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Validated All-in-One™ qPCR Primer for CDC6(NM_001254.3) Search again
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:
Summary
The protein encoded by this gene is highly similar to Saccharomyces cerevisiae Cdc6, a protein essential for the initiation of DNA replication. This protein functions as a regulator at the early steps of DNA replication. It localizes in cell nucleus during cell cyle G1, but translocates to the cytoplasm at the start of S phase. The subcellular translocation of this protein during cell cyle is regulated through its phosphorylation by Cdks. Transcription of this protein was reported to be regulated in response to mitogenic signals through transcriptional control mechanism involving E2F proteins. [provided by RefSeq].
Gene References into function
- Nuclear organization of DNA replication initiation proteins
- CHROMATIN CELLL CYCLE
- downregulation in prostate cancer
- HuCdc6 is cleaved by caspase 3 during apoptosis to prevent a wounded cell from replicating and to facilitate death
- Results show that geminin, cdt1 and cdc6 are differentially regulated during megakaryocytic differentiation and suggest an active role of cdc6 in endomitosis.
- Data show that human Cdc6 (HuCdc6) regulates the onset of mitosis, as overexpression of HuCdc6 in G(2) phase cells prevents entry into mitosis.
- caspase-mediated cleavage of Cdc6 creates a truncated Cdc6 fragment that is retained in the nucleus and induces apoptosis
- endogenous Cdc6 remains nuclear and chromatin bound throughout the entire S period
- Cdc6 expression is regulated during megakaryocytic differentiation through transcriptional mechanisms involving a novel E2 box-GATA element.
- Results further confirm the importance of CDC6 in malignant transformation and in the pathogenesis of cervical dysplasia.
- Androgen receptor may play important role in onset of DNA synthesis in prostate cancer cells by regulating expression and stability of Cdc6, critically required for assembly of pre-replication complex.
- initiation of DNA replication is regulated by p53 through Cdc6 protein stability
- Cdc6 is not only required for G1 origin licensing, but is also crucial for proper S-phase DNA replication that is essential for DNA segregation during mitosis
- aberrant expression of Cdc6 is oncogenic by directly repressing the INK4/ARF locus through the RD(INK4/ARF) element
- Truncated Cdc6 proteins act as dominant-negative inhibitors of replication initiation and disrupt chromatin structure and/or induce DNA damage, leading to ATM/ATR kinase activation and p53-Bax-mediated apoptosis
- These findings demonstrate an important and conserved role for Huwe1 in regulating Cdc6 abundance after DNA damage.
- Cdc6 plays a key role in the sequential molecular events leading to repression of origin licensing and loss of proliferative capacity during execution of the differentiation programme.
- hCdt1 and hCdc6 expression promote malignant behavior
- deregulation of CDC6 expression in human cells poses a serious risk of carcinogenesis [review]
- Data suggest that human Cdc6 functions in several pathways to control the cell proliferation and the cell death.
- PP2A can be targeted in a calcium-regulated manner to Cdc6 via the PR70 subunit, where it plays a role in regulating protein phosphorylation and stability.
- Cdc6 determines utilization of p21(WAF1/CIP1)-dependent damage checkpoint in S phase cells
- rereplication-associated DNA damage triggers Cdt1 and Cdc6 ubiquitination and destruction; this pathway represents an evolutionarily conserved mechanism that minimizes the extent of rereplication
- Polymorphism in the Cdc6 promoter is associated with hepatocellular carcinoma
- A hypothetical model whereby PTEN loss upregulates cell cycle genes such as cdc6 and cyclin E2 that in turn promote metastatic colonization at distant sites.
- Cdc6 mRNA and protein had low expressions in normal oral mucosa but were highly expressed in precancerous lesions and oral squamous cell carcinoma.
