gene, and show that this region has promoter activity.
- Data suggest that the Chk1/Cdc25A/14-3-3 pathway functions to prevent cells from entering into mitosis prior to replicating their genomes to ensure the fidelity of the cell division process.
- Chk1 is a novel Hsp90 client with a role in sensitization of tumor cells to replication stress
- data reveal the very different mode of regulation between CHK1 and CHK2
- CHEK1 interacts with XIAP protein during mitosis.
- The transient slow-down of DNA synthesis was abolished in cells lacking ATR, whereas CHK1-siRNA-treated cells, NBS1 or Fanconi anemia cells showed partial S-phase arrest.
- Brca1 and Chk1 are regulated by MCPH1 during DNA damage in tumor cell lines
- Formation of a stable complex between protein kinase CK2beta and Chk1 is not affected by the modification of Thr213 but it does require the presence of an active Chk1 kinase.
- the Chk1 pathway involves claspin, which functions in checkpoint control [review]
- 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.
- These data further emphasise the role of Chk1 as a molecular target to inhibit in tumors with a defect in the G(1) checkpoint with the aim of increasing the selectivity and specificity of anticancer drug treatments.
- CHK1 inactivation in non-hodgkin's lymphoma occurs by loss of protein expression in a subset of aggressive variants alternatively to ATM, CHK2, and p53 alterations
- role of Chk1 in maintaining tumor cell viability following activation of the replication checkpoint
- Chk1 and Chk2 control the induction of the p53 related transcription factor p73 in response to DNA damage.
- Chk1 and Chk2 have roles in mismatch repair-dependent G2 arrest
- results indicate that the different radiosensitivities & G(2)checkpoint responses are independent of NHEJ, suggesting that CHK1-regulated checkpoint facilitates homologous recombination repair & protects cells from ionizing radiation-induced killing
- possible interplay between tumor protein p53 C-terminal phosphorylation and acetylation, and they provide an additional mechanism for the control of the activity of p53 by Checkpoint kinase 1 and Checkpoint kinase 2
- Chk1 downregulation can not only potentiate DNA-damaging agents, but also enhance the toxicity of anti-microtubule agents.
- Results show that the ATR/checkpoint kinase 1 pathway plays a predominant role in the response to topoisomerase I inhibitors in carcinoma cells.
- Expression of Chk1 blunted induction of gammaH2AX foci by Cdk inhibitors, indicating that Chk1 down-regulation was necessary to elicit the full phenotype.
- loss of PTEN and subsequent activation of AKT impair CHK1 through phosphorylation, ubiquitination, and reduced nuclear localization to promote genomic instability in tumor cells
- ATR phosphorylates Chk1 in cells expressing only a mutant of ATRIP that does not bind to RPA-ssDNA.
- Chk1 is required during normal S phase to avoid aberrantly increased initiation of DNA replication, thereby protecting against DNA breakage.
- results of the present study suggest existence of a checkpoint kinase 1-dependent mechanism for diallyl trisulfide-induced mitotic arrest in human prostate cancer cells
- Synthetized inhibitors are synthetically tractable and inhibit Chk1 by competing for its ATP site.
- cleavage of Claspin by caspase-7 inactivates the Chk1 signaling pathway
- 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.
- Data suggest that the microcephaly observed in patients with MCPH1 deficiencies is due to disruption of the ATR-BRCA1-Chk1 signaling pathway that is also disrupted in Seckel syndrome patients.
- Chk1 plays a primary role in the protection of cells from death induced by replication fork stress, whereas p21 mediates through its role in regulating entry into S phase
- Chk1 is post-translationally chaperoned to an active kinase. This reaction minimally requires Hsp90, Hsp70, Hsp40, Cdc37, and the protein kinase CK2.
- Gene repair directed by oligonucleotides activates a pathway that prevents corrected cells from proliferating in cell culture through the activation of Chk1 and Chk2.
- Chk1 and Claspin proteins regulate each other and thus ensure the proper cell cycle progression and replication checkpoint control.
- CHK1 maintains global replication fork stability in response to DNA damage amd DNA replication inhibitors.
- Chk1-dependent replication checkpoint which slows S phase progression can protect tumour cells against the cytotoxic effects of 5FU.
- These observations imply the regulation of mitotic Chk1 function through Chk1 phosphorylation at novel sites by Cdk1.
- Chk1-mediated G(2)/M cell-cycle arrest by the histamine H1 antagonist, loratidine in a tumor cell line.
- Inhibition of Chk1 by an RNAi approach resulted in an increase in cell death in p53-null cells, showing that the Chk1-dependent G(2) checkpoint protected cells that lacked a functional p53 pathway from oxidative stress
- Critical role in regulating chromosome stability, and in particular, common fragile site stability.
- the Chk1 pathway is regulated through both phosphorylation of Claspin and its controlled degradation.
- Checkpoint kinase 1 (Chk1) is required for mitotic progression through negative regulation of polo-like kinase 1 (Plk1)
- These results suggest that while TopBP1 is a general regulator of ATR, Claspin operates downstream of TopBP1 to selectively regulate the Chk1-controlled branch of the genotoxic stress response.
- Data suggest that degradation of Claspin by SCFbetaTrCP restrains Chk1 activation.
- the Chk1-mediated S-phase checkpoint targets initiation factor Cdc45 via a Cdc25A/Cdk2-independent mechanism
- Either chk1 or plk1-specific antisense oligodeoxynucleotides enhanced DNA damaging agent-induced apoptosis.
- Chk1 can be activated in a claspin-dependent manner leading to cyclin B1 down-regulation and providing the cells of an additional mechanism to inhibit mitosis entry in Hela cells.
- Results show under normal cell cycle conditions and in the absence of DNA damage, CHK1 constitutively phosphorylates CDC25B during interphase and thus prevents the premature initiation of mitosis.
- ataxia-telangiectasia-related protein kinase-Chk1-protein phosphatase 2A regulatory circuit functions to keep Chk1 in a low-activity state during an unperturbed cell division cycle
- Plk1 has a role in mitotic arrest, which is released by Chk1
- Chk1 functions to coordinate mitotic events through regulation of Cdc25B
- Interfering with PCNA function by overexpression of p21 mutant, impaired in its interaction with Cdks but not with PCNA, leads to ATR-dependent Chk1 activation.
- These results suggest a mechanism through which Chk1 could protect against tumorigenesis through its role in spindle checkpoint signaling.
- Chk1-mediated phosphorylation of FANCE is required for a function independent of FANCD2 monoubiquitination.
- the Chk1 framshift mutations might be involved in colorectal tumourigenesis through a defect in response to DNA damage in a subset of sporadic colorectal cancers and HNPCCs.
- Novel substrates for Chk1 and Chk2 were screened using substrate target motifs determined previously by an oriented peptide library approach.
- Inhibition of checkpoint kinase 1 (Chk1) by RNA-mediated interference or drug treatment suppressed DNA-damage-induced centrosome amplification.
- Chk1 regulates the density of active replication origins during the vertebrate S phase.
- Phosphorylation of p53 (Ser15), Chk1 (Ser345), and Chk2 (Thr68) was also observed, suggesting that H/R activates p53 through checkpoint signals.
- zoledronate induces DNA damage and S phase arrest, accompanied by activation of the ATM/Chk1/cdc25 pathway in a human osteosarcoma cell line
- Chk1 is E2F regulated and highly expressed in triple-negative estrogen receptor /progesterone receptor /HER-2 breast carcinomas
- ATR/Chk1 pathway is activated at an early time point after the loss of Geminin and contributes to checkpoint arrest
- Centrosomal Chk1 induces G2/M cell cycle arrest and may evoke centrosome amplification, the latter possibly providing a backup mechanism for elimination of cells with impaired DNA damage checkpoints operating earlier during the cell cycle
- Frequent mutations in CHEK1(5%) damage response axis in colon cancers.
- protein kinase CK2 is involved in cell cycle regulation and indicate the mechanism by which CDC25A turnover might be regulated by Chk1 in the absence of DNA damage.
- the ability of NF-kappaB to regulate the G1-phase expression of key proto-oncogenes is subject to regulation by the integrated activity of IkappaB kinase (IKK)alpha, IKKbeta, Akt and Chk1
- This review of new findings demonstrates that DNA replication fork velocity (fork progression) is coordinated with inter-origin distance and that it can be actively slowed down by Chk1-dependent mechanisms in response to DNA damage.
- Loss of CHK1 function impedes DNA damage-induced FANCD2 monoubiquitination but normalizes the abnormal G2 arrest in Fanconi anemia.
- Abrogation of G2 checkpoint by Geldanamycin may play a central role in sensitizing p53-negative tumor cells to DNA-damaging and decatenation-inhibiting agents.
- suggests the unique role of Chk1 in preventing abrogation of the G2 checkpoint in p53+/+ cells
- Chk1 inhibition activated p53-regulated transcripts including Puma/BBC3 in tetraploid but not in diploid tumor cells
- A side-by-side comparison of the Hsp90-dependent chaperoning of Chk1 to that of the progesterone receptor (PR) was performed to show that these distinct types of clients have different chaperoning requirements.
- Results suggest that apoptosis induced by replication inhibitors in Chk1-depleted cells is dependent upon the helicase cofactor Cdc45.
- CHK1 is a histone H3 threonine 11 kinase that requires DNA damage-induced transcriptional repression.
- CHK1 was at least partially responsible for the lithium arrested hepatocellular carcinoma cell SMMC-7721 at G2/M checkpoint
- Chk1 and Chk2 regulate the functional associations between hBRCA2 and Rad51 in response to DNA damage
- These results demonstrate that phosphorylation of Claspin within the Chk1-binding domain is catalysed by an ATR-dependent kinase distinct from Chk1.
- Hsp72-depleted cells show defect in phosphorylation and activation of the protein kinase Chk1 by genotoxic stresses, such as UVC irradiation or camptothecin.
- findings show that BCL6 can directly bind to a DNA consensus element in the CHEK1 promoter and repress its expression in normal and malignant B-cells
- Chk1 appears to help defend genomic integrity through effects on several other pathways, including Fanconi anemia proteins, the mitotic spindle, and transcription of cell cycle-related genes [review]
- p53 is activated by stimulation of mismatch repair in response to the misincorporation of deoxynucleotides into newly synthesized DNA, long before the lack of pyrimidine nucleoside triphosphates causes the rate of DNA synthesis to slow appreciably.
- a conserved proliferating cell nuclear antigen-interacting protein sequence in Chk1 is required for checkpoint function
- Data show that Chk1 and the Claspin-Timeless module of replication forks not only participate in ATR signaling, but also protect stressed forks independently of ATR.
- Chk1, but neither Chk2 nor MK2, is an important regulator of S phase arrest, and suggest that an additional kinase can contribute to the G(2) arrest.
- Chk1 is the primary signal transducer linking activation of the ATM/ATR kinases to Cdc25A destruction in response to ionizing radiation.
- Mcl-1, perhaps acting as an adaptor protein, in controlling the ATR-mediated regulation of Chk1 phosphorylation
- Chk1 is activated by caspase-mediated cleavage during apoptosis and might be implicated in enhancing apoptotic reactions rather than attenuating the ATR-Chk1 pathway
- These findings systematically dissect the differential roles of Chk1 and Chk2 in a favorable model pursuing camptothecin-driven DNA damage responses.
- the inhibition of the stress response sensor CHEK1 might contribute to the antineoplastic activity of specific DNA-damaging drugs
- study demonstrates that Chk1 inhibition results in the activating phosphorylation of p38 mitogen-activated protein kinase
- Cyclin B1 is an efficacy-predicting biomarker for antineoplastic Chk1 inhibitors.
- Chk1 protein is a molecular target to be inhibited in tumors with a defective G1 checkpoint to increase the selectivity of anticancer treatments.
- Chk1 is phosphorylated at Ser(317) by ATR resulting in stabilization of CKII, which in turn leads to phosphorylation of PTEN at Thr(383)
- HSP90 inhibition abrogates the topoisomerase I poison-induced G2/M checkpoint in p53-null tumor cells by depleting CHK1 and WEE1.
- Chk1-Ser286 and -Ser301 phosphorylation occurs not only in mitosis but also with stalled DNA replication and stimulation of the damage checkpoint.
- Essential function of Chk1 can be uncoupled from DNA damage checkpoint and replication control
- ATR-Chk1 signalling pathway plays a major role in the regulation of death in response to DNA replication stress and that the Chk1-suppressed pathway protecting cells from replication stress is clearly distinguishable from that protecting cells from IR